31. Dosage compensation in drosophila is achieved by-
(1) Selective elimination of maternal X chromosome
(2) Heterochromatization of paternal X chromosome
(3) Hyperactivation of maternal X chromosome
(4) Hyperactivation of paternal X chromosome
Dosage compensation in Drosophila is achieved by the hyperactivation of the paternal X chromosome. This process doubles the transcriptional output from the male’s single X chromosome to balance gene expression with the two X chromosomes present in females.
Explanation of Each Option
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Selective elimination of maternal X chromosome: This does not occur in Drosophila. Selective elimination of an X chromosome is seen in some species but is not the dosage compensation mechanism in Drosophila.
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Heterochromatization of paternal X chromosome: Heterochromatization typically refers to silencing or condensing a chromosome, which reduces expression. This is seen in mammals (X inactivation), not Drosophila where X-linked genes are upregulated in males.
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Hyperactivation of maternal X chromosome: In Drosophila males, there is only one X chromosome, which is paternal-derived in usual genetic crosses, but dosage compensation is not specific to maternal X chromosome hyperactivation.
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Hyperactivation of paternal X chromosome: Correct. In Drosophila, the single X chromosome (often paternal in origin) in males undergoes hyperactivation by the Male-Specific Lethal (MSL) complex, increasing transcription about twofold to match the combined output of females’ two X chromosomes.
Introduction:
Dosage compensation in Drosophila is a crucial genetic mechanism that equalizes the expression of X-linked genes between males and females. Since males have only one X chromosome, this chromosome is hyperactivated to ensure similar gene expression levels as females, who have two X chromosomes. This article explores the mechanisms behind dosage compensation, focusing on the hyperactivation of the paternal X chromosome and contrasting it with other unrelated processes.
Dosage compensation ensures that males (XY) and females (XX) have balanced expression of X-linked genes despite differing numbers of X chromosomes. In Drosophila, this balance is achieved by upregulating transcription from the single male X chromosome approximately twofold. This hyperactivation is mediated by the Male-Specific Lethal (MSL) complex, which acetylates histone proteins, enhancing gene expression along the X chromosome.
Unlike mammals, where one female X chromosome undergoes inactivation through heterochromatization, Drosophila increases gene expression from the male X chromosome. The paternal origin of the male X chromosome is often referenced because the hyperactivation mechanism targets this chromosome directly to compensate for dosage.
Other mechanisms like selective elimination or heterochromatization of the X chromosome are not part of Drosophila dosage compensation but are seen in different species with varying sex chromosome regulation methods.
In summary, the correct mechanism of dosage compensation in Drosophila is the hyperactivation of the paternal X chromosome, distinguishing it from X chromosome inactivation or elimination strategies used elsewhere.
