ArticlePLoS genetics2008
Genetic modifiers of MeCP2 function in Drosophila.
Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 76 citations in OpenAlex.
- Autism: epidemiology, genetics, molecular mechanisms, clinical features, diagnosis, and management.Molecular biomedicine · 2026Review
- Autobehaver: An AI-Based Pipeline for Animal Behavior Analysis.bioRxiv : the preprint server for biology · 2026Article
- MeCP2 interacts with the super elongation complex to regulate transcription.Science advances · 2025Article
- Article
- Revealing function-altering MECP2 mutations in individuals with autism spectrum disorder using yeast and Drosophila.Genetics · 2025Article
- Rett syndrome: advances in Understanding MeCP2 function, potential gene therapies, and public health implications.Molecular biology reports · 2025Review
- Functional assays inGenome research · 2025Review
- Review
- Drosophila models of pathogenic copy-number variant genes show global and non-neuronal defects during development.PLoS genetics · 2020Article
- Genetic Modifiers and Rare Mendelian Disease.Genes · 2020Review
- NCBP2 modulates neurodevelopmental defects of the 3q29 deletion in Drosophila and Xenopus laevis models.PLoS genetics · 2020Article
- Machine Learning Representation of Loss of Eye Regularity in aFrontiers in neuroscience · 2020Article
- Article
- Functional conservation of MBD proteins: MeCP2 and Drosophila MBD proteins alter sleep.Genes, brain, and behavior · 2016Article
- MECP2 impairs neuronal structure by regulating KIBRA.Neurobiology of disease · 2016Article
- Quantitative Assessment of Eye Phenotypes for Functional Genetic Studies Using Drosophila melanogaster.G3 (Bethesda, Md.) · 2016Article
- Drosophila Homolog of Human KIF22 at the Autism-Linked 16p11.2 Loci Influences Synaptic Connectivity at Larval Neuromuscular Junctions.Experimental neurobiology · 2016Article
- Article
- Article
- Astrocyte-specific regulation of hMeCP2 expression in Drosophila.Biology open · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The levels of methyl-CpG-binding protein 2 (MeCP2) are critical for normal post-natal development and function of the nervous system. Loss of function of MeCP2, a transcriptional regulator involved in chromatin remodeling, causes classic Rett syndrome (RTT) as well as other related conditions characterized by autism, learning disabilities, or mental retardation. Increased dosage of MeCP2 also leads to clinically similar neurological disorders and mental retardation. To identify molecular mechanisms capable of compensating for altered MeCP2 levels, we generated transgenic Drosophila overexpressing human MeCP2. We find that MeCP2 associates with chromatin and is phosphorylated at serine 423 in Drosophila, as is found in mammals. MeCP2 overexpression leads to anatomical (i.e., disorganized eyes, ectopic wing veins) and behavioral (i.e., motor dysfunction) abnormalities. We used a candidate gene approach to identify genes that are able to compensate for abnormal phenotypes caused by MeCP2 increased activity. These genetic modifiers include other chromatin remodeling genes (Additional sex combs, corto, osa, Sex combs on midleg, and trithorax), the kinase tricornered, the UBE3A target pebble, and Drosophila homologues of the MeCP2 physical interactors Sin3a, REST, and N-CoR. These findings demonstrate that anatomical and behavioral phenotypes caused by MeCP2 activity can be ameliorated by altering other factors that might be more amenable to manipulation than MeCP2 itself.
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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.