Volume52

Report
of the
Tomato Genetics Cooperative
Number 52 – September 2002
University of Florida
Gulf Coast Research and Education Center
5007 60th
Street East
Bradenton, FL 34203 USA
Foreword
The Tomato Genetics Cooperative, initiated in 1951, is a group of researchers
who share an interest in tomato genetics, and who have organized informally for
the purpose of exchanging information, germplasm, and genetic stocks. The
Report of the Tomato Genetics Cooperative is published annually and contains
reports of work in progress by members, announcements and updates on linkage
maps and materials available. The research reports include work on diverse
topics such as new traits or mutants isolated, new cultivars or germplasm
developed, interspecific transfer of traits, studies of gene function or control or
tissue culture. Relevant work on other Solanaceous species is encouraged as
well.
Membership currently stands at approximately 200 from 34 countries. Requests
for membership (per year) US$15 (plus $5 shipping if international)--should be
sent to Dr. J.W. Scott, Gulf Coast Research and Education Center, 5007 60th
Street East, Bradenton, FL 34203, USA, jwsc@ifas.ufl.edu. Please send only
checks or money orders. Make checks payable to the University of Florida.
We are sorry but we are NOT able to accept cash, wire transfers or credit cards.
Cover photo provided by Roger Chetelat: With Charley Rick’s passing we
have lost one of the great pioneers of tomato genetics who was instrumental in
forming the Tomato Genetics Cooperative. Below is an obituary written by his son
highlighting some aspects of his life and career. It is followed by an article written
by Dick Robinson in 1982 (TGC 32:1-2) that outlines the early history of the
Tomato Genetics Cooperative and Dr. Rick’s critical role in its development. I
know everyone involved in tomato genetics and/or breeding has admiration and
respect for Charley because of his wisdom, accomplishments, and his friendly
demeanor. The main reason I have taken on the editorship of the TGC was
because I considered it an honor to carry on one of Charley’s legacies.
- J.W. Scott

Rick taught and mentored generations of U.S. and international scientists in plant
genetics. His students went on to lead major research institutes, serve as
ministers of agriculture and other governmental roles, and become faculty at
universities on every continent. They have worked on studying and improving
many major crops, including rice, grapes, potatoes, and peppers. His children
continued in academics; his daughter Susan Baldi teaches anatomy and
physiology at Santa Rosa Junior College, and his son John is an archaeologist at
Stanford. Three grandchildren and a great grandchild were his greatest joys in his
last years.
TGC HISTORY Reprinted from TGC Report No. 32, 1982
A HISTORY OF THE TOMATO GENETICS COOPERATIVE
R.W. Robinson
Two graduate students at the University of California at Berkeley, Don Barton and
Allan Burdick, met in the early summer of 1949 with Charley Rick, geneticist at
the Davis campus, for one of their periodic stimulating discussions on tomato
genetics. Their doctoral research on cytogenetics of the tomato had given them
an appreciation for the value of an organization to exchange information on
tomato genetic research, stimulate linkage studies, and preserve and distribute
germplasm, and they urged Rick to consider founding such an organization. The
proposal was further discussed by Burdick, Barton, Rick and others with a
common interest in tomato genetics during a scientific meeting in 1950, probably
at the annual meeting of Genetics Society of America at Columbus, Ohio. The
proposal was received with so much support and enthusiasm that Rick consented
to be Chairman of the Tomato Genetics Cooperative, which was founded in 1950.
The first Report of the TGC was issued in 1951 by C. M. Rick, who served as
editor from then until 1981. The membership of the TGC has grown from 87 in
1951 to 354 thirty years later. It is largely through the efforts of C. M. Rick that
the TGC has become such a useful and renowned publication.
The activities of the TGC are directed by the Coordinating Committee. Members
of the original Coordinating Committee were C. F. Andrus, D. W. Barton, W. H.
Frazier, H. M. Munger, and, as chairman, C. M. Rick. Rick continued to serve as
chairman of the Coordinating Committee for 32 years. Others who have served
on the Coordinating Committee include A. B. Burdick, L. Butler, W. S. Barham, G.
B. Reynard, A. L. Harrison, R. W. Robinson, M. L. Tomes, S. Honma, M. A.
Stevens, and E. C. Tigchelaar.
It soon became apparent to the Coordinating Committee that gene nomenclature
rules were needed for the tomato. The Coordinating Committee appointed a
committee on nomenclature, consisting of D. W. Barton as chairman, L. Butler
and J. A. Jenkins. The Nomenclature Committee formulated nomenclature rules
for tomato mutants, chromosomes, and chromosomal aberrations. The original
nomenclature rules were published in TGC 3, and supplemental rules were given
in TGC 4, 9, 17, 20, and 23.

The Gene List Committee was given the assignment of compiling and publishing
lists of known tomato genes and revising gene symbols when necessary to
conform with nomenclature rules. The first gene list, prepared for TGC 4 by
chairman L. Butler, D. W. Barton, P. A. Young, and C. M. Rick, included 108
tomato genes. The gene list more than doubled in the next five years; 172
additional genes were included in the list in TGC 9. The gene list has continued
to expand, with 99 new genes added to the list in TGC 12, 146 for TGC 17, 88 for
TGC 21, 51 for TGC 23, and 93 additional genes for the list in TGC 29.
The number of tomato genes has grown so large in recent years that there was a
need to categorize them, to classify them into different groups for the
convenience of researchers interested in locating a particular kind of mutant. The
gene list committee, therefore, published in TGC 21 a classification, according to
21 phenotype groups, all of genes known at that time.
The first gene lists for the tomato included sources of seed for each gene. Carl
Clayberg and later Dick Robinson served as coordinators of the stock-keeping
program, assigning volunteers to maintain and distribute seed of each mutant.
This system worked well for many years, but became cumbersome as the
number of known genes greatly increased and some former stock-keepers
retired.
The Tomato Genetics Stock Center was established by C. M. Rick in 1976 to
solve the problem of preserving and making available germplasm for tomato
researchers. The Stock Center published in TGC Reports 27 and 30 lists of
accessions of Lycopersicon and related Solanum species being maintained.
TGC Reports 28 and 31 included lists of mutants in the collection of the Tomato
Genetics Stock Center. Lists in TGC 29 reported other tomato germplasm
maintained by the Stock Center, including allozyme variants, multiple gene
stocks, linkage testers, translocations, tetraploids, trisomics, and cultivars.
For many years, Len Butler coordinated linkage investigations by TGC members.
To prevent duplication in research and to ensure that gene mapping was done
with each of the 12 chromosomes of the tomato, different chromosomes were
assigned to different investigators for linkage testing. In the linkage map
published by Rick and Clayberg in TGC 5, 47 genes were mapped on 11
chromosomes. The linkage map prepared by C. M. Rick for TGC 27 included
288 genes, with each of the 12 chromosomes mapped for marker genes and
position of the centromere.
No history of the TGC would be complete without giving recognition to Dora Hunt,
who has had so much to do with editing the Report, helping with membership
arrangements, and other work for the TGC. Many others have also contributed to
the success of the Tomato Genetics Cooperative, but no one else to the extent of
C. M. Rick. It is largely due to his prodigious efforts that the TGC has prospered
and the tomato has become the pre-eminent plant species for cytogenetic
research. It is a pleasure, on the eve of his retirement, to express gratitude to
Charley Rick for the research, service, and inspiration he has provided for tomato
geneticists.

Professor Charles M. Rick, 1915-2002
Written by his son, John Rick (Stanford Univ., Dept. of Anthropology)
Charles M. Rick, Jr., Professor Emeritus of the University of California, Davis and
the world's foremost authority on tomato genetics, passed away peacefully in the
early morning hours of Sunday, May 5th. Known worldwide for his major scientific
contributions as a plant geneticist and botanist, the majority of Charlie Rick’s
career focused on the genetic variability of the tomato, especially the wild tomato
species distributed widely in western South America and the Galapagos Islands.
In addition to the thorough studies of tomato genes and chromosomes, he
organized numerous plant-collecting expeditions to the Andes to sample the wide
range of genetic variation found in the wild species, but missing from the modern
domestic tomato. Crisscrossing this rugged terrain, he managed to document and
preserve an amazing diversity of tomato varieties with qualities such as disease
resistance that can be bred back into the tomato we know. In his later years, Rick
established and directed the C. M. Rick Tomato Genetics Resource Center at the
Davis campus of the University of California, which serves as a permanent bank
of genetic material for the tomato and other members of the nightshade family.
This center distributes seeds to scientists world-wide, and its holdings include
genetic varieties that have become extinct in the wild.
Born in Reading, Pennsylvania in 1915, Rick grew up working in orchards and
enjoying nature study in the Boy Scouts. He took his B.S. degree at Penn State,
where he met and married the late Martha Overholts, daughter of a well-known
faculty expert on mushrooms. Together they moved to Cambridge,
Massachusetts where he earned his Ph.D. at Harvard in 1940, concentrating on
botany and plant genetics. He had previously established California connections
by working with the Burpee seed company in Lompoc, and as soon as he
finished at Harvard he joined the faculty of the Vegetable Crops Department at
Davis, where he remained for his career of more than 60 years. He taught
temporarily at other universities throughout the world, and remained active in the
field of plant genetics until the age of 85, when health difficulties interfered with
greenhouse and lab work. In the course of his career, Rick accumulated many
honors, including membership in the National Academy of Sciences, and
recognition from dozens of universities and learned societies. He received the
Alexander von Humboldt Award, and was also the first recipient of the Filipo
Maseri Florio World Prize in Agriculture in 1997.
An excellent lecturer, Rick was much sought after by universities who valued both
his rigorous science and his humor and flair for storytelling. A perennial favorite
involved his frustrations in trying to germinate wild tomato seeds collected from
the Galapagos Islands. The emerging mystery of how the plants reproduce in the
wild was only resolved after the seeds were ‘processed’ by passing through the
digestive track of a Galapagos tortoise, resulting in vigorous seedlings. Much of
Rick’s most fascinating work came from a firsthand perception of the plants’ roles
in local environments and their evolving reproductive strategies. Over time, Rick’s
work on tomato genetics established this plant as an important model organism in
the era of genomics.

TABLE OF CONTENTS TGC REPORT 52, 2002
___________________________________________________________________________________
Table of Contents
Foreword………………………………………………………………………………………………...1
Announcements………………………………………………………………………………………..7
Research Reports
Inheritance of resistance to Oidium lycopersici and molecular characterization of resistance
gene in Lycopersicon esculentum var. cerasiforme
Ambrico, A., Longo, O., Schiavone, D., and Ciccarese, F. …………………………….11
Evaluation of tomato breeding material for resistance against late blight pathogen
Bagirova, S.F., Ignatova, S.I., Tereshonkova, T.A., and Gorshkova, N.S. ……………14
Some biochemical and physiological characteristics of transgenic tomato Lycopersicon
esculentum Mill. cv. Ventura
Mapelli, S., Rekoslavskaya, N.I., Salyaev, R. K., Kopytina, T.V., and Ostanina, Y.V. ..18
Introgression of resistance against Mi-1-virulent Meloidogyne spp. from Lycopersicon
peruvianum into L. esculentum
Moretti, A., Bongiovanni, M., Castagnone-Sereno, P., and Caranta, C. ………………21
Differences in susceptibility of pruning wounds and leaves to infection by Botrytis cinerea
among wild tomato accessions
Nicot, P.C., Moretti, A., Romiti, C., Bardin, M., Caranta, C., and Ferrière, H. ………..24
A rise of productivity of transgenic tomato (Lycopersicon esculentum Mill.) by transfer of the
gene iaglu from corn
Rekoslavskaya, N.I., Salyaev, R.K., Mapelli, S., Truchin, A.A., and Gamanetz, L.V. ..27
A new allele at the potato leaf locus derived from L. chilense accession LA 1932 is discovered
in a geminivirus resistance project
Scott, J. W. …………………………………………………………………………………..31
Varietal Pedigrees
Amalia, Mariela
Alvarez, M., Moya, C., Domini, M.E., and Arzuaga, J. ………………………………….35
Ohio OX150 Hybrid Processing Tomato
Francis, D.M., Berry, S.Z., Aldrich, T., Scaife, K., and Bash, W. ….……………………36
Fla. 7771, a medium-large, heat-tolerant, jointless-pedicel tomato
Scott, J.W. …………………………………………………………………………………….38
‘Micro-Tina’ and ‘Micro-Gemma’ miniature dwarf tomatoes
Scott, J.W., Harbaugh, B.K., and Baldwin, E.A. ………………………………………….39
Fla. 7775 and Fla. 7781: Tomato breeding lines resistant to fusarium crown and root rot.
Scott, J.W. and Jones, J.P. ………………………………………………………………40
Stock Lists
Revised List of Monogenic Stocks
Chetelat, R. T. ……………………………………………………………………………….41
Membership List...……………………………………………………………………………………63
Author Index ………………………………………………………………………………………….69

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IN THE ORIGINAL DOCUMENT

ANNOUNCEMENTS TGC REPORT 52, 2002
________________________________________________________________________
From the editor
Regards to the TGC membership from your new editor! First, I would like to give
credit for this report to Ms. Gail Cameron Somodi who has done a large part of
the work. Gail (MS in Plant Pathology) has worked with me for more years than
she would care to count in our bacterial resistance program, and also has
superior editorial and organizational skills. If she was not working for me last year
I may well have not taken on the editorship. I want to also thank former managing
editor Theresa Fulton. I cannot think of anyone else I would rather take over
from. She had things in good order to begin with, and every time we had a
question she was quick to respond. Thanks also to all the contributors of reports
for volume 52 because without you none of this is possible. Finally, thanks for
everyone’s patience with us during the transition. Next year should be more
routine.
The TGC Website has moved and there have been some changes in it. We will
try to update it periodically to keep you abreast of current information and will be
adding links to other relevant tomato genetics addresses. If you have any links to
suggest, send me an email. Many of the old TGC issues are available at the
website thanks to the scanning of Theresa Fulton, Steve Tanksley, and Co. We
hope to keep adding more of them until all are available. The policy will be to wait
a year to put the latest issue on-line, so volume 52 will be on-line in September,
2003. The new web address is:
http://gcrec.ifas.ufl.edu/tgc
There are no longer Associate Editors. I have been trying to set up a Gene List
Committee and the people who have agreed to serve are listed below. The main
function of this committee will be to approve the naming and symbols of new
genes for integration into the tomato gene list. If you are publishing a paper
where you have evidence for a new gene, please bring the paper to the attention
of a committee member and the committee will officially evaluate your evidence
and if approved, it will be listed in the next TGC report. You can also name genes
directly in a TGC paper, of course, and the committee will consider them for
approval.
Gene List Committee:
Jay Scott, University of Florida, Bradenton, FL USA
Roger Chetelat, TGRC, UC Davis, Davis, CA USA
Mathilde Causse, INRA, Montfavet Cedex, France
Pim Lindhout, Wageningen Agricultural Univ., Wageningen,
The Netherlands
Mikel Stevens, BYU, Provo UT, USA
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Managing Editor:
Jay W. Scott
Gulf Coast Research & Education Center
5007 60th
Street East
Bradenton, FL 34203
941-751-7636 ext. 241
e-mail: jwsc@ifas.ufl.edu
Tomato Breeders Roundtable meeting
The next meeting will be held in Park City, Utah, USA from 27-30 April, 2003. For
information about the meeting contact:
Mikel R. Stevens
Department of Agronomy and Horticulture
287 WIDB
Brigham Young University
Provo, UT, 84602
801-378-4032
fax 801-378-2203
e-mail: mikel_stevens@byu.edu
First International Symposium on Tomato Diseases
This meeting will take place from 27-31 October, 2003 at Kusadasi, Turkey. To
find out more about the conference and receive meeting announcements see the
website below:
http://plantdoctor.ifas.ufl.edu/istd.html
Announcement: USDA Funding for Tomato Germplasm Evaluation
Funding will again be available from the USDA, ARS in FY 2003 for evaluation of
tomato germplasm. Evaluation funding will be used on germplasm maintained in
or destined for the National Plant Germplasm System (NPGS). Relevant NPGS
germplasm includes the tomato collection maintained by USDA’s Plant Genetic
Resources Unit in Geneva, New York and the collection at the University of
California, C.M. Rick Tomato Genetics Resource Center, Davis, California.
Proposal guidelines are noted below.
All proposals will be evaluated on the need for evaluation data, national and/or
regional interest in the problem, scientific soundness and feasibility of the
proposal, the likelihood of success, germplasm to be screened, and the likelihood
that data will be entered into NPGS databases and freely shared with the user
community. Proposals will be reviewed by the Tomato Crop Germplasm
Committee (CGC) and applicable ad hoc reviewers and ranked in priority order
for funding. Funding for successful proposals has ranged from $5,000 to
8

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9
$30,000. All proposals and CGC prioritization are forwarded to USDA for a final
decision on funding. Multiple year projects are welcomed, but funding must be
applied for each year and is subject to a progress review.
STANDARD EVALUATION PROPOSAL FORMAT FOR THE NPGS
I. Project title and name, title of evaluators.
II. Significance of the proposal to U.S. agriculture.
III. Outline of specific research to be conducted including the time frame involved
– include the number of accessions to be evaluated.
IV. Funding requested, broken down item by item (no overhead charges are
permitted).
V. Personnel:
a. What type of personnel will be used to perform the research (e.g. ARS,
State, or industry scientist; postdoc; grad student, or other temporary
help).
b. Where will personnel work and under whose supervision.
VI. Approximate resources contributed to the project by the cooperating
institution (e.g. facilities, equipment, and funds for salaries).
The crop curator will enter evaluation data obtained into NPGS databases.
Funding for data entry should be considered when developing proposals.
Evaluation proposals covering several descriptors, such as several diseases,
should give the cost and time frame for each descriptor along with the combined
cost. Funding may only be available to cover one of the projects.
Submission deadline: Electronic submission of proposals is encouraged. Please
submit electronic files (MS Word or WordPerfect) or 10 copies of your proposals
by October 15, 2002 to:
stommelj@ba.ars.usda.gov
John R. Stommel, Chair
Tomato Crop Germplasm Committee
USDA-ARS, Vegetable Laboratory
10300 Baltimore Ave.
Bldg. 010A, BARC-West
Beltsville, MD 20705

RESEARCH REPORTS TGC REPORT 52, 2002
__________________________________________________________________________________________
Inheritance of resistance to Oidium lycopersici and molecular
characterization of resistance gene in Lycopersicon esculentum var.
cerasiforme
Ambrico, A., Longo, O., Schiavone, D., and Ciccarese, F.
Department of Biology and Plant Pathology - University of Bari, Italy
Via G. Amendola 165/A, 70126 Bari, Italy, E-mail: fciccare@agr.uniba.it
Introduction
Powdery mildew caused by Oidium lycopersici is a serious disease of
glasshouse-grown tomato. The use of resistant cultivars is an economical and
ecologically sustainable method of disease control. A resistance source,
incompletely dominant (Ol-1), was found in Lycopersicon hirsutum (Lindhout and
Pet, 1990). In screenings for powdery mildew resistance on numerous
accessions of Lycopersicon species, supplied by the Tomato Genetics
Cooperative, two plants of accession LA-1230 of L. esculentum var. cerasiforme,
showed no symptoms of disease. One symptomless plant was selfed and
progeny (designated LC-95) were resistant.
In this paper, results of research aimed at characterization of a new source
of resistance to powdery mildew are reported. Furthermore random amplified
polymorphic DNA (RAPD) markers linked to resistance gene are screened.
Materials and Methods
Tests on powdery mildew resistance were carried out in a glasshouse at
23±2°C and at 80±5% relative humidity. For studies on inheritance of resistance
identified in L. esculentum var. cerasiforme, a plan of crosses and self-fertilization
was set up. The tomato cultivar ‘Super Marmande’ as susceptible parent and LC-
95 line as resistant were used. The progenies of F1, F2 and backcrosses with the
resistant parent (BC-R) and with susceptible parent (BC-S) were submitted to
artificial inoculation with O. lycopersici. About 200 plants were used for all
generations. Inoculations were carried out by dispersing pathogen conidia,
removed from heavily infected tomato plants, on the leaves of tested plants at the
six-leaf stage. Powdery mildew symptoms were evaluated 20 days after artificial
inoculations considering the percentage of leaf area covered by colonies of O.
lycopersici.
For molecular characterization 240 different primers were tested. RAPD
analysis on the F2 generation was performed according to bulked segregant
analysis (Michelmore et al., 1991). Resistant (R) and susceptible (S) bulks were
tested using DNA extracted from ten healthy (resistant) and ten diseased F2
plants which were seen to be homozygous for the powdery mildew resistant gene
after segregation analysis on F3 plants.
Results and Discussion
All plants of ‘Super Marmande’ cultivar were highly infected. Plants of LC-
95 line were resistant. F1 progeny was susceptible and F2 progeny segregated
resistant/susceptible plants in a ratio of 1:3. All plants of BC-S were susceptible
while the progeny of BC-R segregated in ratio of 1:1 (Tab. 1). The segregation
ratios suggested that resistance to O. lycopersici in LC-95 line of L. esculentum
var. cerasiforme is conferred by a single recessive gene designed ol-2. The
screening on DNA extracted from parents allowed us to characterize only 45
11

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polymorphic primers. On bulks, primer OPU3 (5’-CTATGCCGAC-3’ with a
molecular weight of 2979 bp) showed polymorphism between bulks. With OPU3
primer, a DNA fragment of 1500 bp (designed OPU3 1500) was amplified and by
agarose gel electrophoresis, a well defined band present in the susceptible bulk
but not in the resistant bulk was observed (Fig. 1). The OPU3 marker was closely
linked with susceptibility to O. lycopersici.
Literature cited
Lindhout P. and Pet G., 1990. Resistance to Oidium lycopersici in Lycopersicon
species. Tomato Genetics Cooperative Report 40, 19.
Michelmore R. W., Paran I., Kesseli R. V., 1991. Identification of markers linked
to disease-resistance genes by bulked segregant analysis: a rapid method to
detect markers in specific genomic regions by using segregating populations.
Proceedings of the National Academy of Sciences USA 88: 9828-9832.
Table 1. - Observed segregation for powdery mildew resistance of LC-95 line of
Lycopersicon esculentum var. cerasiforme and goodness of fit test.
Number of plants
Pedigree
Ra
S
Expectedb
ratio
χ2
P
LC-95 72 0 72:0 - -
Super Marmande 0 97 0:97 - -
F1 0 96 0:96 - -
F2 30 70 25:75 1.33 0.25-0.30
BC-R 49 51 50:50 0.04 0.80-0.90
BC-S 0 100 0:100 - -
a
R =resistant and S = susceptible
b
Assuming a single recessive gene for resistance
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Figure 1. Agarose gel showing the RAPD pattern obtained with the OPU3 1500
primer linked to susceptibility to Oidium lycopersici in tomato.
13

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Evaluation of tomato breeding material for resistance against late blight
pathogen
1
Bagirova, S.F., 2
Ignatova, S.I., 2
Tereshonkova, T.A., and 2
Gorshkova, N.S.
1
Department of Mycology and Algology, Moscow State University, Moscow
119899, Russia, e-mail: slana@sbagirova.home.bio.msu.ru
2
All-Russian Research Institute for Vegetable Crops, Mitishi-18, Moscow Region
141018, Russia, e-mail: tter@msk.net.ru
Key words: disease resistance, evaluation, late blight, Phytophthora infestans,
plant breeding, population structure, tomato
Abstract
In three late blight epidemic years (1998-2000) selected tomato breeding material
were evaluated under natural conditions of a severe epiphytotic in greenhouses
in the Moscow Region. More than 1500 tomato lines or hybrids were screened for
resistance against a new more aggressive population of the tomato late blight
pathogen. Eighteen lines were created using different wild tomato species as
resistant sources and these were found to show the greatest resistance to the
late blight. Simultaneously, Phytophthora strains were collected from diseased
plants and studied. High polymorphism of the new sexual population of the late
blight pathogen that was similar to polymorphism of the Mexican populations was
revealed. Our data concerning population diversity suggests that the monitoring
of P. infestans in the Moscow Region is a good model for study of different
aspects of population biology of P. infestans (the spread of new pathotypes, role
of oospores in disease development, interrelationships between the tomato and
potato populations) and for reevaluation of plant breeding material.
Introduction
The most severe plant disease in Russia is late blight. Tomato crop losses in
epidemic years in the Moscow Region can be greater than 80%. Russian
populations of Phytophthora infestans, the causal agent of the late blight, are
characterized by high polymorphism and variability. During the last 15 years there
has been a change of population structure and increase of population size of
strains adopted to parasitize tomatoes (Dyakov Y.T., Rybakova I.N., Dolgova
A.V., Bagirova S.F., 1994). Marked differences between the populations attacking
tomatoes and potatoes were found (Bagirova S.F., An Dzan Li, Dyakov Y.T.,
1998). Until now only one clone has predominated. Tomato late blight has not
been considered such a big problem in the Moscow Region. Variability of new
populations is expressed in differences between strains in the mating types,
virulence, resistance to fungicides, isozymes, mitochondrial and nuclear DNA
(Vorobeva Y.V., Gridnev V.V., Bashaeva E.G., 1991, Gorbunova E. V., Bagirova
S.F., Dolgova A.V., Dyakov Y.T., 1989; Maleeva Yu.V., Naumoff S.P., Yatsentiuk
S.P., Dolgova A.V., Kolesnikov A.A., 1999). With the spread of new strains, the
disease epidemics appeared earlier and developed rapidly. Abundant oospores
are formed in foliage, stem and fruit tissue and are able to overcome cold
Moscow winters (Bagirova S.F., Dyakov Y.T, 1998). The tomato cultivars that
were previously characterized by moderate resistance are now very susceptible
(Ignatova S.I., Gorshkova N.S., Bagirova S.F., 1999). Registered changes of
population composition are similar to replacement of ”old” genotypes by “new”
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ones that are detected in West Europe and North America (Fry W., Goodwin S.,
Matuszak J. et al, 1991; Drenth A., Turkensteen L., Govers F., 1993; Day J.P.,
Shattock R.C., 1997). This changed situation requires reevaluation of tomato
patterns for resistance to the new populations of the late blight pathogen. Our
study was aimed at evaluating tomato breeding material in naturally occurring
epidemics in the Moscow Region.
Materials and methods
During three epidemic years (1998–2000) we screened for resistance to the late
blight tomato collection including more then 1500 tomato accessions of
interspecies hybrids and selected lines. This plant material was obtained from
VNIO (All-Russian Institute for Vegetable Crops, Mitichi, Moscow Region, Russia)
and VIR (Vavilov Plant Research Institute, St. Petersburg, Russia). Evaluation
was carried out in greenhouses of VNIO in Bukovo, the Moscow Region.
The susceptible control genotype was a commercial hybrid widely grown in
Russia, provided by VNIO. The resistant control was West Virginia 63. The
accessions were supplied by VIR. Tomato stem, fruit, and foliage infections were
taken into account. Scale (0-4 marks) for each organ was involved.
Simultaneously Phytophthora isolates were collected from different tomato
organs, and isolated in pure culture on oatmeal agar. Obtained isolates were
assessed for the mating types, resistance to fungicides: dimethomorph and
metalaxyl, pathogenic features, and molecular markers. To assess the mating
type the strains were crossed on oatmeal medium with both the A1 and A2
testers, obtained from the Dep. Mycology and Algology, Moscow State University.
The mating type was determined by inspecting for presence or absence of
oospores in a border zone between grown colonies. Resistance to fungicides was
determined by growing of the isolates on oatmeal medium supplemented with
dimethomorph in concentration 3mg/ml, or with metalaxyl in concentration 10 or
100 mg/ml. Tomato races of the pathogen were defined using a bioassay to
inspect for disease symptom control patterns on Talallixin (Ph-0), Ottawa-30 (Ph-
1), and West Virginia 63 (Ph-2). PCR-tests to define mitochondrial and nuclear
DNA-polymorphism were performed as described elsewhere (Drenth et al, 1993;
Maleeva et al, 1999).
Results
The pathogen attacked all above ground parts of tomato plants: stems, fruits,
foliage branches and even flowers. Data on average severity accounted
separately for each organ were obtained. Eighteen selective lines (Backcrosses,
F3-F8 generations) showed the highest resistance for all organs (0-2 marks).
Susceptible control plants were severely diseased (4 marks). The results are
presented in Table 1. These lines were created involving different tomato wild
species, such as: L. esculentum var. cerasiforme, L. pimpinellifolium, L. hirsutum,
L. hirsutum var. glabratum, L. peruvianum, L. humboldtii, and L. cheesmanii.
15

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Table 1
Disease severity, marksTomato sample
Foliage Stems Fruits
Resistant control 2 1 2
Susceptible control 4 4 4
LLB 98/00-1 1 1 1
LLB98/00-2 2 1 1
LLB 98/00-3 1 0 1
LLB 98/00-4 2 1 1
LLB 98/00-5 1 0 1
LLB 98/00-6 1 0 0
LLB 98/00-7 1 1 2
LLB 98/00-8 2 1 1
LLB 98/00-9 2 1 1
LLB 98/00-10 1 1 1
LLB 98/00-11 2 1 1
LLB 98/00-12 1 0 1
LLB 98/00-13 1 1 2
LLB 98/00-14 2 1 1
LLB 98/00-15 1 0 1
LLB 98/00-16 2 1 1
LLB 98/00-17 1 1 1
LLB 98/00-18 1 1 1
Our data indicate that the most prospective tomato breeding material is based on
a combination of different resistant sources. For example, lines combining
features of interspecies hybrids L. esculentum x L. humboldtii, L. esculentum x L.
pimpinellifolium, L. humboldtii x L.esculentum var. cerasiforme, L. peruvianum x
L. hirsutum var. glabratum, L. hirsutum var. glabratum x L. esculentum var.
cerasiforme, and L. cheesmanii x L. humboldtii.
Collected Phytophthora strains appeared to be susceptible to both metalaxyl in
concentration 10 and 100 mg/ml and dimethomorph in concentration 3 mg/ml.
Tomato strains were distinct from those isolated from the potato crops in the
same region. Highly resistant metalaxyl strains predominated in those
populations. Tested tomato strains differed in molecular markers and
aggressiveness. Both A1 and A2 strains were found. Data on population structure
confirm high polymorphism of Phytophthora in the new sexual population.
The most aggressive strains will be used in laboratory bio-assays for further
screening selected tomato genotypes for the late blight resistance.
References:
Bagirova S.F., Dyakov Yu.T. 1998.Ob uchastii oospor v vesenem vozobnovlenii
Infekcii fitoftoroza tomata (The role of oospores in overwintering of
Phytophthora infestans on tomato crops).Selskoxozyistvennaya biologiya. 3:
69-72.
16

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Bagirova S.F., An Zan Li, Dyakov Yu.T. 1998. Mexanizmy geneticheskoy izolycii
specificheskix patogennyx form Phytophthora infestans v polovyx i bespolyx
populyciyax (Mechanisms of genetic isolation for specific pathogenic forms of
Phytophthora infestans in sexual and asexual populations). Mikologia i
fitopatologia.32: 47-50.
Day J.P., Shattock R.C. 1997 Aggressiveness and other factors relating to
displacement of populations of Phytophthora infestans in England and Wales.
Eur. J. Plant. Pathol. 103:379-391.
Drenth A., Turkensteen L., Govers F. 1993 The occurrence of the A2 mating
type of Phytophthora infestans in the Netherlands: significance and
consequences. Netherlands J. Plant Pathology. 99: 57-67.
Dyakov Yu.T., Rybakova I.N., Dolgova A.V. Bagirova S.F. 1994. Divergencia
populyciy fitopatogennogo griba Phytophthora infestans v svyzi so
specializaciey k rasteniym-xozyevam. (Divergent evolution of plant pathogenic
fungi Phytophthora infestans in connection to specialization to host plants).
Zurnal obshey biologii. 55:179-188.
Fry W.E., Goodwin S.B., Matuszak J. et al. 1992. Population genetics and
intercontinental migrations of Phytophthora infestans. Annu. Rev. Phytopathol.
30:107-129.
Gorbunova E.V., Bagirova S.F., Dolgova A.V., Dyakov Yu.T. 1989.Vegetativnaya
nesovmestimost y fitopatogennogo griba Phytophthora infestans (Vegetative
incompatibility in Phytophthora infestans). DAN SSSR. 304: 1245-1248.
Maleeva Yu.V., Naumoff D.G.., Yatsentiuk S.P., Dolgova A.V., Kolesnikov A.A.
1999. Changes in the composition of populations of Phytophthora infestans in
Russia in the 1990s based on the results of mitochondrial DNA analysis.
Genetika. 35:1170-1181.
Vorobeva Yu.V., Gridnev V.V., Bashaeva E.G. et. al. 1991. O poyvlenii izolytov
A2 tipa sovmestimosti Phytophthora infestans na territorii SSSR (About
appearance of the A2 mating type of Phytophthora infestans in USSR).
Mikologiya i fitopatologiya. 25: 62-67.
Acknowledgements:
The work was partly supported by ISTC.
We acknowledge the support granted by RFFI “Leading scientific schools”.
17

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Some biochemical and physiological characteristics of transgenic tomato
Lycopersicon esculentum Mill. cv. Ventura
2
Mapelli S., 1
Rekoslavskaya N. I., 1
Salyaev R. K., 1
Kopytina T. V., 1
Ostanina Y. V.
1
Siberian Institute of Plant Physiology and Biochemistry, Siberian Branch of RAS, PO
Box 1243, Irkutsk, Russia, e-mail phytolab@sifibr.irk.ru
2
Istituto Biologia Biotecnologia Agraria, C.N.R., via Bassini 15, Milan, Italy, e-mail
mapo@ibv.mi.cnr.it
The aim of the project was to create the transgenic plants with high energy of
growth and improved productivity via the transfer of the gene iaglu encoding the
enzyme UDPG-transferase in maturing corn endosperm (Zea mays L.). UDPG-
transferase (indoleacetic acid glucose synthase by trivial name) is converted IAA to IAA-
glucose, the stored, but easily transported and hydrolysable, form of this phytohormone.
In a previous report transgenic tomato plants (Lycopersicon esculentum Mill.) were
obtained in which there was a good correlation between the enhanced auxin status,
higher growth activity and improved productivity of transgenic plants in comparison with
controls. Here comparisons between control and transgenic to have indication of fruits
quality are presented.
Some biochemical and physiological characteristics were presented in Table 1. The
dry matter of control plants were higher in leaves but not in fruits. The water content in
leaves of transgenic plants was correlated with higher content of indoleacetic acid (IAA)
which usually increased the hydraulic pressure in cells. Contents of sugars and organic
acids were quite the same in fruits both from transgenic and control plants but the
content of vitamin C was higher in control fruits.
Table 1. Characteristics of fruits of L. esculentum Mill. cv. Ventura
Dry matter (%)___
Leaves Fruits
Sugars
(% of d. m.)
Organic acids*
(% of d. m.)
Vitamin C
(% of d. m.)
Control 11.2±0.9 6.1±0.1 3.5±0.1 0.47±0.01 0.439±0.0033
Transgenic 8.9±0.5 6.3±0.1 3.5±0.1 0.51±0.01 0.369±0.0032
*Calculated as malic acid equivalents.
We reported that the yield of red fruits in transgenic Ventura tomato plants was up to
1.3 time of the control Ventura plants and the size of red mature fruits were larger. The
dry matter data in Table 1 showed that fruit enlargement was not due to the water
accumulation and dilution of cell contents. The quality and taste of transgenic tomato
was appreciated to be about the same as in control ones.
The total amino acids contents were measured in fruits and in leaves (Table 2),
because leaves were suggested to be a source of amino acids for fruits. In green and
red fruits the contents of total free amino acids were higher when excluding slightly
lower content of Phe in green fruits. Analyzing the L-amino acids composition it was
18

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found that amounts of Lys, Arg, Asp, Glu, Val, Met, Leu, iLeu, Tyr and Phe were higher
in transgenic fruits and the content of Pro, Gly and Ala were lower. If the change in
amino acids composition in fruit and the increase in vitamin C can be accompanied with
change in other substances (i.e. carotenoids) and influence the fruit nutritional value will
be a point to investigate. Larger pool of lower molecular weight compounds, such as
amino acids, in plants has the role to balance the osmotic pressure in cells in order to
overcome water stress.
Table 2. Total amino acids contents in leaves and fruits of tomato cv. Ventura
(nmol/g fresh weight).
Leaves Green fruits Red fruits
Control 4206.2 5208.4 5557.5
Transgenic 4931.3 6349.1 8899.5
Leaves of transgenic plants cv Ventura contained more water then the control
(Table 1), perhaps the abundance of low molecular weight compounds balanced the
osmotic pressure in cells in order to maintain water content high and to overcome
drought and water stress.
Measurement of leaf gas exchange (Table 3) indicated that the Ventura transgenic
plants have higher net carbon dioxide assimilation and lower stomatal conductance and
water transpiration indicating a possible higher efficiency of water use.
Table 3. Comparison of leaf gas exchange between control and transgenic tomato.
Net
photosynthesis
Water vapor
transpiration
Stomatal
Conductance
µmol m-2
s-1
mmol m-2
s-1
mol m-2
s-1
30th June
Control 11.20±0.2199 11.07±0.003483 1.791± 0.7129
Transgenic 13.35±0.2610 9.073±0.003649 0.8248±0.1983
31st July
Control 12.56±0.6676 12.40±0.1264 1.647±0.6759
Transgenic 15.55±0.4139 9.888±0.09210 0.8225±0.2395
During Siberian summer the tomato cultivation occurred under a plastic greenhouse
and hot temperatures occurred sometimes. In this condition both control and transgenic
plants wilted but the recovery was faster in transgenic tomato plants than in control
19

______________________________________________________________________
ones. This evidence supports the idea about more favorable relationship between water
use and growth capacity of the iaglu transgenic tomato plants.
Recently a tryptophan racemase was found in wheat leaves (Rekoslavskaya et
al.1999) that was activated during drought and osmotic stresses. As a result the amino
acid D-tryptophan appeared as if it was used for IAA biosynthesis as an additional and
direct precursor source during period of recovery after drought. Preliminary studies of
the tryptophan racemase activity were carried out in excised tomato leaves. In turgid
control tomato leaves the activity was lower than in transgenic. Artificially wilting the
leaves, placing on 0.5M mannitol solution, the activity of tryptophan racemase increased
in leaves of transgenic plants and diminished in control leaves.
As a whole the insertion of iaglu gene in tomato plants seems to have effects useful
in tomato cultivation and productivity.
Literature Cited
Rekoslavskaya N. I., Yurjeva O. V., Salyaev R. K., Mapelli S., Kopytina T. V., 1999.
Bulgar. J. Plant Physiol. 25: 39-49.
20

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Introgression of resistance against Mi-1-virulent Meloidogyne spp. from
Lycopersicon peruvianum into L. esculentum
1
Moretti, A., 2
Bongiovanni, M., 2
Castagnone-Sereno, P., 1
Caranta, C.
1
INRA, Genetics and Breeding of Fruits and Vegetable, Dom. St Maurice, BP94, 84143
Montfavet cedex, France. E-mail : caranta@avignon.inra.fr
2
INRA, Interactions Plantes Micro-organismes et Santé Végétale, 123 Boulevard F.
Meilland, BP 2078, 06606 Antibes cedex, France. E-mail : pca@antibes.inra.fr
Root-knot nematodes (Meloidogyne spp.) are one of the main pathogens of
tomato crops worldwide. Up to now, all tomato cultivars with resistance to Meloidogyne
originated from a single resistant L. peruvianum interspecific F1 plant carrying the
dominant gene Mi-1 (Smith, 1944). Mi-1 is effective against M. incognita, M. arenaria
and M. javanica but there have been several reports of field or laboratory-selected
isolates from the three species able to reproduce on tomato plants with Mi-1
(Castagnone-Sereno et al., 2001). Moreover, the need for introgression of additional
resistance genes against root-knot nematodes increased with the prohibition of the
nematicide methyl bromide, from 2005 in all the European Union.
Among the resistance sources and genes against nematodes available in wild
tomato species, the Mi-3 gene from L. peruvianum family VWP2x4 is of particular
interest since it is effective against M. incognita strains virulent on Mi-1 and also confers
resistance at 32°C (Yaghoobi et al., 1995).
Seeds from the L. peruvianum family VWP2x4 homozygous for Mi-3 (based on
DNA marker NR14) were kindly provided by V. Williamson (Univ. California, Davis,
USA). This material was also homozygous for Mi-1 as indicated by the DNA marker
REX-1. Five plants VWP2x4 homozygous for both Mi-3 and Mi-1 were hybridized with L.
esculentum Momor sp. (an INRA near isogenic line in the Moneymaker type containing
the Ve, Frl and Tm-22
resistance genes and the sp gene, Laterrot, 1996) used as the
female parent. Buds were emasculated and immediately pollinated with pollen from L.
peruvianum; the same buds were pollinated at least two other times at 2-days intervals.
Fruits were harvested 30-32 days after. The 371 fruits obtained presented 0 to 3 seeds
per fruit; among them, a single one presented an immature embryo. Classical embryo
rescue technique leads to a single F1 hybrid plant (Smith, 1944).
Cuttings of the interspecific F1 hybrid were evaluated for resistance against M.
incognita, M. arenaria, M. javanica using both Mi-1-avirulent and Mi-1-virulent isolates
and also against M. hapla (not controlled by Mi-1) during two independent tests (Table
1). Resistance evaluation was performed as described in Castagnone-Sereno et al.
(2001) and the behavior of the interspecific F1 hybrid was compared with those of the L.
esculentum Saint Pierre (susceptible to Meloidogyne spp.) and Piersol (homozygous for
Mi-1).
As expected, L. esculentum Saint Pierre is highly susceptible to all strains of M.
incognita, arenaria, javanica and hapla. L. esculentum Piersol is resistant only against
M. incognita Antibes, M. arenaria Marmande and M. javanica Avignon ; this resistance
spectrum results from the presence of Mi-1. On the contrary, the Mi-1-virulent isolates
reproduce well on Piersol. Both the parental line L. peruvianum VWP2x4 and the
21

______________________________________________________________________
interspecific F1 hybrid are completely resistant to M. incognita, including strains able to
overcome Mi-1. Interestingly, they are also partially resistant to M. arenaria and M.
javanica strains able to overcome Mi-1. This resistance spectrum probably results from
the presence of Mi-3 or other unknown resistance genes. As already known for Mi-1,
Mi-3 does not control M. hapla.
In order to continue introgression into L. esculentum and to better characterize
resistance against Mi-1-virulent strains, the F1 hybrid was back-crossed with L.
esculentum Momor sp. (used as the female parent). Among the 109 fruits obtained, the
embryo rescue technique led to 10 BC1 plants. This material is currently being
evaluated for resistance against Mi-1-virulent and -avirulent Meloidogyne spp.
Literature cited:
Castagnone-Sereno, P., Bongiovanni, M., Djian-Caporalino, C. 2001. New data on the
specificity of the root-knot nematode resistance genes Mi1 and Mi3 in pepper.
Plant Breeding 120 : 429-433.
Laterrot, H. 1996. Twenty near isogenic lines in Moneymaker type with different genes
for disease resistances. TGC Report 46.
Smith, P.G. 1944. Embryo culture of a tomato species hybrid. Proc. Am. Soc. Hort. Sci.
44 : 413-416.
Yaghoobi, J., Kaloshian, I., Wen, Y., Williamson, V.M. 1995. Mapping a new nematode
resistance locus in Lycopsersicon peruvianum. Theor. Appl. Genet. 91 : 457-464.
22

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Table 1 : Screening for Meloidogyne spp. resistance in the interspecific F1 hybrid
(Momor sp X VWP2x4).
Nematode strains L.
esculentum
Saint Pierre
L.
esculentum
Piersol (Mi1)
Interspecific F1
(Momor sp x
VWP2x4)
L. peruvianum
VWP2x4
M. incognita
Antibes (avira
.) 43b
(6)c
0 (6) 0 (13)*
Adiopodoumé
(avir.)
46.2 (12) 0 (12) 0 (29)
Adiopodoumé (vir.) 47.2 (12) 45.6 (12) 0.2 (26)
N'Gorom (vir.) 30.6 (6) 19.3 (6) 0 (10)
Valbonne (vir.) 46.2 (6) 46.3 (6) 0.2 (14)* 0.4 (27)
M. arenaria
Marmande (avir.) 40.2 (6) 0 (6) 0.1 (13)*
Saint Vincent (vir.) 46 (12) 45.8 (10) 6.6 (25)
Grau du Roi (vir.) 29.8 (6) 13.5 (6) 7.4 (13)*
Chateau-Belair
(vir.)
31.3 (6) 28.4 (6) 9.5 (10)
M. javanica
Avignon (avir.) 37 (6) 0 (6) 0 (13)*
Canaries (vir.) 31.8 (6) 37.8 (6) 2.5 (13)* 15.8 (26)
Turquie (vir.) 46 (6) 39.2 (6) 3.1 (10)
M. hapla
La Môle 14.7 (6) 30.2 (6) 15.3 (10)
* indicates that resistance was assessed during two independent tests.
a
Avir. indicates Meloidogyne isolates that are avirulent on tomato plants with Mi-1 ; vir.
indicates Meloidogyne isolates that are virulent on tomato plants with Mi-1.
b
Average number of egg masses 8 weeks after inoculation with 50 J2.
c
number of evaluated cuttings.
23

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Differences in susceptibility of pruning wounds and leaves to infection by
Botrytis cinerea among wild tomato accessions
1
Nicot, P. C., 2
Moretti A., 1
Romiti, C., 1
Bardin, M., 2
Caranta C., 1
Ferrière H.
INRA, 1
Plant Pathology Unit, and 2
Genetics and Breeding of Fruits and Vegetable,
Domaine. St Maurice, BP 94, 84143 Montfavet cedex, France.
E-mail : Philippe.Nicot@avignon.inra.fr
Control of gray mold caused by Botrytis cinerea, a key problem in greenhouse
production of tomato, has mostly been focused on cultural methods and the use of
fungicides and biological control agents (Nicot and Baille, 1996). Recent reports on
possible sources of partial resistance in Lycopersicon esculentum and related species
(Chetelat and Stamova, 1999, Egashira et al., 2000, Nicot et al., 2000) have prompted
interest in the possibility of breeding tomatoes less susceptible to B. cinerea. The
purpose of the present study was to explore the potential of different tomato accessions
as possible sources of resistance in a germplasm collection maintained at the plant
breeding unit of INRA-Avignon. Work was focused on wild tomatoes in the genus
Lycopersicon.
Plants were grown in a greenhouse in individual pots containing a type P3
horticultural mix (De Baat, Coevorden, The Netherlands) and watered daily with a
nutrient solution. The plants were staked and axillary shoots were removed regularly to
maintain a plant architecture (single stem) similar to that in commercial production.
After 8 weeks of growth, the plants had 10-12 leaves for most accessions. Some
species such as L. hirsutum and L. pimpinellifolium tended to have more (12-14) while
others such as L. pennellii tended to have fewer (9) leaves per plant.
To mimic leaf pruning, a common agricultural practice in greenhouse production,
three leaves were removed from the lower part of each of five plants per accession,
leaving 5-10 mm petiole stubs on the stems. Each pruning wound was inoculated with
10µl of a spore suspension containing 107
conidia of B. cinerea per ml from a 10-day
old colony on Potato Dextrose Agar. To minimize genetic variability among spores of
the pathogen, a mono-ascospore isolate was used (isolate SAR 11092, kindly provided
by M. Boccara, University of Paris-6). After complete absorption of the inoculum into
the wounds (10-15 minutes), the plants were transferred to a growth chamber and
incubated in conditions conducive to disease development. The wounds were
examined for infection and the length of each developing stem lesion was recorded 4, 7,
and 14 days after inoculation. Sporulation occurred rapidly on lesions and the
manipulation of plants for disease rating contributed to the dispersion of abundant
secondary inoculum throughout the air of the growth chamber. The resulting leaf
infections were recorded at 14 days after inoculation on a scale from 0 (no lesion) to 5
(up to 50% of necrotic leaf area). On many accessions, intumescences developed on
stems and/or leaves, presumably in relation with the confined environment in the growth
chamber (Moreau et al., 1997). They were rated as described by Moreau et al. (1997),
on a scale from 0 (no intumescence) to 4 (up to 30% of leaf or stem surface covered).
Three independent trials were conducted.
24

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Wound infection was recorded on all accessions. In all cases the pathogen was
able to colonize the petiole stub, but significant quantitative differences were observed
among accessions for the subsequent development of stem lesions (Table 1). Stem
colonization was most severe on the fixed line Mospomorist of L. esculentum, used as a
susceptible control, and it was least severe among accessions of L. hirsutum and L.
peruvianum. For these less susceptible accessions, the size of the stem lesions rarely
increased beyond the diameter of the petiole.
Partial resistance was also observed on leaves. Compared to L. esculentum,
symptoms were significantly reduced on several accessions such as L. chmielewskii
731089 and L. chilense LA1969 (Table 1). There was little correlation between
susceptibility of stem and leaf tissue (r² < 0.04), and the accessions with significantly
smaller stem lesions were equally or more susceptible to leaf infection than L.
esculentum. However, the development of Botrytis lesions on the leaves appeared to
be partially related to that of intumescences (Table 1).
Stem lesions represent the most frequent and the most damaging of Botrytis
symptoms in heated glasshouses where excess humidity is usually avoided. In this
context, the high level of partial resistance to stem colonization found within the species
L. hirsutum appears promising for breeding less susceptible tomatoes. Further work
has been focused on the genetics, mechanisms and durability of partial resistance.
Literature cited :
Chetelat, R.T., Stamova, L. 1999. Tolerance to Botrytis cinerea. Acta Horticulturae
487:313-316.
Egashira, H., Kuwashima, A., Ishiguro, H., Fukushima, K., Kaya, T., Imanishi, S. 2000.
Screening of wild accessions resistant to gray mold (Botrytis cinerea Pers.) in
Lycopersicon. Acta Physiologiae plantarum 22:324-326.
Moreau, P., Thoquet, P., Laterrot, H., Moretti, A., Olivier, J., Grimsley, N.H. 1997. A
locus, ltm, controlling the development of intumescences, is present on
chromosome 7. TGC Report 47:15-16.
Nicot P.C., Baille A. 1996. Integrated control of Botrytis cinerea on greenhouse
tomatoes. In: C.E. Morris, P.C. Nicot and C. Nguyen Thé (eds.). Aerial Plant
Surface Microbiology. Plenum Publisher New York, ISBN 0-306-45382-7. pp 169-
189.
Nicot P.C., Pellier A.L., Moretti A., Caranta C., Rousselle P. 2000. Resistance of
tomato to Botrytis cinerea. 12th. International Botrytis Symposium, Reims,
2000/07/03-08. University of Reims Champagne-Ardenne, Reims, France.
Abstract .P77.
Acknowledgements: This work was supported in part by private breeders: Gautier
Graines, Rijk-Zwaan France SARL, Seminis Vegetable Seeds France S.A., Syngenta
Seeds S.A.S., Takii Recherche France S.A., Tézier S.A., Vilmorin.
25

______________________________________________________________________
Table 1 : Susceptibility of Lycopersicon accessions to Botrytis cinerea and to
development of intumescences.
stem lesions1
leaf lesions2
intumescences3
L. hirsutum LA1777 2,0 a 2,7 cde 2,5 defg
L. hirsutum PI247087 4,2 ab 3,5 def 3,4 ghi
L. hirsutum H2 4,2 ab 2,3 bc 1,7 bcdef
L. hirsutum G11560 4,7 ab 2,9 cde 2,9 fghi
L. hirsutum PI134417 5,1 ab 3,5 def 2,6 efgh
L. peruvianum CMV - Sel
INRA
5,3 ab 2,7 cde 2,1 bcdef
L. peruvianum PI 128660 5,4 ab 2,4 bcd 2,2 cdefg
L. hirsutum B 6,0 ab 3,6 ef 3,8 hi
L. pimpinellifolium L3708 6,5 ab 3,0 cde 1,7 bcdef
L. chilense LA1969 7,4 ab 0,1 a 0,4 ab
L. peruvianum D4xD5 7,6 ab 3,0 cde 2,2 cdefg
L. hirsutum PI134498 8,0 ab 1,0 ab 0,0 a
L. pennellii Clayberg 8,5 ab 1,5 b 0,0 a
L. chmielewskii 731089 8,6 ab 0,3 a 0,1 a
L. pimpinellifolium WVA700 11,6 abc 2,7 cde 1,5 abcde
L. hirsutum PI390660 13,4 bc 1,1 ab 1,0 abc
L. pimpinellifolium WVA106 14,4 bc 3,0 cde 1,3 abcd
L. pimpinellifolium hirsute 19,7 c 4,6 f 3,9 i
L. pennellii LA716 19,9 c 1,9 bc 0,1 a
L. esculentum Mospomorist 20,4 c 2,2 bc 0,0 a
1
lesion size (mm) 14 days after inoculation (average for 3 replicated independent tests);
numbers followed by different letters were statistically different (p<0.05) according to
Tukey's HSD test
2
average disease index 14 days after inoculation (average for 2 replicated independent
tests); numbers followed by different letters were statistically different (p<0.05)
according to Tukey's HSD test
3
average index of intumescence on leaves 7 days after inoculation (average for 2
replicated independent tests); numbers followed by different letters were statistically
different (p<0.05) according to Tukey's HSD test
26

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A rise of productivity of transgenic tomato (Lycopersicon esculentum Mill.) by
transfer of the gene iaglu from corn
1
Rekoslavskaya N. I., 1
Salyaev R. K., 2
Mapelli S., 1
Truchin A. A., 1
Gamanetz L. V.
1
Siberian Institute of Plant Physiology and Biochemistry, Siberian Branch of RAS, PO
Box 1243, Irkutsk, Russia, e-mail: phytolab@sifibr.irk.ru
2
Istituto Biologia Biotecnologia Agraria, C.N.R., via Bassini 15, Milan, Italy, e-mail
mapo@ibv.mi.cnr.it
The creation of transgenic plants with the aim to increase productivity and to gain
resistance to unfavorable natural and abiotic factors as a result of transgenesis is
currently a promising task. The transfer and integration of the maize iaglu gene into
Solanum plants was shown earlier to improve an auxin status expressed in an elevated
content of free and bound indoleacetic acid (IAA) and accelerated growth and root
formation in transgenic plants (Zhukova et al. 1997; Gamanetz et al. 1998).
Tomato seeds, of Ventura and Verlioka varieties, obtained from in vitro transformed
plant were utilized to confirm gene insertion and evaluate the effect on plant morphology
and productivity. Tomato seedlings cv. Bumerang were infected with transconjugant in
planta without step of cultivation in vitro. The efficiency of plant transformation was
assessed by the activity of the markers and target enzymes, β-glucuronidase (GUS)
(Table 1), neomycinphosphotransferase (Table 2) and UDPG-transferase, respectively
in leaves of adult plants.
Table 1. The activity of β-glucuronidase in leaves of tomato L. esculentum cv.
Ventura
Fluorescence Impulses
(10 4
/mg protein/hr)
Control 6.2
Transgenic 428.6
The data from Sephadex G-25 column eluates of tomato leaves enzyme extracted
in K/Na phosphate buffer.
In crude extracts from leaves of transgenic tomato cv. Verlioka, the activity of GUS
was 284.1±59.1 x 10 4
fluorescence impulses/gram of dry matter, comparing to the
activity of 62.5±4.2 x 10 4
fluorescence impulses/gram of dry matter measured in the
controls.
The transgenesis of tomato hybrid plants Bumerang was confirmed by expression of
GUS-activity with color substrate 5-bromo-4-chloro-3-indolyl- β-glucuronide due to the
appearance of blue zones in trichoblasts on stems of transgenic plants after incubation
of small cuttings.
27

______________________________________________________________________
Table 2. Content of chlorophyll in leaves of tomato cv. Ventura exposed to
kanamycin.
Kanamycin (mg/l)
0 50 100 200 300
Control 34.0±0.4 33.8±0.0 22.2±0.2 13.5±0.6 10.1±0.1
Transgenic 51.1±0.3 42.0±0.4 34.6±0.6 29.8±0.3 28.0±0.1
To check the presence of the nptII expression, the developed leaves of both types
of plants were placed in kanamycin solution for seven day and differences between
them were evaluated thereafter as a diminishing of chlorophyll content (Table 2). The
integration of target iaglu gene in the tomato varieties was confirmed with PCR where
the amplification products of corresponding size were found in electrophoresis agarose
gels.
The growth and productivity can be supported by strengthening of the auxin status
expressed in enhanced IAA biosynthesis, IAA binding activity and IAA bounded
hydrolysis (Table 3). The content of free endogenous IAA in leaves of the transgenic
tomato was actually two-fold higher calculated by both fresh and dry weights.
The activity of UDPG-transferase, the enzyme coded by iaglu gene, was higher in
the cytosol from transgenic tomato plants. The activity of amidohydrolase in transgenic
tomato leaves as compared to the control was 14 times higher in Sephadex G-25
purified enzyme fractions. The substrate of this enzyme is the product of iaglu UDPG-
transferase.
It is likely that the balance between synthesis, conjugation, transport and hydrolysis
results in higher content and action of endogenous IAA in the transgenic tomato.
Table 3. The auxin status of control and transgenic tomato plants cv. Ventura
IAA
(nmol per g fr wt)
UDPG-transferase
(nmol/mg protein/hr)
Amidohydrolase
(nmol/mg protein/hr)
Control 64±4 139.9 278±0.2
Transgenic 112±29 286.3 3875±22
Varieties of transgenic tomato plants obtained by transformation grew faster than
the control ones, formed wider leaf blades, and had larger mass of shoots and stems
and more developed root system (Table 4). The transgenic plants were distinguished by
formation of a greater number of root primordia (more than 100) along the stem. They
started blooming earlier and formed greater amount of trusses and fruits, as well the red
fruits yield of the transgenic Ventura, Verlioka and Bumerang varieties were heavier
(Table 5) and harvest time occurred 7-10 days earlier.
28

______________________________________________________________________
Table 4. A morphometric analysis of control and transgenic tomatoes growing in soil
Height
(cm)
Leaves
number
Mean leaf
area
(mm 2
)
Upper part
(g)
Root
(g)
Ventura cv.
Control 70.6±4.7 9.1±0.7 281.3±8.3 310.0±35.7 37.8±6.5
Transgenic 88.8±6.5 10.7±0.8 351.7±19.5 423.3±60.0 64.5±8.0
Verlioka cv.
Control 49.0±5.6 9.5±0.7 375.0±1.7 333.3±89.8 28.2±1.2
Transgenic 118.2±21.6 30.0±5.0 1250.0±5.4 1133.3±189.0 38.1±3.1
The determination was performed in the stage of fruit ripening. Fruit weight
excluded.
Table 5. Characteristics of tomato fruits
Yield per plant
(g)
Weight of red fruit
per plant (g)
Number red fruits
per plant
Ventura cv.
Control 6021 4613 224
Transgenic 8006 7023 301
Verlioka cv.
Control 3159 1640 99
Bumerang hybrid
Control 4649 3290 133
Therefore, transgenesis and expression of the iaglu gene enhanced the auxin status
of the transgenic plants that appeared to be a stimulating factor providing faster plant
growth, floral development as well as the improvement of productivity in genetically
modified tomato plant.
29

______________________________________________________________________
Literature Cited:
− Rekoslavskaya, N. I., Gamanetz, L. V., Bryksina, I. V., Mapelli, S. and Salyaev, R. K.
(1998). Obtaining of transgenic tomato (Lycopersicon esculentum Mill.) and potato
(Solanum tuberosum L.) by transfer of the ugt gene from corn. Rep. Tom. Genet.
Coop., 48: 40-42.
− Zhukova, V. M., Rekoslavskaya, N. I., Salyaev, R. K. and Yurieva, O. V. (1997).
Transformation of plants via shoot regeneration from infected with agrobacteria
axillary buds of Solanum illustrated with the gene iaglu. Biotechnology (Russian), 5:
15-21.
30

______________________________________________________________________
A new allele at the potato leaf locus derived from L. chilense accession LA 1932
is discovered in a geminivirus resistance project.
Scott, J.W.
University of Florida, IFAS, Gulf Coast Research & Education Center, Bradenton, FL
34203
The potato leaf (c) locus has been mapped to chromosome 6 near the sp and B loci
Tanksley et al., 1992; Weide et al., 1993). In 1990 we discovered resistance to the
geminivirus, tomato mottle virus (ToMoV), in several accessions of L. chilense (Scott
and Schuster, 1991). Resistance was introgressed into tomato by crossing entirely with
cut leaf recurrent parents. Nevertheless, we began to find potato leaf segregants in
determinate plants derived from LA 1932 (and LA1961). The potato leaf trait seemed to
be associated with ToMoV resistance and potato leaf was used along with sp to anchor
RAPD markers linked to resistance loci (Griffiths, 1998; Griffiths and Scott, 2001). In
that research it was observed that the potato leaf type observed was not as easily
identified as with c genotypes.
To determine if the LA 1932
derived potato leaf was in fact
an allele at the c locus, an
inbred with the trait, 745-Y1,
was crossed with c leaf
accessions LA 2510 and LA
2513 and Fla. 7781 (c+).
Subsequently, F2 seed was
obtained for each cross.
Parents, F1 and F2 generations
were grown in Todd planter flats
in a greenhouse in spring,
2002. Plants were rated as wild
type (cut leaf), potato leaf (c), or
LA 1932 potato leaf (Fig. 1)
when seedlings were at the 2-3
leaf stage. The LA 1932 derived
potato leaf is not as distinctive
as c, the leaf generally has a
lower length to width ratio, is
more rounded than pointed, and
has a small serration in the leaf
margin (Fig. 1). As can be seen
in Fig. 1d, the axillary leaflets
often connect to the terminal
leaflet unlike c where they are
generally separate. The LA 1932
31

______________________________________________________________________
potato leaf margin sometimes has a few rather wide and deep serrations (Fig 1e), but it
can be accurately identified with practice. The new phenotype was a monogenic
recessive to wild type based on the F1 and F2 results (Table 1). The new phenotype was
a monogenic dominant to c. The data suggest the new phenotype is allelic to c although
there were 2 plants that appeared to be wild type in the 745-Y1 x LA 2510 F2. These
may have been misclassified (although they were grown out and checked later) or due
to some type of error in the experiment. A closely linked gene to c can not be ruled out,
but it is felt that another allele at the c locus provides the best fit to the data. The symbol
c2
is thus proposed for the potato leaf allele derived from LA 1932.
It is surprising that this allele emerged from a cross of two non-potato leaf parents.
Possibly LA 1932 (sp+) is heterozygous for c2
, although I do not remember seeing
indeterminate potato leaf plants in any of our work. Apparently LA 1932 has a gene
linked on the opposite side of the sp locus (or very close to it) that is epistatic to c2
expression. The tomato yellow leaf curl virus (TYLCV) resistant variety ‘Tyking’ also has
a potato leaf type. Furthermore, we tested Henri Laterrot’s CHILTYLIC94-3 population
in 1995 and found a few plants showed ToMoV resistance. A few generations of
resistance selection followed and derived homozygous resistant lines all had potato
leaves. Since ‘Tyking’ is in the pedigree of the CHILTYLC94-3 population, this could
have been the source of the potato leaf. No allelism work has been done with c2
and
these other genotypes or with cint
which has some similarity to c2
but a different length
/width ratio (see images in the TGRC website). It does seem probable that these
genotypes have a geminivirus resistance gene in the c region of chromosome 6. Lines
derived from LA 1932 with ToMoV and TYLCV resistance without c2
have recently been
developed, indicating the linkage between c2
and the resistance gene has been broken.
Literature Cited
Griffiths, P.D. 1998. Inheritance and linkage of geminivirus resistance genes derived
from Lycopersicon chilense Dunal in tomato (Lycopersicon esculentum Mill.). PhD diss.,
Univ. of Florida, Gainesville.
Griffiths, P.D. and J.W. Scott. 2001. Inheritance and linkage of tomato mottle virus
resistance genes derived from Lycopersicon chilense accession LA 1932. J. Amer. Soc.
Hort. Sci. 126(4):462-467.
Scott, J.W. and D.J. Schuster. 1991. Screening of accessions for resistance to the
Florida tomato geminivirus. TGC Rpt. 41:48-50.
Tanksley, S. et al. 1992. High density molecular linkage maps of the tomato and potato
genomes. Genetics 132:1141-1160.
Weide, R. et al. 1993. Integration of the classical and molecular linkage maps of tomato
chromosome 6. Genetics 135:1175-1186.
32

______________________________________________________________________
33
Table 1. Segregation of leaf type for two types of potato leaf parents, a wild type
parent, derived F1 and F2 generations, and chi square analyses for goodness of fit to
single dominant gene models.
Leaf Morphology
Genotype Generation
Cut
(c+)
New
Potato
Standard
Potato(c)
Expected
Ratio χ2
p
LA 2510 (c) P1A 0 0 24 0:0:1 - -
LA 2513 (c) P1B 0 0 24 0:0:1 - -
745-Y1 (from
LA1932)
P2 0 24 0 0:1:0 - -
Fla. 7781 (7781)(c+) P3 23 0 0 1:0:0 - -
(745-Y1 x 7781) F1 15 1 0 1:0:0 - -
(745-Y1 x LA 2510) F1 0 23 0 0:1:0 - -
(745-Y1 x LA 2513) F1 0 24 0 0:1:0 - -
(745-Y1 x 7781)Bk F2 250 85 0 3:1:0 0.016 .9
(745-Y1 x LA
2510)Bk
F2 0 219 74 0:3:1 0.012 .9-
.975
(745-Y1 x LA
2513)Bk
F2 2z
226 84 0:3:1 0.727 .5-.1
z
Not included in chi-square calculations.

VARIETAL PEDIGREES TGC REPORT 52, 2002
____________________________________________________________________________________
Alvarez, M.; Moya, C.; Dominí, M.E. and Arzuaga, J.; 2002. Instituto Nacional de Ciencias
Agrícolas (INCA), La Habana, Cuba. Released 1997.
Amalia, Mariela
Pedigree:
Mariela
Amalia
Campbell-28
INCA 3A
Caraibe
Línea C-3
HC-2580
Línea 35
Campbell-28
INCA-3
Characteristics:
Amalia
Fruit: Red, slightly flattened globe, joint, tolerant to cracking and rots, high soluble solids,
average weight 125 g.
Plant: Determinate (sp), small, resistant to Fusarium (I) and Stemphylium (Sm), good fruit set.
Utility and Maturity: Fresh market cultivar widely adapted to tropical environments, early
maturity.
Mariela
Fruit: Red, flattened globe with slightly green - shouldered, joint, average weight 150g.
Plant: Determinate (sp), good fruit protection, resistant to Fusarium (I) and Stemphylium (Sm).
Utility and Maturity: Good for fresh market.
35

____________________________________________________________________________________
Ohio OX150 Hybrid Processing Tomato
David M. Francis, Stan Z. Berry, Troy Aldrich, Ken Scaife, and Winston Bash
Horticulture and Crop Science
The Ohio State University, OARDC
1680 Madison Ave.
Wooster, OH 44691
Introduction: Ohio OX150 is an early to early-mid season processing tomato (Lycopersicon
esculentum Mill.) hybrid adapted to high population transplant culture, machine harvest, and
bulk handling under humid growing environments. It is suited for the production of peeled,
whole-canned, and diced tomato products.
Origin: Ohio OX150 is the F1 hybrid resulting from the cross of the inbred line O88119
described by Berry et al. (1995) and Ohio 9242. ‘Ohio 9242’ is an F8 selection derived by
single seed decent from the F6 selection A1816. The selection A1816 is derived from a cross
between ‘Ohio 832’ (Berry et al., 1986) variant ‘O9149’ (Montagno et al., 1988) and ‘Ohio
8556’ (Berry et. al., 1993).
______
| O88119
|
|
‘Ohio OX150’ ____ |
| _____
| | Ohio 832 (variant O9149)
| |
|______Ohio 9242 _______
|
|
|_____ Ohio 8556
Fig. 1. Pedigree of ‘Ohio OX150’
Description: Ohio OX150 vines are medium in size, semi-prostrate, and determinate (sp).
Foliage cover is excellent for ensuring good fruit quality and at maturity the vines cover the row
area uniformly. The average maturity from transplant to harvest of ‘Ohio OX150’ is 97.1 days
over four years of field testing, comparable to the early season standard, ‘Ohio 7983’ (Berry et
al., 1992).
The average machine harvest yield of Ohio OX150 was 32.8 T/A over four years of
testing, outperforming the major early season varieties open pollinated variety Ohio 7983 and
comparing favorably to OX 52 (Francis et al., 2000) (though differences were not always
significant). Yields of ‘Ohio OX150’ were comparable to the main-season open pollinated
variety Ohio 8245 and the main-season hybrid Heinz 9423. Yields were somewhat less than
the major main-season variety Peto 696 (Table 1).
36

____________________________________________________________________________________
Fruit of ‘Ohio OX150’ average 2.1 oz with two to three locules. The shape is ovate.
Fruit have a small stem scar and core, are uniform ripening (u), are attached by a jointless
pedicel (j2
), and are heterozygous for the crimson (ogc
/+) locus. The color of fruit from ‘Ohio
OX150’ is excellent.
Table 1. Summary statistics for maturity, mechanical harvest yield, and fruit quality for
OX 150 over four years.
Days to Yield color Force to
Variety Harvest T/A L Chroma Hue puncture (Kg) Brix
O 7983 96.2 27.6 41.6 35.9 44.0 5.5 5.32
OX 52 97.1 36.1 41.9 36.1 45.1 5.0 4.72
OX 150 97.1 32.8 40.0 35.0 43.0 5.3 4.65
TR 12 98.2 33.1 40.1 36.2 42.6 5.6 5.11
H 9423 101.5 30.1 43.3 40.6 41.2 7.2 5.00
PS 696 101.8 36.8 42.6 37.3 44.8 5.6 5.02
O 9242 102.7 26.7 38.8 35.4 38.8 4.9 5.31
O 8245 103.7 29.7 42.8 37.3 44.6 5.8 5.16
mean 99.8 31.6 41.4 36.7 43.0 5.6 5.04
LSD
(0.05)
NS NS 2.5 1.7 NS 0.6 0.31
LSD
(0.30)
4.2 5.1 1.2 0.8 2.5 0.3 0.16
References:
Berry, S.Z. and W.A. Gould. 1986. ‘Ohio 832’ Tomato. HortScience 21:334.
Berry, S.Z. K.L. Weise, and W.A. Gould. 1992. “Ohio 7983” Processing Tomato. Hortscience
27: 939.
Berry, S.Z., K.L. Wiese, and T.S. Aldrich. 1993. “Ohio 8556” Processing Tomato.
HortScience 28:751.
Berry, S. Z., T.S. Aldrich, K.L. Wiese, and W.D. Bash. 1995. ‘Ohio OX38” Hybrid Processing
Tomato. Hortscience 30:159.
Francis, D. M., S. Berry, T. Aldrich, K. Scaife, W. Bash. 2000. ‘Ohio OX 52’ Processing
Tomato. Report of the Tomato Genetics Cooperative Vol 50
Montagno, T. J., R.D. Lineberger, and S.Z. Berry. 1989. Somaclonal and radiation induced
variation in Lycopersicon esculentum. Environmental and Experimental Botany. 29:401-408.
37

____________________________________________________________________________________
Scott, J.W. 2000. Fla. 7771, a medium-large, heat-tolerant, jointless-pedicel tomato.
HortScience 35(5):968-969.
FLORIDA 7771
Fla. 1B
648
648
Cl 123
C-28 C-28
Burgis
Pedigree:
7060
Horizon
F4
F4
F6
Suncoast
Suncoast
F5
F1
F6
F7
F5
F3
F7
7340
F5
7340
7095
F5
648
E03
6120
Hayslip
Fla. 1C
Horizon
7182
F5
7319
F5
7546B
F5
F7
Fla. 7771
F7
Characteristics:
Fruit: flat-round shape, light green shoulder, slightly pale interior color, medium-large fruit,
medium firmness, n-2
Plant: sp, I, I-2, Sm, medium vine with erect leaves in top
Utility and maturity: Early-midseason fresh market breeding line combining jointless pedicel,
medium large fruit size and heat-tolerance (33-22 C, high relative humidity) with minimal
fruit defects for breeding of same
38

____________________________________________________________________________________
Scott, J.W., B.K. Harbaugh, and E.A. Baldwin. 2000. ‘Micro-Tina’ and ‘Micro-Gemma’
miniature dwarf tomatoes. HortScience 35(4):774-775.
MICRO-TINA
MICRO-GEMMA
Pedigree:
Micro-Tina
F10
Micro-Gemma
F10
P 270248 (‘Sugar’)I
P 270248 (‘Sugar’)I
Micro-Tom
Fla. 7565 (related to ‘Micro-Gold’)
Characteristics:
Fruit: Very small (7g), tri-locular, flat-round shape, u, Micro-Gemma has gold color (r,Y),
sweeter flavor than Micro-Tom or Micro-Gold (plus 1 Brix)
Plant: sp, d, I, Sm, diminutive size of plant organs similar to ‘Micro-Tom’
Utility and maturity: Micro-Tina is 1 week earlier than Micro-Gemma and Micro-Tom, for
small pots or hanging baskets and patio gardens
39

____________________________________________________________________________________
40
Scott, J.W. and John Paul Jones. 2000. Fla. 7775 and Fla. 7781: Tomato breeding lines
resistant to fusarium crown and root rot. HortScience 35(6):1183-1184.
FLORIDA 7775
FLORIDA 7781
Ohio 89-1
Suncoast
Suncoast
F4
F4
7181
F4
7228
F8
F5
F5
7464
F6
Suncoast
Suncoast
Suncoast
NC 8276
NC 8276
F3
F3
F3
Horizon
7198
F4
7197
F3
E01
Hayslip
Horizon
7182
7440
F5
7340
F5
7340
F5
7182
F9
7182
F9
7647B
F8
7647B
F8
F5
F6
Fla. 7781
F13
Fla. 7775
F9
Pedigree:
Characteristics:
Fruit: flat-round shape, light-green shoulder, ogc
, Fla. 7775 has medium size, jointless (j- 2)
pedicels and is very firm, Fla. 7781 is medium-large, has jointed pedicels, and is firm
Plant: sp, I, I-2, Ve, Sm, Frl, Fla. 7775 also has Tm-2 (OPB 12 SCAR marker) and a
open vine, Fla. 7781 has a larger vine
Utility and maturity: Midseason fresh market breeding lines for fusarium crown and root rot
resistance breeding

STOCK LISTS TGC REPORT 52, 2002
_____________________________________________________________________________________________
41
Revised List of Monogenic Stocks
Chetelat, R. T.
C.M. Rick Tomato Genetics Resource Center, Dept. of Vegetable Crops, Univ. of California,
Davis, CA 95616
The following list of 994 monogenic stocks (at 614 loci) is a revision of the list issued in
TGC 49. For other types of accessions, see TGRC stock lists published in TGC vols. 51 (Wild
Species Stocks), and 50 (Miscellaneous Stocks). Certain obsolete or unavailable items have
been deleted, newly acquired stocks have been added, inaccuracies corrected, and gene
symbols revised to reflect allele tests or other information. Recently acquired morphological
mutants include a stock of Xa-2 that forms twin spots due to chromosome breakage (provided
by M. Koornneef), and a source of yvms
, an unstable allele characterized by yellow/green
sectoring (M. Ramanna). New alleles and NIL stocks of hp and hp-2 (A. van Tuinen) and the
corolla intensifier Bco (R. Chetelat) were also added. Introgressed disease resistance genes
include I-3 for Fusarium wilt (J. Scott) and Cmr for CMV (B. Stamova). Other genes
introgressed from wild relatives include sucr for sucrose accumulation (R. Chetelat) and Rg-1
for enhanced shoot regeneration from tissue culture (M. Koornneef).
Instances of demonstrated allelism between mutants are incorporated into this list.
These include the old gold (og) and crimson (ogc
) mutations, which are null alleles at the Beta
(B) locus, recessive to both the dominant (B) and wild type (B+
) alleles (PNAS 97:11102), for
which we propose the symbols Bog
and Bc
, respectively. Other new allele designations include
comin
(TGC 46:15) and PtoPto-2
(TGC 41:27). Conversely, the hairless mutation in accession 3-
417, which is not allelic to hl (TGC 37:43), is listed herein as hl-2. Finally, the symbol for the
gene encoding resistance to Fusarium oxysporum f. sp. radicis-lycopersici (FORL) has been
corrected from Fr-1 to Frl.
This stock list includes only accessions we consider to be the primary sources for
individual mutations: usually the original source (often isogenic in a known background), and
any nearly isogenic lines into which the mutation has been bred. Most stocks are homozygous
and true-breeding. However, male-steriles, other inherited sterilities, homozygous-inviable
mutants, and other stocks that are too difficult to maintain as homozygotes, are propagated via
heterozygotes (seed usually provided as F2’s).
Additional information on these stocks, including phenotypes, references, images,
chromosomal locations, etc., can be obtained through our website (http://tgrc.ucdavis.edu).
TGC members are encouraged to submit stocks of verified monogenic mutants not listed here
to the TGRC for maintenance and distribution.
Table 1. List of monogenic stocks, including gene and allele symbols, locus name, synonyms,
phenotypic classes, source of mutation, background genotype, isogenicity, and accession
number. The original mutant allele at a locus is designated by ‘--‘, and provisional alleles by
‘prov#’; under SYNONYMS, superscripted alleles are indicated by ‘^’. Abbreviations used for
phenotypic categories (CLASS) and background genotypes (BACK) are defined in Tables 2 and
3 respectively. Sources of mutations are spontaneous (SPON), or induced by chemical agents
(CHEM) or irradiation (RAD). Isogenicity (ISO) indicates whether a mutation is isogenic (IL),
nearly isogenic (NIL), or nonisogenic (NON) in a particular accession.
GENE ALLELE LOCUS NAME SYNONYMS CLASS SOURCE BACK ISO ACC#
a -- anthocyaninless a1 A* SPON X NON LA0291
a -- anthocyaninless a1 A* SPON AC NIL LA3263
a prov2 anthocyaninless a A* CHEM VF36 IL 3-414

_____________________________________________________________________________________________
42
a prov3 anthocyaninless a A* CHEM VF36 IL 3-415
aa -- anthocyanin absent A* SPON MD IL LA1194
aa -- anthocyanin absent A* SPON AC NIL LA3617
Abg -- Aubergine P* SPON X NON LA3668
abi -- aborted inflorescence M* CHEM CSM NON 3-803
Aco-1 1 Aconitase-1 V* SPON pen NON LA2901
Aco-1 2 Aconitase-1 V* SPON pim NON LA2902
Aco-2 2 Aconitase-2 V* SPON chm NON LA2905
acr -- acroxantha acr1 D*JK RAD CR IL LA0933
ad -- Alternaria alternata resistance Q* SPON X NON LA1783
Adh-1 1 Alcohol dehydrogenase-1 V* SPON VCH NON LA2416
Adh-1 2 Alcohol dehydrogenase-1 V* SPON par NON LA2417
Adh-1 n Alcohol dehydrogenase-1 V* CHEM MM IL LA3150
Adh-2 1 Alcohol dehydrogenase-2 V* SPON hir NON LA2985
adp -- adpressa K*J RAD AC NIL LA3763
adp -- adpressa K*J RAD CR IL LA0661
adu -- adusta adu1 H*K RAD CR IL LA0934
ae -- entirely anthocyaninless a332 A* RAD CG NIL LA3018
ae -- entirely anthocyaninless a332 A* RAD AC NIL LA3612
ae -- entirely anthocyaninless a332 A* RAD KK IL LA1048
ae 2 entirely anthocyaninless A* CHEM UC82B IL 3-706
ae afr entirely anthocyaninless afr, ap A* RAD CT IL LA2442
ae prov3 entirely anthocyaninless ae A* CHEM VCH IL 3-620
aeg -- aegrota H* RAD CR IL LA0537
aer -- aerial roots R* SPON X NON LA3205
aer-2 -- aerial roots-2 R* SPON X NON LA2464A
af -- anthocyanin free a325 A*I RAD RCH IL LA1049
af -- anthocyanin free a325 A*I RAD AC NIL LA3610
Af -- Anthocyanin fruit P* SPON X NON LA1996
afe -- afertilis afe1 N*CJK RAD RR IL LA0935
afl -- albifolium af B*G SPON XLP IL 2-367
afl -- albifolium af B*G SPON AC NIL LA3572
ag -- anthocyanin gainer A* SPON GS5 NON LA0177
ag -- anthocyanin gainer A* SPON AC NIL LA3163
ag 2 anthocyanin gainer A* SPON che NON LA0422
ag 2 anthocyanin gainer A* SPON AC NIL LA3164
ag-2 -- anthocyanin gainer-2 A* SPON AC NIL LA3711
ah -- Hoffman’s anthocyaninless ao, a337 A* SPON OGA IL LA0260
ah prov2 Hoffman’s anthocyaninless ah A* CHEM MM IL 3-302
ah prov3 Hoffman’s anthocyaninless ah A* CHEM VCH IL 3-607
ah prov6 Hoffman’s anthocyaninless ah A* SPON PSN IL LA0352
ah prov7 Hoffman’s anthocyaninless ah A* CHEM MM IL 3-343
ai -- incomplete anthocyanin a342 A* RAD KK IL LA1484
ai -- incomplete anthocyanin a342 A* RAD AC NIL LA3611
ai 2 incomplete anthocyanin am, a340 A* RAD KK IL LA1485
al -- anthocyanin loser a2 A* SPON AC NIL LA3576
alb -- albescent G*C SPON AC NIL LA3729
alb prov2 albescent alb G*C CHEM VCH IL 3-625
alc -- alcobaca P* SPON X NON LA2529

_____________________________________________________________________________________________
43
alc -- alcobaca P* SPON RU NIL LA3134
alu -- alutacea alu1 C*K RAD CR IL LA0838
an -- anantha an^1, an^2, ca L*N RAD CR IL LA0536
ap -- apetalous L*N SPON ESC IL 2-009
ap -- apetalous L*N SPON AC NIL LA3673
apl -- applanata J*K RAD LU IL LA0662
apn -- albo-punctata G*BJK CHEM VF36 IL 3-105
Aps-1 1 Acid phosphatase-1 V* SPON VCH NIL LA1811
Aps-1 2 Acid phosphatase-1 V* SPON chm NON LA1812
Aps-1 n Acid phosphatase-1 V* SPON pim NON LA1810
Aps-2 1 Acid phosphatase-2 V* SPON SM NON LA1814
Aps-2 2 Acid phosphatase-2 V* SPON che NON LA1815
Aps-2 3 Acid phosphatase-2 V* SPON par NON LA1816
Aps-2 n Acid phosphatase-2 V* SPON che NON LA1813
are -- anthocyanin reduced A* CHEM VF36 NON 3-073
Asc -- Alternaria stem canker resistance Q* SPON X NON LA2992
at -- apricot P* SPON AC NIL LA3535
at -- apricot P* SPON X NON LA0215
at -- apricot P* SPON RU NIL LA2998
atn -- attenuata at E*AJK RAD AC NIL LA3829
atn -- attenuata at E*AJK RAD RR IL LA0587
atv -- atroviolacium A* SPON AC NIL LA3736
au -- aurea C*B RAD AC NIL LA3280
au (1s) aurea au^2, au, brac C*B RAD CR IL LA0538
au 6 aurea yg^6, yg-6,
au^yg-6, yo
C*B SPON RCH IL LA1486
au 6 aurea yg^6, yg-6,
au^yg-6, yo
C*B SPON AC NIL LA2929
au tl aurea C*B SPON VF145 IL 2-655A
au w aurea w616 C*B CHEM MM IL LA2837
aus -- austera J*KT RAD LU IL LA2023
aut -- aureata C*F SPON X NON LA1067
aut -- aureata C*F SPON AC NIL LA3166
auv -- aureate virescent F*C CHEM VF36 IL 3-075
avi -- albovirens avi1 C*BGN RAD CR IL LA0936
aw -- without anthocyanin aba, ab, a179 A* SPON AC NIL LA3281
aw -- without anthocyanin aba, ab, a179 A* SPON per NON LA0271
aw prov3 without anthocyanin aw A* CHEM VF36 IL 3-121
aw prov4 without anthocyanin aw A* CHEM VCH NON 3-603
aw prov5 without anthocyanin aw A* CHEM VCH NON 3-627
B -- Beta-carotene P* SPON X NON LA2374
B -- Beta-carotene P* SPON RU NIL LA3000
B -- Beta-carotene P* SPON E6203 NIL LA3898
B -- Beta-carotene P* SPON O8245 NON LA3899
B og Beta-carotene og L*P SPON chi NON LA0294
B og Beta-carotene og L*P SPON PSN NIL LA0348
B og Beta-carotene og L*P SPON unk NON LA0500
B c Beta-carotene og^c, Crn, Cr,
crn-2, cr-2
P*L SPON AC NIL LA3179
crn-2, cr-2
P*L SPON X NON LA4025
crn-2, cr-2
P*L SPON PCV NON LA0806
B c Beta-carotene og^c, Crn, Cr, P*L SPON X NON LA4026

_____________________________________________________________________________________________
44
crn-2, cr-2
bc -- bicolor bi U*JKT RAD CR IL LA0588
Bco -- Brilliant corolla L* SPON M82 NON LA4067
bi -- bifurcate inflorescence M* SPON X NON LA1786
bip -- bipinnata J* RAD LU IL LA0663
bip -- bipinnata J* RAD AC NIL LA3765
bip prov2 bipinnata bip J* CHEM VCH IL 3-602
bk -- beaked O* SPON X NON LA0330
Bk-2 -- Beaked-2 O* SPON X NON LA1787
bl -- blind K* SPON X NON LA0059
bl -- blind K* SPON AC NIL LA3745
bl 2 blind to^2 K* SPON LU IL LA0980
bl to blind to K*JLO RAD CR IL LA0709
bls -- baby lea syndrome alm A*K SPON X NON LA1004
bls -- baby lea syndrome alm A*K SPON AC NIL LA3167
bls prov2 baby lea syndrome bls A*K CHEM VCH IL 3-610
Bnag-1 1 Beta-N-acetyl-D-glucosaminidase-1 V* SPON pen NON LA2986
br -- brachytic K* SPON X NON LA2069
brt -- bushy root R* SPON X NON LA2816
brt-2 -- bushy root-2 R* SPON X NON LA3206
bs -- brown seed S* CHEM AC NIL LA2935
bs-2 -- brown seed-2 S* SPON PLB IL LA1788
bs-4 -- brown seed-4 S* RAD MM IL LA1998
btl -- brittle stem J*Y SPON X NON LA1999
bu -- bushy fru K*JM SPON AC NIL LA2918
bu -- bushy fru K*JM SPON X NON LA0897
bu ab bushy fru^ab K*JM RAD RR IL LA0549
bu cin bushy cin K*JM SPON HSD IL LA1437
bu cin-2 bushy cin-2 K*JM SPON HSD IL LA2450
bu hem bushy fru^hem K*JM RAD CR IL LA0604
bul -- bullata C*JK RAD CR IL LA0589
buo -- bullosa buo1 J*O RAD pim IL LA2000
c -- potato leaf J* SPON AC NIL LA3168
c int potato leaf int J* RAD CR IL LA0611
c int potato leaf int J* RAD AC NIL LA3728A
c prov2 potato leaf c J* CHEM MM IL 3-345
c prov3 potato leaf c J* CHEM VCH IL 3-604
car -- carinata J*DLO RAD CR IL LA0539
car-2 -- carinata-2 car2 J*K RAD pim IL LA2001
cb -- cabbage J*K AC NIL LA3819
cb-2 -- cabbage leaf-2 J*K RAD X NON LA2002
cb-2 -- cabbage leaf-2 J*K RAD AC NIL LA3169
ccf -- cactiflora N*LO CHEM CSM IL 3-805
Cf-1 -- Cladosporium fulvum resistance-1 Cf, Cf1, Cfsc Q* SPON X NON LA2443
Cf-1 3 Cladosporium fulvum resistance-1 Cf-5, Cf5 Q* SPON X NON LA2447
Cf-1 3 Cladosporium fulvum resistance-1 Cf-5, Cf5 Q* SPON MM NIL LA3046
Cf-2 -- Cladosporium fulvum resistance-2 Cf2, Cfp1 Q* SPON X NON LA2444
Cf-2 -- Cladosporium fulvum resistance-2 Cf2, Cfp1 Q* SPON MM NIL LA3043
Cf-3 -- Cladosporium fulvum resistance-3 Cf3, Cfp2 Q* SPON X NON LA2445
Cf-3 -- Cladosporium fulvum resistance-3 Cf3, Cfp2 Q* SPON MM NIL LA3044

_____________________________________________________________________________________________
45
Cf-4 -- Cladosporium fulvum resistance-4 Cf-1^2, Cf4 Q* SPON MM NIL LA3045
Cf-4 -- Cladosporium fulvum resistance-4 Cf-1^2, Cf4 Q* SPON X NON LA2446
Cf-4 -- Cladosporium fulvum resistance-4 Cf-1^2, Cf4 Q* SPON AC NIL LA3267
Cf-6 -- Cladosporium fulvum resistance-6 Q* SPON X NON LA2448
Cf-7 -- Cladosporium fulvum resistance-7 Q* SPON X NON LA2449
Cf-9 -- Cladosporium fulvum resistance-9 Q* SPON MM NIL LA3047
cg -- congesta cg1 K*J RAD RR IL LA0831
ch -- chartreuse L* SPON PSN IL 2-253
ch -- chartreuse L* SPON AC NIL LA3720
ci -- cincta ci1 K* RAD CR IL LA0938
cit -- citriformis O*JK RAD RR IL LA2024
cjf -- confunctiflora L*N SPON PTN IL LA1056
ck -- corky fruit O* SPON X NON LA2003
cl-2 -- cleistogamous-2 cl2 L*N SPON SM IL 2-185
cla -- clara C*A RAD LU IL LA0540
clau -- clausa ff, vc J*LO RAD LU IL LA0591
clau -- clausa ff, vc J*LO RAD X NON LA0719
clau -- clausa ff, vc J*LO RAD AC NIL LA3583
clau ff clausa J*LO SPON VFSM IL 2-505
clau ics clausa ics J* SPON PTN IL LA1054
clau ics clausa ics J* SPON AC NIL LA3713
clau prov2 clausa clau J*LO SPON X IL LA0509
clau vc clausa J*LO SPON X NON LA0896
cls -- clarescens C*K RAD RR IL LA2025
clt -- coalita J* RAD LU IL LA2026
cm -- curly mottled G*JNO SPON PCV NON LA0272
cm -- curly mottled G*JNO SPON AC NIL LA2919
cma -- commutata K*DHJ RAD RR IL LA2027
Cmr -- Cucumber mosaic resistance Q* SPON X NON LA3912
cn -- cana ca D*K RAD RR IL LA0590
co -- cochlearis J*D RAD CR IL LA0592
coa -- corrotundata coa1 J*KLT RAD CR IL LA0940
com -- complicata K*J RAD CR IL LA0664
com in complicata in K*DJ RAD CR IL LA0610
com in complicata in K*DJ RAD AC NIL LA3715
con -- convalescens E*FK RAD CR IL LA0541
con -- convalescens E*FK RAD AC NIL LA3671
cor -- coriacea K*J RAD CR IL LA0666
cor -- coriacea K*J RAD AC NIL LA3743
cpa -- composita cpa1 M*K RAD RR IL LA0833
cpt -- compact K*EJ SPON XLP IL 2-377
cpt -- compact K*EJ SPON AC NIL LA3723
Cri -- Crispa H*JU RAD CR IL LA0667
Crk -- Crinkled J*T SPON X NON LA1050
crt -- cottony-root R* SPON RCH NON LA2802
cta -- contaminata cta1 K*HJN RAD RR IL LA0939
ctt -- contracta K*J RAD LU IL LA2028
Cu -- Curl J*KT SPON STD IL LA0325
Cu -- Curl J*KT SPON AC NIL LA3740
cu-2 -- curl-2 cu2 J* RAD CT IL LA2004
cu-3 -- curl-3 J*KT SPON pim NON LA2398
cul -- culcitula K*U RAD RR IL LA2029
cur -- curvifolia J*EK RAD RR IL LA0668

_____________________________________________________________________________________________
46
cv -- curvata cu K*JT RAD LU IL LA0593
cv 2 curvata acu K*JT RAD CR IL LA0660
cva -- conversa K*D RAD CR IL LA0665
cvl -- convoluta cvl1 K*J RAD RR IL LA0830
Cvx -- Convexa J* SPON X NON LA1151
d -- dwarf robîmm K*JT SPON GRD NIL LA3031
d -- dwarf robîmm K*JT SPON STN NIL LA0313
d -- dwarf robîmm K*JT SPON FB NIL LA3022
d b dwarf K*JTL SPON RR IL LA3865
d cr dwarf rob^crisp K*JT RAD CR IL LA0570
d im dwarf K*JT RAD CR IL LA0571
d prov2 dwarf d K*JT CHEM VCH IL 3-623
d provcr-2 dwarf d^cr K*JT CHEM VF36 IL 3-420
d provcr-3 dwarf d^cr K*JT CHEM VF36 IL 3-422
d x dwarf K*JT SPON PCV NON LA1052
d x dwarf K*JT SPON AC NIL LA3615
d x dwarf K*JT SPON VAN NIL LA3902
d x dwarf K*JT SPON SPZ IL LA0160
d-2 -- dwarf-2 rob2, rob II, d2 K*N RAD RR IL LA0625
dc -- decomposita dc1 J* RAD RR IL LA0819
dd -- double dwarf d^xx K*J SPON X NON LA0810
de -- declinata K*JU RAD RR IL LA0594
de -- declinata K*JU RAD AC NIL LA3742
deb -- debilis H*BCJ RAD CR IL LA0542
deb -- debilis H*BCJ RAD AC NIL LA3727
dec -- decumbens K*R RAD LU IL LA0669
def -- deformis J*LN RAD RR IL LA0543
def -- deformis J*LN RAD AC NIL LA3749
def 2 deformis vit J* RAD CR IL LA0634
def-2 -- deformis J*LN RAD AC NIL LA2920
Del -- Delta P* SPON RU NIL LA2996A
Del -- Delta P* SPON M82 NON LA4099
Del -- Delta P* SPON AC NIL LA2921
deli -- deliquescens K*CJ RAD RR IL LA0595
dep -- deprimata T*J RAD CR IL LA0544
depa -- depauperata K*CJ RAD RR IL LA0596
depa -- depauperata K*CJ RAD AC NIL LA3725
det -- detrimentosa C*KF RAD RR IL LA0670
det 2 detrimentosa C*KF RAD RR IL LA0820
Df -- Defoliator Y*H SPON par NON LA0247
dg -- dark green T* SPON MP IL LA2451
dgt -- diageotropica lz-3 K*R SPON VFN8 IL LA1093
Dia-2 1 Diaphorase-2 V* SPON pen NON LA2987
Dia-3 1 Diaphorase-3 V* SPON X NON LA3345
dil -- diluta D*JK RAD CR IL LA0545
dil -- diluta D*JK RAD AC NIL LA3728
dim -- diminuta A*DK RAD LU IL LA0597
dim-2 -- diminuta-2 dim2 A*K RAD AC NIL LA3170
dis -- discolor D*F RAD CR IL LA0598
div -- divaricata C*AJK RAD CR NON LA0671
div -- divaricata C*AJK RAD AC NIL LA3818
dl -- dialytic I*LN SPON SM IL 2-069
dl -- dialytic I*LN SPON AC NIL LA3724

_____________________________________________________________________________________________
47
dl S dialytic L*N SPON VF36 NIL LA3906
dlb -- dilabens dlb1 C*JK RAD CR IL LA0829
dm -- dwarf modifier d2 K* SPON X NON LA0014
dmd -- dimidiata K*JU RAD LU IL LA2033
dmt -- diminutiva K* CHEM VF36 IL 3-007
dp -- drooping leaf J*KT RAD CT IL LA2526
dps -- diospyros P* SPON X NON LA1016
dpy -- dumpy K*J SPON X NON LA0811
dpy -- dumpy K*J SPON AC NIL LA3171
dpy prov2 dumpy dpy K*J CHEM VCH IL 3-630
dpy prov3 dumpy dpy K*J SPON ANU IL LA1053
drt -- dwarf root R* CHEM X NON LA3207
ds -- dwarf sterile N*K SPON EPK IL 2-247
ds -- dwarf sterile N*K SPON AC NIL LA3767
dt -- dilatata dt1 C*JK RAD CR IL LA0828
dtt -- detorta J*K RAD LU IL LA2030
du -- dupla J*KU RAD LU IL LA2034
dv -- dwarf virescent F*D SPON X NON LA0155
e -- entire b J* SPON AC NIL LA2922
e prov3 entire e J* CHEM VCH IL 3-616
eca -- echinata K* RAD RR IL LA2035
el -- elongated e O* SPON AC NIL LA3738
ele -- elegans E*JK RAD CR IL LA0546
ele -- elegans E*JK RAD AC NIL LA3825
ele 2 elegans ang E*JK RAD CR IL LA0586
elu -- eluta E*K RAD LU IL LA0547
em -- emortua em1 H*K RAD AC NIL LA3817
em -- emortua em1 H*K RAD RR IL LA0827
en -- ensiform J* SPON X NON LA1787
ep -- easy peeling O* RAD MM IL LA1158
ep -- easy peeling O* RAD AC NIL LA3616
Epi -- Epinastic J*K SPON VFN8 IL LA2089
er -- erecta K*JT RAD CR IL LA0600
era -- eramosa era1 B*JK RAD CR IL LA0850
Est-1 1 Esterase-1 V* SPON pim NON LA1818
Est-1 1 Esterase-1 V* SPON cer IL LA2415
Est-1 4 Esterase-1 V* SPON par NON LA1821
Est-1 5 Esterase-1 V* SPON pen NON LA2419
Est-1 n Esterase-1 V* SPON pim NON LA1817
Est-4 4 Esterase-4 V* SPON PCV NON LA2425
Est-4 7 Esterase-4 V* SPON cer NON LA2428

_____________________________________________________________________________________________
48
ete -- extenuata ete1 K*JN RAD CR IL LA0942
ex -- exserted stigma L*N SPON SM IL 2-191
exl -- exilis ex D*JK RAD CR IL LA0601
exs -- excedens exs1 K*J RAD CR IL LA0852
f -- fasciated fruit O*L SPON ESC NON LA0517
f D fasciated fruit O*L SPON PCV NON LA0767
fa -- falsiflora fa1 M*N RAD RR IL LA0854
fcf -- fucatifolia fcf1 D*CK RAD CR IL LA0945
fd -- flecked dwarf G*DK RAD BK NON LA0873
fd -- flecked dwarf G*DK RAD AC NIL LA3750
Fdh-1 1 Formate dehydrogenase-1 V* SPON pen IL LA2989
fe -- fertilis J*LO RAD LU IL LA0672
fer -- fe inefficient B* X NON LA2994
fgv -- fimbriate gold virescent F*CJ SPON VF36 IL LA1143
fir -- firma K*JM RAD CR IL LA0602
fl -- fleshy calyx O* SPON X NON LA2372
fla -- flavescens D*JK RAD LU IL LA0548
fla -- flavescens D*JK RAD AC NIL LA3565
flav -- flavida C* RAD LU IL LA0603
flc -- flacca K*HW RAD RR IL LA0673
flc -- flacca K*HW RAD AC NIL LA3613
fld -- flaccida fld1 K*HJT RAD RR IL LA0943
fle -- flexifolia fle1 A*J RAD AC NIL LA3764
fn -- finely-netted D* RAD X NON LA2481
fn -- finely-netted D* RAD PSP IL LA2005
fr -- frugalis K*JT RAD CR IL LA0674
frg -- fragilis frg1 D*CJK RAD CR IL LA0864
fri 1 far red light insensitive AY* CHEM MM IL LA3809
Frl -- FORL resistance Fr1, Fr-1 Q* SPON AC NIL LA3273
Frl -- FORL resistance Fr1, Fr-1 Q* SPON VGB NON LA3841
Frs -- Frosty spot Nec H* SPON X NON LA2070
frt -- fracta K*JT RAD LU IL LA2038
fsc -- fuscatinervis dkv E* SPON VF145 IL LA0872
ft -- fruiting temperature O* SPON X NON LA2006
fu -- fusiformis C*JK RAD CR IL LA0605
fu -- fusiformis C*JK RAD AC NIL LA3070
fua -- fucata fua1 E*K RAD CR IL LA0944
fug -- fulgida fug1 E*BK RAD RR IL LA0946
ful -- fulgens E* RAD CR IL LA0550
ful 2 fulgens ful1^2 E* RAD RR IL LA0843
ful-3 -- fulgens-3 E* SPON VF36 IL LA1495
fus -- fulgescens E* RAD LU IL LA2039
Fw -- Furrowed J*KN SPON AC NIL LA3300
Fw -- Furrowed J*KN SPON PSN IL LA0192
fx -- flexa K* RAD LU IL LA2037
fy -- field yellow E* SPON AC NIL LA3295
ga -- galbina ga1 D*BE RAD CR IL LA0836
ga -- galbina ga1 D*BE RAD AC NIL LA3828
gas -- gamosepala gas1 D*JL RAD RR IL LA0947
gbl -- globula K*JU RAD LU IL LA2032
Ge c Gamete eliminator N* SPON CR NON LA0533

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