Synthesis of Ribonucleic Acid by the X-Chromosomes of Drosophila melanogaster and the Problem of Dosage Compensation

Mukherjee, A. S.; Beermann, Wolfgang

doi:10.1038/207785a0

Cited by 184 publications

(66 citation statements)

References 6 publications

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“…This observation indicates that similar levels of G6PD enzyme activity in the two sexes (Seecof et al, 1969) is due to the steady-state level of G6PD mRNA. Also, it supports the previous conclusions, based on studies using salivary gland chromosomes (Mukherjee and Beermann, 1965), that dosage compensation is the result of increased transcriptional activity of the male X chromosome. Our results do not, however, eliminate differential RNA processing and/or RNA turnover rates as possible mechanisms for generating equivalent levels of G6PD mRNA in the two sexes.…”

Section: (B) Wpd Mrnasupporting

confidence: 90%

“…[3H]Uridine incorporation into the single polytenic X chromosome of male larval salivary glands and the paired X chromosomes of females is equivalent (Mukherjee and Beermann, 1965), suggesting that dosage compensation is a ~~sc~ption~ phenomenon. Since this observation suggests that the steady-state level of mRNA encoded by X-linked dosage compensated gene sequences is equivalent in males and females, we determined the relative level of G6PD mRNA in the two sexes.…”

Section: (B) Measurement Of G6pd Mrna Size and Relative Abundancy In mentioning

confidence: 99%

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Isolation and characterization of the glucose-6-phosphate dehydrogenase gene of Drosophila melanogaster

Ganguly

Manning

1985

Gene

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Section: (B) Wpd Mrnasupporting

confidence: 90%

Section: (B) Measurement Of G6pd Mrna Size and Relative Abundancy In mentioning

confidence: 99%

Isolation and characterization of the glucose-6-phosphate dehydrogenase gene of Drosophila melanogaster

Ganguly

Manning

1985

Gene

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“…The first evidence that dosage compensation in Drosophila is achieved by regulating the transcription of X-linked genes was obtained more than 30 years after Muller's seminal observations, by A.S. Mukherjee and W. Beermann (Mukherjee and Beermann 1965). Using transcription autoradiography of the giant polytenic chromosomes of larval salivary glands, a molecular technique that represented the state of the art at that time, these investigators observed that the level of [ 3 H]uridine incorporation by the single X in males and both Xs in females was equivalent.…”

Section: The Phenomenon Of Dosage Compensation Was Discovered In Drosmentioning

confidence: 99%

Dosage Compensation inDrosophila

Lucchesi

Kuroda

2015

Cold Spring Harb Perspect Biol

185

173

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SUMMARYDosage compensation in Drosophila increases the transcription of genes on the single X chromosome in males to equal that of both X chromosomes in females. Site-specific histone acetylation by the malespecific lethal (MSL) complex is thought to play a fundamental role in the increased transcriptional output of the male X. Nucleation and sequence-independent spreading of the complex to active genes serves as a model for understanding the targeting and function of epigenetic chromatin-modifying complexes. Interestingly, two noncoding RNAs are key for MSL assembly and spreading to active genes along the length of the X chromosome.

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“…N Drosophila, dosage compensation occurs by an upregulation of transcription from the X chromosome in males (Mukherjee and Beermann 1965;Belote and Lucchesi 1980;Straub et al 2005). The best-characterized mechanism of upregulation depends on the male-specific activity of the malespecific lethal (MSL) complex (Gelbart and Kuroda 2009), which binds to sites on the X chromosome and enhances the rate of transcript elongation (Larschan et al 2011).…”

mentioning

confidence: 99%

Sex-Specific Pattern Formation During Early Drosophila Development

2013

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The deleterious effects of different X-chromosome dosage in males and females are buffered by a process called dosage compensation, which in Drosophila is achieved through a doubling of X-linked transcription in males. The male-specific lethal complex mediates this process, but is known to act only after gastrulation. Recent work has shown that the transcription of X-linked genes is also upregulated in males prior to gastrulation; whether it results in functional dosage compensation is not known. Absent or partial early dosage compensation raises the possibility of sex-biased expression of key developmental genes, such as the segmentation genes controlling anteroposterior patterning. We assess the functional output of early dosage compensation by measuring the expression of even-skipped (eve) with high spatiotemporal resolution in male and female embryos. We show that eve has a sexually dimorphic pattern, suggesting an interaction with either X-chromosome dose or the sex determination system. By manipulating the gene copy number of an X-linked transcription factor, giant (gt), we traced sex-biased eve patterning to gt dose, indicating that early dosage compensation is functionally incomplete. Despite sex-biased eve expression, the gene networks downstream of eve are able to produce sex-independent segmentation, a point that we establish by measuring the proportions of segments in elongated germ-band embryos. Finally, we use a whole-locus eve transgene with modified cis regulation to demonstrate that segment proportions have a sexdependent sensitivity to subtle changes in Eve expression. The sex independence of downstream segmentation despite this sensitivity to Eve expression implies that additional autosomal gene-or pathway-specific mechanisms are required to ameliorate the effects of partial early dosage compensation. IN Drosophila, dosage compensation occurs by an upregulation of transcription from the X chromosome in males (Mukherjee and Beermann 1965;Belote and Lucchesi 1980;Straub et al. 2005). The best-characterized mechanism of upregulation depends on the male-specific activity of the malespecific lethal (MSL) complex (Gelbart and Kuroda 2009), which binds to sites on the X chromosome and enhances the rate of transcript elongation (Larschan et al. 2011). MSL activity is inhibited in females by the translational repression of Msl2 protein, which is necessary for complex formation, by the protein product of the sex-determination gene Sex-lethal (Sxl) (Kelley et al. 1995). The canonical MSL-dependent mechanism does not appear to be active prior to gastrulation as msl2 transcript is not detected until cleavage cycle 14 (Lott et al. 2011) and the earliest expression of Msl3 protein in male embryos is detected only at stage 6 (gastrulation) (Rastelli et al. 1995;Franke et al. 1996;Cline 2005).Despite the lack of MSL-dependent dosage compensation during the blastoderm stage, the transcription of X-linked genes expressed before gastrulation is, in fact, elevated in males (Lott et al. 2011). With the exc...

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Synthesis of Ribonucleic Acid by the X-Chromosomes of Drosophila melanogaster and the Problem of Dosage Compensation

Cited by 184 publications

References 6 publications

Isolation and characterization of the glucose-6-phosphate dehydrogenase gene of Drosophila melanogaster

Isolation and characterization of the glucose-6-phosphate dehydrogenase gene of Drosophila melanogaster

Dosage Compensation inDrosophila

Sex-Specific Pattern Formation During Early Drosophila Development

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