Heterosis, also known as hybrid vigor, refers to the increased or superior characteristics of offspring compared to their parents. This document discusses the history and genetic models of heterosis. It was first described by Charles Darwin and later termed "heterosis" by Shull. Genetic models like dominance, overdominance, and epistasis aim to explain the superior performance of hybrids. While early models focused on alleles, more recent research explores the role of epigenetic factors like DNA methylation and how interaction between genetic and epigenetic variations contribute to heterosis. The molecular basis remains complex and varies depending on organism, population, and trait.

3.  Refers to the phenomenon in which hybrid progeny of two inbred varieties
exhibits enhanced growth or agronomic performance.
 Heterosis was first described by Charles Darwin (Darwin 1876) and
independently rediscovered by Shull (1908) and East(1908).
(‘‘I raised close together two large beds of self-fertilised and crossed seedlings
from the same plant of Linaria vulgaris. To my surprise, the crossed plants
when fully grown were plainly taller and more vigorous than the self-fertilized
ones.’’ - Charles Darwin )
 Term coined by “SHULL” in (1952) as “ stimulation of heterozygosity”.

4. QUANTITATIVE DEFINITION
MID-PARENT HETEROSIS:
It indicates that a trait
displays hybrid performance
that is significantly better
than the average(mid-
parent) valve.
BEST-PARENT HETEROSIS:
Indicates that a hybrid trait
performs significantly better
than the better of two
homozygous parents.AA BB AB(case1) AB(case2)
OffspringParents
Mid –parent
heterosis
Best- parent
heterosis
Performance
Best-parent
Mid-parent
Mid parent Heterosis (MH) = [ (F1- MP)/ MP ] x 100
Better parent (BP) = [ (F1- BP)/ BP ] x 100

5. GENETIC MODELS FOR HETEROSIS
Dominance
True/Pseudo
Over-dominance
Epistasis

6. DOMINANCE MODEL:
The dominance hypothesis explains heterosis by the complementing action of
superior dominant alleles from both parental inbred lines at multiple loci over the
corresponding unfavorable alleles, leading to improved vigor of hybrid plants
OVERDOMINANCE MODEL:
Over-dominance hypothesis attributes heterosis to allelic interactions at one or
multiple loci in hybrids that result in superior traits as compared to

7. •PSEUDO-OVERDOMINANCE:
The genetic intermediate of dominance and ODO IS Pseudo-ODO, which is actually a
case of simple dominance complementation, because of tight repulsion phase
linkage and appears to be ODO.
•EPISTASIS MODEL:
The epistasis hypothesis considers epistatic interactions between nonallelic genes at
two or more loci as the main factor for the superior phenotypic expression of a trait
in hybrids (Powers 1945).

8.  Cancelling of deleterious
or inferior allells
 Heterosis depend on
number of dominant
genes.
 Both parents should
differ in dominant genes.
 According to Panday
Complementation across
loci must be cumulative
to produce a superior
phenotype.
DISCUSSION ON DOMINANCE
MODEL
AA CC EEbb aadd cc ddee BB
*
Aa Cc EeBb dd
P1 P2
F1

9. 0
1
2
3
4
5
6
7
Progressive heterosis refers to
the fact that double cross hybrid
autotetraploids (ABCD) typically
show greater vigor than single
cross hybrids (AABB; CCDD and so
on).
 Increasingly superior alleles at
any one locus must be added to
the genotype with each different
genome introduced in the
tetraploid without contributing
inferior alleles at other loci. The
probability of this occurring is low.
This observation argues against
simple complementation as the
sole basis of heterosis; therefore,
there must be an additional
molecular explanation.
PROGRESSIVE
HETEROSIS

10. DISCUSSION ON OVER-
DOMINANCE
• This model proposes that allelic
interactions at a single heterozygous locus
result in a synergistic effect on vigor that
surpasses both homozygous parents.
• No assumption of dominant- recessive
relationship.
• Both alleles function together.
• Single or small segment of genomes are
responsible for heterosis.
• East (1936) postulated that divergence of
alleles brought together in heterozygotes,
tend to increase the vigour of
heterozygote.
*
P1 P2
A’ A
B” B”
F1
A’
A’
A
A
BB
BB”
A1A4>A1A3>A1A2------------- so on
OVER-DOMINANCE

11. EPISTASIS AS GENETIC MODEL FOR
HETEROSIS
•
• Evidence that the interaction of favorable alleles at different loci
contributed by the two parents, which themselves may show additive,
dominant, or overdominant action
• The genetic background and allelic interactions therein can have an
effect on the heterotic contributions of individual loci.

12. QUANTITATIVE GENETICS OF HETEROSIS
Classical approaches of quantitative genetics to elucidate the genetic basis of heterosis
include :
1.Generation means or diallel analyses and
2.Estimates of variance components reflecting different types of genetic effects .
Comstock and Robinson (1952) used generation mean to estimate the average degree of
dominance, but it ignores the effects of epistasis in estimates of additive and dominance
variance components.
The triple testcross (TTC) design provides a test for contribution of epistasis to
heterosis.

13. Genetic basis
of heterosis
were coined
before the
molecular
concepts of
genetics were
formulated and
are not directly
connected with
Molecular
principles.
AT MOLECULAR
LEVEL TWO
MODELS ARE
USED TO EXPLAIN
HETEROSIS.
One model considers that
in hybrids having two
different kinds of alleles
an allelic expression in
additive manner occurs
.
In the second model the
combination of
different alleles causes
gene expression
changes in hybrids that
deviate relative to mid-
parent.

14. QTL AND HETEROSIS
Molecular breeding may act one of the promising approach to un reveal genetic
basis of heterosis.
Mainly used to identify genes or genomic regions that contribute heterosis for trait
of interest, that may be used in MAS to increase performance of hybrids but still
challenging.
Numerous QTLs with different levels of dominant, over dominant, and epistatic
effects have been mapped for heterosis in Rice (Li et al., 2001;Luo et al. (2001),
and Mei et al. (2003, 2005),

15. CONCLUSIONS FROM THESE QTL AND MARKER BASED STUDIES.
 The specifically detected QTL indicate that different factors are of relevance
under different conditions and it is difficult to decipher molecular basis using
only one hypothesis actually may be caused by combinations of these mutually
nonexclusive mechanisms
The complex trait ‘heterosis’ is expected to be reflected by many genes, their
wide genomic distribution, the combination and interaction of which may
depend on the organism and trait under study .
QTL may not always directly control an individual agronomic trait but may
instead be regulatory in nature, mediated by multi subunit complexes, are
dosage dependent that would contribute to the multigenic control of the
ultimate phenotype .
There is variation in the relative level of heterosis for different traits between
different hybrids. This variation suggests that the same set of genes does not
control all heterotic responses.

16. A CAUSE OF HETEROSIS
EPIGENETICS AS
“Epigenetics” refers to heritable
(through mitosis or meiosis) alterations in
gene expression that are independent of
DNA sequence: different epigenetically
regulated forms of a gene are known as
epialleles.
Epigenetic information systems, could
generate epigenetic variation/epiallels that
had never been considered as the cause of
phenotypic variation .
In addition, local chromatin status,
mediated through epigenetic
modification, can potentially affect gene
expression in cis (at the gene itself) or in
trans (by regulating loci indirectly).
TYPES
DNA
METHYLATION
HISTONE
MODIFICATION
RNAINTERFERANCE
siRNAs, miRNAs etc
CHROMATIN REMODLING

17. DNA methylation is a biochemical process where a methyl
group is added to the cytosine or
adenine DNA nucleotides.
 Conversion of cytosine to 5 methyl cytosine.
DNA methylation does not change the DNA sequence and its function, but
does change its expression level, referred as an epigenetic change.
Associated with gene silencing, and genes with abundant 5-methylcytosine in
their promoter region are usually transcriptionally silent.

18. Basically heterosis is a result of ‘‘different alleles’’
being present at loci that contribute to the regulatory
hierarchies that control quantitative traits .
These ‘‘different alleles’’, however, can arise from
differently methylated DNA. If so, homozygosity of
methylated DNA in such regulatory factors suppresses
gene expression, while its heterozygosity regulates.

19. Heterosis in rice
National Key Laboratory of Crop Genetic Improvement
Experiment,
They use rice as the model system.
They make a cross between Zhenshan 97 and Minghui 63 to
derive an F2:3 population and an "immortalized" F2 population .
 The hetrosis is due the involvement of large numbers of
two-locus interactions, or epistasis, underlying the genetic
basis of quantitative traits.But the contributions of the genetic
components varied with traits

20. Overdominance/pseudo-overdominance is the most
important contributor to heterosis of yield, no. of grains/
panicle, and grain weight.
Dominance × dominance interaction is important for
heterosis of tillers per plant and grain weight and has
roles in yield and grain number.
Single-locus dominance has relatively small
contributions in all of the traits.
The RNA fragments were sequenced and mapped to
the rice linkage map, which provided insights into the
understanding. They analyses ,both combining genetic
and molecular approaches will eventually lead to the
characterization of the biological mechanisms of
heterosis.

21. . Despite the use of advanced technologies it still
remains un clear what is the actual cause of heterosis.
However one common theme through out the century
was that heterosis is complex issue, that is organism ,
population and trait dependent.
 Genetic and molecular approaches lead to the
characterization of the biological mechanisms of heterosis

22. Thanks for patience
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