ArticleMolecular and cellular biology2005
The MRG domain mediates the functional integration of MSL3 into the dosage compensation complex.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 56 citations in OpenAlex.
- Two Chinese patients with Basilicata-Akhtar syndrome caused by novelTranslational pediatrics · 2025Article
- Convergent evolution of H4K16ac-mediated dosage compensation in the ZW species Artemia franciscana.PLoS genetics · 2025Article
- Sex Chromosome Dosage Compensation in Insects.Insects · 2025Review
- Processivity and specificity of histone acetylation by the male-specific lethal complex.Nucleic acids research · 2024Article
- Loss of function of male-specific lethal 3 (Msl3) does not affect spermatogenesis in rodents.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Article
- Tip60's Novel RNA-Binding Function Modulates Alternative Splicing of Pre-mRNA Targets Implicated in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- JASPer controls interphase histone H3S10 phosphorylation by chromosomal kinase JIL-1 in Drosophila.Nature communications · 2019Article
- De novo mutations in MSL3 cause an X-linked syndrome marked by impaired histone H4 lysine 16 acetylation.Nature genetics · 2018Article
- Divergent actions of long noncoding RNAs on X-chromosome remodelling in mammals and Drosophila achieve the same end result: dosage compensation.Journal of genetics · 2015Review
- Arabidopsis MRG domain proteins bridge two histone modifications to elevate expression of flowering genes.Nucleic acids research · 2014Article
- The Drosophila over compensating males gene genetically inhibits dosage compensation in males.PloS one · 2013Article
- Structural insight into the regulation of MOF in the male-specific lethal complex and the non-specific lethal complex.Cell research · 2012Article
- Finding a balance: how diverse dosage compensation strategies modify histone h4 to regulate transcription.Genetics research international · 2012Article
- Role of the ATPase/helicase maleless (MLE) in the assembly, targeting, spreading and function of the male-specific lethal (MSL) complex of Drosophila.Epigenetics & chromatin · 2011Article
- Structure and mechanisms of lysine methylation recognition by the chromodomain in gene transcription.Biochemistry · 2011Review
- Structural basis for MOF and MSL3 recruitment into the dosage compensation complex by MSL1.Nature structural & molecular biology · 2011Article
- Structural and biochemical studies on the chromo-barrel domain of male specific lethal 3 (MSL3) reveal a binding preference for mono- or dimethyllysine 20 on histone H4.The Journal of biological chemistry · 2010Article
- Conditional inactivation of MRG15 gene function limits survival during larval and adult stages of Drosophila melanogaster.Experimental gerontology · 2010Article
- A new strategy for isolating genes controlling dosage compensation in Drosophila using a simple epigenetic mosaic eye phenotype.BMC biology · 2010Article
- Drosophila dosage compensation: a complex voyage to the X chromosome.Development (Cambridge, England) · 2009Review
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5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The male-specific-lethal (MSL) proteins in Drosophila melanogaster serve to adjust gene expression levels in male flies containing a single X chromosome to equal those in females with a double dose of X-linked genes. Together with noncoding roX RNA, MSL proteins form the "dosage compensation complex" (DCC), which interacts selectively with the X chromosome to restrict the transcription-activating histone H4 acetyltransferase MOF (males-absent-on-the-first) to that chromosome. We showed previously that MSL3 is essential for the activation of MOF's nucleosomal histone acetyltransferase activity within an MSL1-MOF complex. By characterizing the MSL3 domain structure and its associated functions, we now found that the nucleic acid binding determinants reside in the N terminus of MSL3, well separable from the C-terminal MRG signatures that form an integrated domain required for MSL1 interaction. Interaction with MSL1 mediates the activation of MOF in vitro and the targeting of MSL3 to the X-chromosomal territory in vivo. An N-terminal truncation that lacks the chromo-related domain and all nucleic acid binding activity is able to trigger de novo assembly of the DCC and establishment of an acetylated X-chromosome territory.
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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.