ArticleGenetics2005
Gene expression analysis of the function of the male-specific lethal complex in Drosophila.
Article in Genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- Genome-Wide Identification of Long Noncoding RNA and Their Potential Interactors inInternational journal of molecular sciences · 2022Article
- Modulation of Global Gene Expression by Aneuploidy and CNV of Dosage Sensitive Regulatory Genes.Genes · 2021Article
- Interaction of Male Specific Lethal complex and genomic imbalance on global gene expression in Drosophila.Scientific reports · 2021Article
- Non-canonical Drosophila X chromosome dosage compensation and repressive topologically associated domains.Epigenetics & chromatin · 2018Article
- Dosage-Dependent Expression Variation Suppressed on theG3 (Bethesda, Md.) · 2018Article
- Dosage compensation of the sex chromosomes and autosomes.Seminars in cell & developmental biology · 2016Review
- Male-Killing Spiroplasma Alters Behavior of the Dosage Compensation Complex during Drosophila melanogaster Embryogenesis.Current biology : CB · 2016Article
- Variation in transcriptome size: are we getting the message?Chromosoma · 2015Review
- Facts and artifacts in studies of gene expression in aneuploids and sex chromosomes.Chromosoma · 2014Review
- Transcriptional control of a whole chromosome: emerging models for dosage compensation.Nature structural & molecular biology · 2014Review
- Male X-linked genes in Drosophila melanogaster are compensated independently of the Male-Specific Lethal complex.Epigenetics & chromatin · 2013Article
- Dosage compensation and inverse effects in triple X metafemales of Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Male-specific lethal complex in Drosophila counteracts histone acetylation and does not mediate dosage compensation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Dosage compensation in Drosophila melanogaster: epigenetic fine-tuning of chromosome-wide transcription.Nature reviews. Genetics · 2012Review
- Dosage compensation of the sex chromosomes.Annual review of genetics · 2012Review
- Article
- X-chromosome hyperactivation in mammals via nonlinear relationships between chromatin states and transcription.Nature structural & molecular biology · 2011Article
- The nucleosome remodeling factor.FEBS letters · 2011Review
- Sub-cellular internalization and organ specific oral delivery of PABA nanoparticles by side chain variation.Journal of nanobiotechnology · 2011Article
- Expression in aneuploid Drosophila S2 cells.PLoS biology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Dosage compensation refers to the equal expression of X-linked genes despite the difference in copy number between the two sexes. The male-specific lethal (MSL) complex is concentrated on the X chromosome in males. A gene expression assay for embryos was developed to examine the function of this complex. In mutant male embryos without either the MSL complex or MOF histone acetylase, dosage compensation is retained but autosomal expression is increased. Dosage compensation is lost in the double-mutant embryos. In embryos in which the MSL complex and MOF are targeted to the X chromosomes in females, the results are consistent with previous surveys showing that in general the X expression remains unchanged, but autosomal expression is reduced. Mutations in the ISWI chromatin-remodeling component cause increases specifically of X-linked genes in males. Thus, the function of the MSL complex in conjunction with ISWI is postulated to override the effect on gene expression of high histone acetylation on the male X. The basic determinant of dosage compensation is suggested to be an inverse dosage effect produced by an imbalance of transcription factors on the X vs. the autosomes. 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.