A dominant gene V in humans causes certain areas of the skin to become depigmented, a condition called "vitiligo." Albinism is the complete lack of pigment production and is produced by the recessive genotype aa. The albino locus is epistatic to the vitiligo locus. Another gene locus, the action of which is independent of the previously mentioned loci, is known to be involved in a mildly anemic condition called "thalassemia." (a) When the adult progeny from parents both of whom exhibit vitiligo and a mild anemia is examined, the following phenotypic proportions are observed : 1/16 normal : 3/16 vitiligo : 1/8 mildly anemic : 1/12 albino : 3/8 vitiligo and mildly anemic : 1/6 albino and mildly anemic. What is the mode of genetic action of the gene for thalassemia? (b) What percentage of the viable albino offspring in part (a) would carry the gene for vitiligo? (c) What percentage of viable offspring with symptoms of mild anemia also show vitiligo?
To determine the mode of genetic action of the gene for thalassemia, we need to analyze the phenotypic ratios observed in the offspring.
(a) The observed phenotypic ratios are as follows:
- 1/16 normal
- 3/16 vitiligo
- 1/8 mildly anemic
- 1/12 albino
- 3/8 vitiligo and mildly anemic
- 1/6 albino and mildly anemic
From these ratios, we can see that the phenotypic proportions of vitiligo and mild anemia are the same (3/8 each) in the offspring. This indicates that the gene for thalassemia is showing a complementary gene interaction with the gene for vitiligo.
A complementary gene interaction occurs when the presence of two recessive alleles at different gene loci is required to produce a specific phenotype. In this case, the presence of both the recessive alleles for thalassemia and the recessive allele for vitiligo is needed to cause the phenotype of vitiligo and mild anemia.
(b) To determine the percentage of viable albino offspring that would carry the gene for vitiligo, we need to consider the genotypes of the albino individuals. We know that the albino locus is epistatic to the vitiligo locus, meaning that the presence of the albino allele masks the expression of the vitiligo allele.
Given that the albino genotype is aa, which represents homozygosity for the albino allele, it means that both alleles are "a" and there is no presence of the V allele. Therefore, none of the viable albino offspring would carry the gene for vitiligo.
(c) To determine the percentage of viable offspring with symptoms of mild anemia (which we know is caused by the gene for thalassemia) that also show vitiligo, we need to consider the genotypes that exhibit mild anemia.
From the phenotypic ratios given, we can see that the proportions for mild anemia are 1/8 mildly anemic, 3/8 vitiligo and mildly anemic, and 1/6 albino and mildly anemic.
If we add up these ratios, we find that the total percentage of viable offspring with mild anemia is (1/8) + (3/8) + (1/6) = 5/12.
Out of these mild anemic individuals, we need to determine how many also exhibit vitiligo. From the given ratios, we see that the proportion of individuals with vitiligo and mild anemia is 3/8. Therefore, the percentage of viable offspring with symptoms of mild anemia that also show vitiligo would be (3/8) / (5/12) = 9/20 or 45%.
To summarize:
(a) The mode of genetic action of the gene for thalassemia is a complementary gene interaction with the gene for vitiligo.
(b) None of the viable albino offspring would carry the gene for vitiligo.
(c) 45% of viable offspring with symptoms of mild anemia also show vitiligo.