Most alleles of the Drosophila cut (ct) gene are stable. For example, all progeny from crossing ct1 to ct2 to yield ct1 /ct2 heterozygotes have \"cut\" wings. ct1 is a strong allele with severe cutting of the wings. ct2 and another allele, ctMR2, are weaker with only moderate cutting of the wings. When ctMR2 homozygotes are crossed to ct1 homozygotes, three kinds of progeny are produced, 95% have a moderate cutting of the wings (as expected for ctMR2 / ct1 ), 2.5% have wild-type wings and 2.5% have more severe cut wings like ct1 homozygotes. a) How do you explain the high frequency of reversion to wild-type? b) How do you explain the high frequency of progeny with the more severe cut phenotype? Solution B) high frequency of phenotype for the more severe cut progeny can be explained by a dominant epistasis. Epistasis, is a type of GENE interaction but not allele interaction. Here one gene either masks or modifies the expression of the other gene . The gene that masks the expression is called EPISTATIC and the gene that is getting masked or modified is called the HYPOSTATIC gene. Epistasis is a gene interaction and not an allele interaction, in this way it is different from dominance. In epistasis, the ratio turns out to be less than 4 , as in an usual Di hybrid cross. A) the occurrence of the wild type wing is also due to the epistatic nature of the ct1 gene, which expresses itself , regardless of the second gene. In case where there are no Dominant alleles of the ct1 gene and also, none of the ctMR2 gene, the reversion to the wild type gene could be seen as none of the other alleles would express themselves..

1. Most alleles of the Drosophila cut (ct) gene are stable. For example, all progeny from crossing
ct1 to ct2 to yield ct1 /ct2 heterozygotes have "cut" wings. ct1 is a strong allele with severe
cutting of the wings. ct2 and another allele, ctMR2, are weaker with only moderate cutting of the
wings. When ctMR2 homozygotes are crossed to ct1 homozygotes, three kinds of progeny are
produced, 95% have a moderate cutting of the wings (as expected for ctMR2 / ct1 ), 2.5% have
wild-type wings and 2.5% have more severe cut wings like ct1 homozygotes. a) How do you
explain the high frequency of reversion to wild-type? b) How do you explain the high frequency
of progeny with the more severe cut phenotype?
Solution
B) high frequency of phenotype for the more severe cut progeny can be explained by a dominant
epistasis. Epistasis, is a type of GENE interaction but not allele interaction. Here one gene either
masks or modifies the expression of the other gene . The gene that masks the expression is called
EPISTATIC and the gene that is getting masked or modified is called the HYPOSTATIC gene.
Epistasis is a gene interaction and not an allele interaction, in this way it is different from
dominance. In epistasis, the ratio turns out to be less than 4 , as in an usual Di hybrid cross.
A) the occurrence of the wild type wing is also due to the epistatic nature of the ct1 gene, which
expresses itself , regardless of the second gene. In case where there are no Dominant alleles of
the ct1 gene and also, none of the ctMR2 gene, the reversion to the wild type gene could be seen
as none of the other alleles would express themselves.