• Corpus ID: 19051713

Role of the male specific lethal (msl) genes in modifying the effects of sex chromosomal dosage in Drosophila.

@article{Bhadra1999RoleOT,
  title={Role of the male specific lethal (msl) genes in modifying the effects of sex chromosomal dosage in Drosophila.},
  author={Utpal Bhadra and Manika Pal‐Bhadra and James A. Birchler},
  journal={Genetics},
  year={1999},
  volume={152 1},
  pages={
          249-68
        }
}
Immunostaining of chromosomes shows that the male-specific lethal (MSL) proteins are associated with all female chromosomes at a low level but are sequestered to the X chromosome in males. Histone-4 Lys-16 acetylation follows a similar pattern in normal males and females, being higher on the X and lower on the autosomes in males than in females. However, the staining pattern of acetylation and the mof gene product, a putative histone acetylase, in msl mutant males returns to a uniform genome… 

Figures and Tables from this paper

Interaction Study of the Male Specific Lethal (MSL) Complex and Trans-Acting Dosage Effects in Metafemales of Drosophila melanogaster
TLDR
There is a lower autosomal level of histone acetylation compared to the normal metafemales, suggesting a nullifying effect on the negative dosage effect of the X chromosome as previously hypothesized to occur in normal males.
Gene Expression Analysis of the Function of the Male-Specific Lethal Complex in Drosophila
TLDR
The sequestration of the MSL complex to the male X may have evolved to counteract a similar effect on the autosomes and to prevent an overexpression of the X chromosome in males that would otherwise occur due to the high levels of histone acetylation.
Histone acetylation and gene expression analysis of sex lethal mutants in Drosophila.
TLDR
This report examines how mutations in the principal sex determination gene, Sex lethal (Sxl), impact the H4 acetylation and gene expression on both the X and autosomes and finds that when Sxl expression is missing in females, it is found that the sequestration occurs concordantly with reductions in autosomal H4Lys16 acetylations and gene Expression on the whole.
Dosage Dependent Gene Regulation and the Compensation of the X Chromosome in Drosophila Males
TLDR
Evidence is described for a model that dosage compensation is caused by an 'inverse dosage effect’ that results from an altered stoichiometry of transcriptional regulators on the X versus the autosomes that causes a two-fold increase in target gene expression throughout the genome.
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TLDR
It is found that long, non-ubiquitously expressed genes tend to rely less on the MSL-complex for their compensation and genes that in addition are far from High Affinity Sites tend to not bind the complex at all or very weakly.
roX RNAs Are Required for Increased Expression of X-Linked Genes in Drosophila melanogaster Males
TLDR
The results implicate failure to compensate X-linked genes, rather than inappropriate upregulation of autosomal genes at ectopic sites of MSL binding, as the primary cause of male lethality upon loss of roX RNAs.
Male-specific lethal complex in Drosophila counteracts histone acetylation and does not mediate dosage compensation
TLDR
The data indicate that the male-specific lethal (MSL) complex does not mediate dosage compensation directly, but rather, its activity overrides the high level of histone acetylation and counteracts the potential overexpression of X-linked genes to achieve the proper twofold up-regulation in males.
Drosophila MSL complex globally acetylates H4 Lys16 on the male X chromosome for dosage compensation
TLDR
Almost all active genes on the X chromosome are associated with robust H4 Lys16 acetylation (H4K16ac), the histone modification catalyzed by the MSL complex, suggesting a common principle for the establishment of active and silenced chromatin domains.
Re-evaluation of the function of the male specific lethal complex in Drosophila.
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