UNIT 2 – Gene Action and Interactions (Q&A) | MZO-002 MSCZOO | IGNOU

SAQ 1

Fill in the blanks with appropriate word:

a) A condition in which a gene or gene pair suppresses or hinders the expression of another non-allelic gene is called ...................... .
Answer: epistasis

b) The phenotype effect gets enhanced because of the effect of ....................... genes.
Answer: cumulative or additive 

c) Red eye colour in Drosophila melanogaster is due to the deposition of pigment ...................... .
Answer: drosopterins

d) Progeny shows a ratio of ........................ in case of duplicate dominant epistasis. 
Answer: 15 : 1

e) Epistasis in which a dominant allele at one locus can mask the expression of both (dominant and recessive) alleles at the second locus occurs due to .......................... gene interaction.
Answer: inhibitory

SAQ 2

State whether these statements are 'True' or 'False.'

a) Pleiotropy occurs when a gene shows a complementary gene interaction with another gene.
Answer: False

b) Pleiotropic effects of albinism include impaired vision and a higher risk of skin cancer.
Answer: True

c) Mutation in the gene encoding phenylalanine hydroxylase leads to uraemia.
Answer: True

d) Pleiotropic effects of sickle cell anemia result due to haemolysis and blockages of blood vessels.
Answer: False

e) Persistent lung infections and salty skin occur when there is a mutation in the CFTR gene.
Answer: False

SAQ 3

State whether the following statements are 'True' or 'False'

a) Phenocopies are inherited by the offspring.
Answer: False

b) Father with blood type AB has a son showing blood group O.
Answer: True

c) Prototrophs do not require supplementation of minimum culture medium to grow.
Answer: False

d) Rose comb allele in chickens is dominant over pea comb allele.
Answer: True

e) Hemophilia is a sex-linked dominant disorder.
Answer: True

SAQ4

Match the terms given in column A with the appropriate description in column B

Answer: a) → iii;     b) → v;     c) → iv;     d) → i;     e) ii

TERMINAL QUESTIONS

1. What is the difference between dominance and epistasis? Why didn't any dihybrid crosses studied by Mendel show epistasis?

To understand the difference, we need to know that both dominance and epistasis are related to how genes express themselves, but they work at different levels.

Dominance

Dominance happens between alleles of the same gene. In a pair of alleles (like Aa), the dominant allele masks or hides the effect of the recessive one. For example, in pea plants, tall (T) is dominant and dwarf (t) is recessive. So in genotype Tt, the plant will be tall, because the dominant T shows its effect and t remains hidden.

So, dominance is an interaction between two alleles of the same gene, present at the same locus (same position on homologous chromosomes).

Epistasis

Epistasis happens between alleles of different genes, located at different loci. In this, one gene can mask or modify the effect of another gene. The gene that does the masking is called the epistatic gene and the gene whose expression is affected is called the hypostatic gene.

For example, in Labrador dogs, one gene controls the pigment colour (black or brown), and another gene controls whether pigment is deposited in fur or not. Even if a dog has the gene for black or brown colour, if it has two recessive alleles (ee) at the second locus, no pigment is deposited and the dog will be yellow. So, the e gene is epistatic over the pigment gene.

So, epistasis is interaction between two different genes, where one gene changes or hides the effect of another gene.

Why Mendel's Dihybrid Crosses Did Not Show Epistasis?

Mendel studied seven different characters in pea plants like seed shape, seed colour, flower position, pod shape, etc. In all these characters, each trait was controlled by a single gene with clear dominant and recessive alleles and the genes were independent of each other, not interfering with each other's expression.

So, when he did dihybrid crosses, like round-yellow (RRYY) × wrinkled-green (rryy), the two genes for shape and colour acted independently. There was no gene masking another gene's expression. Hence, he always got the classic 9:3:3:1 phenotypic ratio, which is seen only when there is no epistasis.

Also, Mendel was very careful in choosing traits that were independent and clear in expression. Modern science now knows that many genes do show epistasis, but Mendel was lucky that his selected traits did not. If epistasis was present, the phenotypic ratios would have been different, like 12:3:1 or 9:7 or 13:3, etc.

So, Mendel's dihybrid crosses didn't show epistasis because he unknowingly selected traits controlled by independent and non-interacting genes.

2. a) Can marriage between two albinos produce children with normal pigmentation?

No, marriage between two albinos cannot produce children with normal pigmentation.

This is because albinism is caused by a recessive allele and albino individuals have the genotype aa (homozygous recessive). Since both parents have only recessive alleles (aa × aa), all their children will also receive one a allele from each parent, resulting in genotype aa, which means all children will also be albino.

So, it is genetically impossible for them to have a child with normal pigmentation.

b) A person has met with an accident and needs blood transfusion. However, when tested for blood group, his blood was found to agglutinate blood of types A, B as well as O. His both parents have blood group A. What is the genotype of this person for this trait? How can we explain these observations?

Normally, humans have four main blood groups: A, B, AB and O. These are decided by a gene with three alleles: Iᴬ, Iᴮ and i. The alleles Iᴬ and Iᴮ are dominant and code for A and B antigens on red blood cells, while the i allele is recessive and does not produce any antigen. Blood group O people have genotype ii and their red blood cells show no A or B antigens.

But these A or B antigens are not formed directly. They are actually built upon a base molecule called the H antigen. This H antigen works like a platform or foundation where A or B sugars attach to form the A or B antigen. The H antigen itself is made by a completely different gene, called the H gene, which has two forms:
  • H (dominant) – makes the H antigen normally
  • h (recessive) – does not make the H antigen
If a person has hh genotype, then no H antigen is formed, so even if the person has Iᴬ or Iᴮ alleles, the A or B antigen cannot be displayed on red blood cells. In this condition, the person's red blood cells appear to be without any antigen, just like group O, but their immune system reacts not only to A and B antigens but also to H antigen. This condition is called the Bombay phenotype.

Now, in this question, the person's blood agglutinates (clumps) with A, B and O blood, which is unusual because:
  • A and B blood groups contain A or B antigens, and also H antigen
  • O group does not have A or B antigens, but still has H antigen
Since this person's blood reacts even to O group, it clearly shows that his blood lacks the H antigen and has developed anti-H antibodies, which attack even the H antigen found in O blood. This is only possible in Bombay phenotype, where genotype is hh.

Now, the parents are both A blood group, which means they could be IᴬIᴬ or Iᴬi. Also, they might each carry one recessive h allele: Hh. In that case, they can pass Iᴬ or i and h to their child. If the child receives Iᴬ or i from both sides and h from both sides, then their genotype becomes:
  • ABO system: IᴬIᴬ or Iᴬi
  • H gene: hh
Due to hh, the person cannot express A antigen, even though their ABO genotype is A type. That's why the blood behaves like O, but is not truly O, it is Bombay phenotype, which was first discovered by Dr. Y. M. Bhende in 1952 in Bombay, hence the name.

This person cannot receive blood from A, B or O donors, because their blood contains anti-A, anti-B and also anti-H antibodies. So, they can only receive blood from another Bombay phenotype individual, which is very rare.

Final Genotype of this person:

  • ABO gene: IᴬIᴬ or Iᴬi
  • H gene: hh

3. How is recessive epistasis different from duplicate recessive epistasis?

In classical Mendelian genetics, one gene controls one trait. But in real life, many traits are controlled by two or more genes and sometimes one gene can affect or interfere with the expression of another gene. This interaction is called epistasis. Here, we will compare two types: recessive epistasis and duplicate recessive epistasis. Both involve two genes, but the way they interact is different.

Recessive Epistasis

Recessive epistasis occurs when the recessive alleles of one gene (in homozygous form) can mask or suppress the effect of another gene. In this case, the second gene can be dominant or recessive, but its expression will not appear if the first gene is homozygous recessive.

This means one gene (called the epistatic gene) is stronger and can block the phenotype controlled by the second gene (called the hypostatic gene), but only when present in recessive form.

Example:

A good example is coat colour in mice. One gene (A) controls pigment production. If the mouse has at least one dominant allele A, pigment is produced. The second gene (B) controls the pigment type (black or brown). But if the mouse has genotype aa, no pigment is produced, so the coat is white. Here, gene A is epistatic to gene B. Even if B is dominant (BB or Bb), it cannot show its effect if A is aa.

The typical F2 phenotypic ratio in recessive epistasis is 9:3:4.

Duplicate Recessive Epistasis

Duplicate recessive epistasis is also called complementary gene interaction. Here, both genes are equally important and both must have at least one dominant allele to show the trait. If either gene is homozygous recessive, the phenotype will not be expressed.

This means the recessive allele of any one gene can block the full expression of the trait. Both genes work together to complete the biochemical pathway that produces the phenotype.

Example:

A well-known example is flower colour in sweet pea plant (Lathyrus odoratus). Here, gene C and gene D are both required for purple flower colour. If any of these genes is in homozygous recessive condition (cc or dd), the plant will have white flowers. Only when both genes have at least one dominant allele (meaning at least one C and one D allele), the plant will produce purple flowers. In this case, both cc and dd act as epistatic forms. 

The typical F2 phenotypic ratio in duplicate recessive epistasis is 9:7, where 9 plants have purple flowers and 7 have white flowers.

4. Iᴬ, Iᴮ, i, H genes govern blood group antigens A and B. Using Punnett square, show the ratio of different phenotypes obtained on crossing two heterozygotes, IᴬIᴮHh × IᴬIᴮHh. Which factors contribute to the typical phenotypic ratio?

Cross: IᴬIᴮHh × IᴬIᴮHh

This cross involves two genes:
  • ABO gene (Iᴬ, Iᴮ, i) which determines A, B, AB and O blood group.
  • H gene (H, h) which controls expression of ABO antigens. The hh genotype leads to Bombay phenotype, which lacks A and B antigens regardless of ABO genotype.

Step 1: Gametes

Each parent can produce these gametes: IᴬH, Iᴬh, IᴮH, Iᴮh

Step 2: Punnett Square Results

Using the Punnett square, the possible genotypes and phenotypes are:

1. Genotype combinations:

  • Total 16 combinations from 4×4 grid.

2. Now we separate them based on phenotype:

A. With at least one H allele (HH or Hh): Normal ABO expression

These will express normal A, B, AB and O groups.

B. With hh genotype: Bombay phenotype

Regardless of ABO genotype, these individuals cannot express A or B antigens.
So, they appear as O group but are genetically different. Called Bombay phenotype.

Final Phenotypic Ratio

After counting all combinations from the Punnett square:
  • AB: 6
  • A: 2
  • B: 2
  • O (normal): 1
  • Bombay phenotype (hh): 5
So, phenotypic ratio is:
AB : A : B : O : Bombay = 6 : 2 : 2 : 1 : 5

Factors Contributing to This Phenotypic Ratio

1. Codominance of Iᴬ and Iᴮ: Both are expressed in AB group.

2. H gene epistasis: hh genotype prevents expression of ABO antigens.

3. Independent assortment: ABO gene and H gene are inherited independently.

5. Define and distinguish sex-linked, sex-limited and sex-influenced characters.

In genetics, traits can be influenced or expressed differently depending on the sex of the individual. Some traits are linked to sex chromosomes, while others are affected by hormonal or physiological differences between males and females. To describe these traits more precisely, geneticists use three main terms: sex-linked, sex-limited and sex-influenced traits. Although these terms may sound similar, they refer to different types of genetic expression related to sex. Understanding the distinction among these three is important for grasping how certain traits are inherited and expressed differently in males and females.

1. Sex-linked characters:

These are traits controlled by genes that are located on the sex chromosomes, usually on the X chromosome in humans. Because males have only one X chromosome (XY) and females have two (XX), the pattern of inheritance and expression is different in both sexes. Most sex-linked traits are X-linked, and very few are Y-linked. An example is haemophilia and red-green colour blindness, which are X-linked recessive traits.

2. Sex-limited characters:

These are traits that are controlled by autosomal genes, meaning they are not located on sex chromosomes, but they are expressed only in one sex, due to the presence of sex hormones or other physiological differences. These traits are inherited by both sexes but are phenotypically visible only in one. For example, milk production in female mammals and beard growth in human males.

3. Sex-influenced characters:

These are also controlled by autosomal genes, but their expression is influenced by the sex of the individual. In this case, a gene may behave as dominant in one sex and recessive in the other. This means the same genotype can produce different phenotypes in males and females. An example is pattern baldness in humans, which behaves as dominant in males and recessive in females.

Differences Between Sex-Linked, Sex-Limited and Sex-Influenced Characters

The following comparison highlights how these three types of traits differ from each other across multiple biological aspects:

1. Based on chromosomal location:

Sex-linked traits are genes found on the sex chromosomes, mostly on the X chromosome. Their inheritance depends on the sex of the individual because males and females have different sex chromosomes.

Sex-limited traits are controlled by genes on autosomes (non-sex chromosomes) but show up only in one sex, usually because of hormones that switch these genes on or off in that sex.

Sex-influenced traits are also on autosomes, but their expression changes depending on whether the individual is male or female, due to differences in hormones.

2. Based on expression in sexes:

Sex-linked traits are expressed more commonly in males, because they have only one X chromosome. For example, a male with one recessive allele for haemophilia on X will express the trait.

Sex-limited traits are expressed only in one sex, even though both sexes may carry the gene. For example, milk production appears only in females.

Sex-influenced traits are expressed in both sexes, but differently. For example, baldness is more frequent in males because the gene behaves dominantly in them but recessively in females.

3. Based on hormonal control:

Sex-linked traits are generally not regulated by hormones but depend on the presence of X or Y chromosomes.

Sex-limited traits are directly regulated by sex hormones, such as estrogen and testosterone. For example, testosterone promotes beard growth, a sex-limited male trait.

Sex-influenced traits are partially regulated by hormones, which influence gene dominance. For example, testosterone enhances the expression of baldness.

4. Based on inheritance pattern:

Sex-linked traits follow non-Mendelian patterns, especially criss-cross inheritance (mother to son, father to daughter).

Sex-limited traits follow typical Mendelian autosomal inheritance, but phenotypically expressed in only one sex.

Sex-influenced traits also follow autosomal Mendelian inheritance, but expression is modified by sex.

5. Based on genotype-to-phenotype relationship:

In sex-linked traits, even a single recessive allele on the X chromosome can cause the trait in males.

In sex-limited traits, the genotype may be present in both sexes, but phenotype appears only in one sex. For example, male and female birds may carry the same genotype for feather pattern, but expression is sex-limited.

In sex-influenced traits, same genotype shows different dominance in males and females. For example, a heterozygous male (Bb) for baldness will show baldness, but a heterozygous female (Bb) may not.

6. Whether the oat grains are red or non-red is determined by the dominant allele R and its recessive allele r. Non-red grain (rr) may be yellow or white, these traits being determined by a dominant allele Y (yellow) or its recessive allele y (white). A cross between plants heterozygous for both pairs of genes produced 101 red, 23 yellow and 8 white offspring.

a) What ratio does the data represent?

b) What genotypes could be found among the red offspring?

c) What genotypes would be found among the yellow offspring?

In this case, two gene pairs control oat grain colour:
  • R (dominant) gives red colour.
  • r (recessive) gives non-red and in that case:
    • Y (dominant) gives yellow
    • y (recessive) gives white
So, colour depends on R and Y gene interaction.

Parents are heterozygous: RrYy × RrYy

This cross gives a 12:3:1 phenotypic ratio:
  • Red (R present): 12 parts
  • Yellow (rrY_): 3 parts
  • White (rryy): 1 part

a) What ratio does the data represent?

12 : 3 : 1 Phenotyic Ratio

b) What genotypes could be found among the red offspring?

Red offspring genotypes: RRYY, RRYy, RRyy, RrYY, RrYy, Rryy

c) What genotypes would be found among the yellow offspring?

Yellow offspring genotypes: rrYY, rrYy

7. How did Morgan discover X-linkage in Drosophila?

The discovery of X-linkage was one of the most important milestones in classical genetics. This concept was first established by Thomas Hunt Morgan in 1910 during his genetic experiments on the fruit fly, Drosophila melanogaster. Morgan's work not only confirmed Mendel's laws but also extended them by explaining how certain traits are inherited through the sex chromosomes, especially the X chromosome.

How did Morgan discover X-linkage in Drosophila?

Thomas Hunt Morgan discovered X-linkage in Drosophila melanogaster through careful breeding experiments that studied the inheritance of eye color. This discovery was very important because it showed that genes are located on chromosomes, supporting the chromosome theory of inheritance.

Morgan started his research with fruit flies that normally had red eyes. One day, he found a male fly with white eyes, which was a rare mutation. To understand how this trait was inherited, he crossed this white-eyed male with normal red-eyed females. The first generation (F1) offspring all had red eyes, which showed that red eye color is dominant over white eye color.

Next, Morgan crossed the F1 flies with each other to produce the second generation (F2). Here he noticed something interesting. Among the F2 offspring, all the white-eyed flies were males, while females had only red eyes. This was unusual because, according to Mendel's laws, a recessive trait like white eyes should have appeared in both males and females equally if the gene was on an autosome (non-sex chromosome). The fact that only males showed the white-eyed trait suggested a different pattern of inheritance. After this discovery, Morgan proposed that the gene for eye color was located on the X chromosome, which is one of the sex chromosomes.

In fruit flies, males have one X and one Y chromosome (XY), while females have two X chromosomes (XX). Because males have only one X chromosome, if they inherit the recessive white-eye allele on their single X chromosome, they will show white eyes. Females, on the other hand, need two copies of the recessive allele (one on each X chromosome) to have white eyes. Since the white-eyed female was rare and the mutation was recessive, most females were red-eyed because they usually carried at least one dominant red allele.

Importance of Morgan’s Discovery

Morgan's discovery of this inheritance pattern provided the first clear evidence of sex-linked inheritance, which is when genes are located on sex chromosomes and affect males and females differently. This work was crucial in proving that chromosomes carry genes and that the position of a gene on a chromosome influences how it is inherited.

This discovery also explained why some traits, like certain types of color blindness and hemophilia in humans, are more common in males, because these traits are controlled by genes on the X chromosome. Morgan's work opened a new chapter in genetics by linking specific genes to specific chromosomes, helping to explain the inheritance of many sex-linked traits.

8. Give two examples of gene interaction resulting in the formation of structural proteins.

Gene interaction refers to a situation where two or more genes influence the same trait. In the case of structural proteins, sometimes the final functional protein is not made from a single gene product but is the result of the combination of different polypeptides produced by different genes. Such interaction is especially important in the formation of complex structural proteins that require the association of multiple chains to become functional. Two good examples of this kind of gene interaction are seen in haemoglobin and MHC (Major Histocompatibility Complex) molecules.

1. Haemoglobin (HbA)

Haemoglobin is the oxygen-carrying protein found in red blood cells. The adult type of haemoglobin, called HbA, is a tetramer made up of two alpha-globin chains and two beta-globin chains. These chains are coded by different genes:
  • The alpha-globin gene is located on chromosome 16.
  • The beta-globin gene is located on chromosome 11.
Both these gene products interact and combine with heme groups to form the complete, functional haemoglobin molecule. If either of the chains is defective or missing, the structure and function of haemoglobin is affected, leading to disorders like thalassemia and sickle cell anaemia. This is a clear example of inter-genic interaction, where two gene products come together to form one structural protein.

2. MHC Molecule

MHC (Major Histocompatibility Complex) proteins are essential structural components of the immune system. They are responsible for presenting antigens to T cells. Two main types of MHC molecules show gene interaction during their structural formation:
  • MHC Class I molecules are formed by the interaction of:
    • One alpha-chain, coded by a gene on chromosome 6 and One beta2-microglobulin, coded by a gene on chromosome 15.
  • MHC Class II molecules are formed by:
    • One alpha-chain and One beta-chain, both coded by different genes within the MHC gene cluster on chromosome 6.
In both MHC Class I and II, the chains must combine properly to form the complete structural molecule. Without this gene interaction, the MHC proteins cannot function in antigen presentation.









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