ArticleEpigenetics & chromatin2013
Male X-linked genes in Drosophila melanogaster are compensated independently of the Male-Specific Lethal complex.
Article in Epigenetics & chromatin, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Adult expression of Semaphorins and Plexins is essential for motor neuron survival.Scientific reports · 2023Article
- Modulation of RNA stability regulates gene expression in two opposite ways: through buffering of RNA levels upon global perturbations and by supporting adapted differential expression.Nucleic acids research · 2022Article
- The role of H3K36 methylation and associated methyltransferases in chromosome-specific gene regulation.Science advances · 2021Article
- Article
- Faint gray bands in Drosophila melanogaster polytene chromosomes are formed by coding sequences of housekeeping genes.Chromosoma · 2020Article
- Article
- RNA-on-X 1 and 2 in Drosophila melanogaster fulfill separate functions in dosage compensation.PLoS genetics · 2018Article
- Non-canonical Drosophila X chromosome dosage compensation and repressive topologically associated domains.Epigenetics & chromatin · 2018Article
- RNA sequencing reveals a complete but an unconventional type of dosage compensation in the domestic silkwormRoyal Society open science · 2017Article
- Article
- Primary Sex Determination in Drosophila melanogaster Does Not Rely on the Male-Specific Lethal Complex.Genetics · 2016Article
- Dosage Compensation in the African Malaria Mosquito Anopheles gambiae.Genome biology and evolution · 2016Article
- Proximity ligation assays of protein and RNA interactions in the male-specific lethal complex on Drosophila melanogaster polytene chromosomes.Chromosoma · 2015Article
- X Chromosome and Autosome Dosage Responses in Drosophila melanogaster Heads.G3 (Bethesda, Md.) · 2015Article
- Increased expression of X-linked genes in mammals is associated with a higher stability of transcripts and an increased ribosome density.Genome biology and evolution · 2015Article
- Review
- Article
- Non-coding roX RNAs prevent the binding of the MSL-complex to heterochromatic regions.PLoS genetics · 2014Article
- Facts and artifacts in studies of gene expression in aneuploids and sex chromosomes.Chromosoma · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn organisms where the two sexes have unequal numbers of X-chromosomes, the expression of X-linked genes needs to be balanced not only between the two sexes, but also between X and the autosomes. In Drosophila melanogaster, the Male-Specific Lethal (MSL) complex is believed to produce a 2-fold increase in expression of genes on the male X, thus restoring this balance.
resultsHere we show that almost all the genes on the male X are effectively compensated. However, many genes are compensated without any significant recruitment of the MSL-complex. These genes are very weakly, if at all, affected by mutations or RNAi against MSL-complex components. In addition, even the genes that are strongly bound by MSL rely on mechanisms other than the MSL-complex for proper compensation. We find 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.
conclusionsWe conclude that most of the compensation of X-linked genes is produced by an MSL-independent mechanism. Similar to the case of the MSL-mediated compensation we do not yet know the mechanism behind the MSL-independent compensation that appears to act preferentially on long genes. Even if we observe similarities, it remains to be seen if the mechanism is related to the buffering that is observed in autosomal aneuploidies.
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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.