Includes information regarding interaction of genes

1. Interaction of Genes
Interaction of Genes
Dr. A. S. Wabale
Dr. A. S. Wabale
Assistant Professor and Research Guide
Assistant Professor and Research Guide
Post Graduate Department of Botany and Research Centre,
Post Graduate Department of Botany and Research Centre,
Padmashri Vikhe Patil College of Arts, Science and Commerce,
Padmashri Vikhe Patil College of Arts, Science and Commerce,
Pravaranagar
Pravaranagar-
- 413 713
413 713
dranilwabale78@gmail.com
dranilwabale78@gmail.com

2. • Non-epistatic genetic interactions- complementary genes (9:7)
• Duplicate Genes (15:1)
• Epistatic genetic interactions- Masking genes (12:3:1)
• Supplementary genes (Recessive epistasis-9:3:4)
• Inhibitory genes(13:3)
• Lethal genes (2:1)-Concept, Inheritance of coat colour in mice
• Inheritance of sickle cell anemia
CONTENTS
CONTENTS

3. Generally while studying Mendel's dihybrid crosses, it is found that two
genes control two different characters. It is, however, not necessary that a single
character is controlled by one gene only, instead it may be controlled by more
than one gene. In such a situation when two or more than two genes come
together to give rise to a particular phenotype is termed as interaction of genes.
e.g. Gene-A is responsible for phenotype-A and Gene-B is responsible
for phenotype-B, both ‘A’ and ‘B’ when present together may give rise to a
phenotype-C. If ‘A’ and ‘B’ are two genes, both dominant over their recessive
alleles ‘a’ and ‘b’, then the interaction will depend upon
v The presence of both dominant alleles
v Absence of ‘A’
v Absence of ‘B’
v Absence of both ‘A’ and ‘B’
Such a type of interaction is called as interaction of genes
INTRODUCTION
INTRODUCTION

4. If two genes are involved in a specific pathway OR responsible for producing a particular
phenotype, such a interaction is called as complementary gene interaction.
W. Bateson and R. C. Punnett observed that when two white flowered varieties of sweet pea,
Lathyrus odoratus are crossed, F1 progeny had all coloured flowers. When F2 progeny
obtained from F1 was classified, plants with coloured flowers and those with white flowers
were obtained in 9:7 ratio which was the modification of 9:3:3:1 ratio
I.e. A pea plant with white flowers (genotype =CCpp) is crossed to a plant with white flowers
(genotype =ccPP), the F1 plant will have purple colored flowers and a CcPp genotype. The
normal ratio from selfing dihybrid is 9:3:3:1, but interactions of the ‘C’ and ‘P’ genes give a
modified 9:7 ratio. The following table describes the interactions for each genotype and
how the ratio occurs.
Genotype Flower Color Enzyme Activities/TH>
9 C_P_ Flowers colored; anthocyanin produced Functional enzymes from both genes
3 C_pp Flowers white; no anthocyanin produced p enzyme non-functional
3 ccP_ Flowers white; no anthocyanin produced c enzyme non-functional
1 ccpp Flowers white; no anthocyanin produced c and p enzymes non-functional
COMPLEMENTARY GENE INTERACTION
COMPLEMENTARY GENE INTERACTION

5. Complementary gene action: Enzyme-C and enzyme-P cooperate to make a
product, therefore they complement one another
Purple
pigment
Colorless
intermediate
Colorless
precursor
COMPLEMENTARY GENE INTERACTION
COMPLEMENTARY GENE INTERACTION

6. A Cross Producing a 9:7 ratio
9 C_P_ : 3 C_pp : 3 ccP_ : 1 ccpp
purple white
COMPLEMENTARY GENE INTERACTION
COMPLEMENTARY GENE INTERACTION

7. Phenotypes: Kernel Color in Wheat
• For this type of pathway a functional enzyme ‘A’ or ‘B’ can
produce a product from a common precursor. The product
gives color to the wheat kernel. Therefore, only one dominant
allele at either of the two loci is required to generate the
product.
• Thus, if a pure line wheat plant with a colored kernel (genotype
= AABB) is crossed to plant with white kernels (genotype =
aabb) and the resulting F1 plants are selfed, a modification of
the dihybrid 9:3:3:1 ratio will be produced. The following table
provides a biochemical explanation for the 15:1 ratio.
• If we sum the three different genotypes that will produce a
colored kernel we can see that we can achieve a 15:1 ratio.
Because either of the genes can provide the wild type
phenotype, this interaction is called duplicate gene action.
Genotype Kernel Phenotype Enzymatic Activities
9 A_B_ colored kernels functional enzymes from both genes
3 A_bb colored kernels functional enzyme from the A gene pair
3 aaB_ colored kernels functional enzyme from the B gene pair
1 aabb colorless kernels non-functional enzymes produced at both genes
DUPLICATE GENES
DUPLICATE GENES

8. Phenotype: Fruit Shape of Shepherds Purse
i.e. Capsella modification of mendelian ratio 15:1
Both enzymes ‘A’ and ‘B’ make product ‘C’,
therefore they duplicate each other
TV, Tv, tV gives triangular shape and tv- gives ovate
shape
DUPLICATE GENES
DUPLICATE GENES
Precursor Product
Genotype- TV, Tv, tV
Enzyme
Enzyme
Genotype- tv
TV
TV
Tv
Tv
tV
tV
tv
tv
TTVV TTVv TtVV TtVv
TTVv TTvv TtVv Ttvv
TtVV TtVv ttVV ttVv
TtVv Ttvv ttVv ttvv
TTVV
Triangular
ttvv
Ovate
x
F1 generation TtVv
All Triangular
F2 generation- 15:1

9. Epistasis is a form of gene interaction in which one gene masks the
phenotypic expression of another.
n The alleles that are masking the effect are called epistatic alleles
n The alleles whose effect is being masked are called the hypostatic
alleles.
n Epistasis can be described as either recessive epistasis or dominant
epistasis.
EPISTATIC GENE INTERACTION
EPISTATIC GENE INTERACTION

10. Brown Dog (bbii) X White Dog (BBII)
Gametes BI bI Bi bi
BI BBII
(W)
BbII
(W)
BBIi
(W)
BbIi
(W)
bI BbII
(W)
bbII
(W)
BbIi
(W)
bbIi
(W)
Bi BBIi
(W)
BbIi
(W)
BBii
(B)
Bbii
(B)
bi BbIi
(W)
bbIi
(W)
Bbii
(B)
bbii
(Br)
F2 Generation- 12:3:1
A condition in which out of two pairs
of genes the dominant allele, (i.e. gene
A) masks the activity of other allelic
pair (Bb) is called as dominant
epistasis. The dominant epistatic gene
‘A’ suppresses the expression of
hypostatic gene ‘B’ or ‘b’.
Example: In dogs white coat colour
appears to be dominant. It develops
due to the action of epistatic gene ‘I’
which prevents the formation of
pigment, controlled by hypostatic gene
‘B’. Hypostatic gene ‘B’ produces black
coat whereas its allele ‘b’ produces
brown colour when gene ‘I’ is
recessive. When two white dogs are
crossed, they produce white, black and
brown colour in the ratio of 12:3:1. The
white dogs in this case posses gene for
black and brown colour but does not
produce the pigment due to the
presence of gene ‘I’ in dominant state.
DOMINANT EPISTASIS: (12:3:1 RATIO)
DOMINANT EPISTASIS: (12:3:1 RATIO)
bi
BI
All white (BbIi)
F1 Generation

11. RECESSIVE EPISTASIS/SUPPLEMENTARY GENE ACTION: (9:3:4 RATIO)
RECESSIVE EPISTASIS/SUPPLEMENTARY GENE ACTION: (9:3:4 RATIO)
Example- Colour Coat in Mice (9:3:4)
AC- Agouti/ Gray colour
aC- Black colour
Ac, ac- White colour
In mice agouti (gray) colour is due to the
dominant gene-’A’. The dominant gene-’C’ in
absence of dominant gene-’A’ gives black
colored mice and in presence gives agouti
mice.
But dominant gene-’A’ is unable to produce
agouti colour in presence of recessive gene-
’c’.
Therefore recessive gene-’c’ acts as a epistatic
over dominant gene-’A’. F2 Generation- 9:3:4
Gametes AC Ac aC ac
AC AACC
(Gray)
AACc
(Gray)
AaCC
(Gray)
AaCc
(Gray)
Ac AACc
(Gray)
AAcc
(White)
AaCc
(Gray)
Aacc
(White)
aC AaCC
(Gray)
AaCc
(Gray)
aaCC
(Black)
aaCc
(Black)
ac AaCc
(Gray)
Aacc
(White)
aaCc
(Black)
aacc
(White)
Parents Gray Mice X White/Albino mice
(AACC) (aacc)
Gametes AC ac
F1 Generation AaCc
All Gray mice
Epistasis due to recessive gene is known
as recessive epistasis. i.e. out of the two
pairs of genes, the recessive epistatic
gene masks the activity of dominant
gene of the other gene locus. The
dominant ‘A’ gene express itself only in
presence of dominant ‘C’ gene. If
recessive ‘c’ gene is present the
character of dominant ‘A’ gene is
masked.

12. Example Maize Aleurone Colour (13:3 ratio)
One dominant gene- ‘R’ produces concerned
phenotype (red colour) and its recessive allele- ‘r’
produces contrasting phenotype (white colour).
The second dominant allele- ‘I’ has no effect on
the concerned phenotype (colour) but stops the
expression of dominant gene- ‘R’, so when both
dominant alleles are present, phenotype (white
colour) as that of recessive homozygote is
produced.
‘RI’- White
‘Ri’- Red
‘rI’- White
‘Ri’- White
Gametes RI Ri rI ri
RI RRII
(White)
RRIi
(White)
RrII
(White)
RrIi
(White)
Ri RRIi
(White)
RRii
(Red)
RrIi
(White)
Rrii
(Red)
rI RrII
(White)
RrIi
(White)
rrII
(White)
rrIi
(White)
ri RrIi
(White)
Rrii
(Red)
rrIi
(White)
rrii
(White)
INHIBITORY GENE INTERACTION (13:3 RATIO)
INHIBITORY GENE INTERACTION (13:3 RATIO)
F2 Generation- 13:3
Aleurone Layer
White
Seed
Red
Seed
Parents RRII X rrii
(White Aleurone) (White Aleurone)
Gametes RI ri
F1 Generation RrIi
(All White Aleurone)

13. Gametes Y y
Y YY
Dies
Yy
y Yy yy
LETHAL GENES (2:1 RATIO)
LETHAL GENES (2:1 RATIO)
L. Cuenot, French geneticist studied the
inheritance of mouse body colour that did not fit
the expected mendelian segregation pattern.
It was found that yellow body colour was
dominant over normal brown colour controlled by
a single gene designated as ‘Y’. It was found that
yellow mice never obtained in homozygous
condition i.e. YY
When yellow mice were crossed among
themselves, the F2 generation obtained in 2:1 ratio
instead of 3:1. The brown mice were pure and
were therefore homozygous and yellow individuals
as usual were heterozygous
The results were explained with the assumptions
that allele ‘Y’ (yellow body colour) which was
dominant in heterozygous condition was
responsible for lethality in homozygous condition.
i.e. Whenever a homozygous individual for ‘Y’ is
produced, the lethal character will express itself
and the individual will die. Thus homozygous
yellow will never be produced
Yellow (Yy) Yellow (Yy)
X
F2 Generation- 2:1

14. Sickle Cell Anemia is a genetic disorder that affects erythrocytes (RBC’s) causing them to
become sickle or crescent shape due to abnormality of hemoglobin molecules. Dr. Earnest E.
Irons was the first to observe these type of cells in the year 1904.
It is an inherited form of anemia in which there are not enough healthy red blood cells (RBC’s)
to carry adequate oxygen throughout the body.
Normally, red blood cells are flexible and round, moving easily through the blood vessels. In
sickle cell anemia, the RBC’s become rigid and sticky with sickle or crescent moon shape. So
the name Sickle Cell
These irregularly shaped cells get stuck in small blood vessels, slowing down or blocking blood
flow and oxygen to parts of body. HbS is a gene responsible for sickle cell hemoglobin that
cause sickle cell anemia.
INHERITANCE OF SICKLE CELL ANEMIA
Normal
Red
Blood
Cell
Sickle
Cell
Sickle Cell blocking
blood flow
Unrestricted blood flow

15. WHEN ONE PARENT IS A PATIENT AND
ANOTHER IS A CARRIER
WHEN ONE PARENT IS CARRIER
WHEN BOTH PARENTS ARE PATIENTS WHEN BOTH PARENTS ARE CARRIERS
PATIENTS UNAFFECTED CARRIERS
MOTHER WITH SICKLE
CELL ANEMIA
HbSS
CARRIER FATHER
HbAS
CARRIER FATHER
HbAS
UNAFFECTED MOTHER
HbAA
CARRIER FATHER
HbAS
CARRIER MOTHER
HbAS
MOTHER WITH SICKLE
CELL ANEMIA
HbSS
FATHER WITH SICKLE
CELL ANEMIA
HbSS
HbSS HbSS
HbAS
HbAS HbAS HbAS
HbAA
HbAA
HbAS HbSS
HbAS
HbAA
HbSS HbSS
HbSS
HbSS
50% with SCA
50% Carriers
50% without SCA
50% Carriers
All with SCA 25% without SCA
25% with SCA
50% Carriers

16. ASSIGNMENT
ASSIGNMENT
DEFINITION
• Interaction of Genes
• Complementary Interaction
• Epistasis
• Dominant Epistasis
• Recessive Epistasis
• Supplementary Interaction
• Duplicate Genes
• Lethal Genes
• Inhibitory Genes
SHORT QUESTIONS
• Describe in brief complementary gene interaction with example
• Explain dominant epistasis
• Comment on recessive epistasis
• Write a note on duplicate genes
• Comment on lethal genes
• Write a note on inhibitory genes
LONG QUESTIONS
• What is epistasis? Describe dominant and recessive epistasis with suitable examples.
• What is sickle cell anemia? Explain inheritance of sickle cell anemia in detail.