{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xu SJ"],"funding":["NIDA NIH HHS","NIGMS NIH HHS"],"pagination":["2943-2966.e8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8454057"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["109(18)"],"pubmed_abstract":["Neuronal alternative splicing is a key gene regulatory mechanism in the brain. However, the spliceosome machinery is insufficient to fully specify splicing complexity. In considering the role of the epigenome in activity-dependent alternative splicing, we and others find the histone modification H3K36me3 to be a putative splicing regulator. In this study, we found that mouse cocaine self-administration caused widespread differential alternative splicing, concomitant with the enrichment of H3K36me3 at differentially spliced junctions. Importantly, only targeted epigenetic editing can distinguish between a direct role of H3K36me3 in splicing and an indirect role via regulation of splice factor expression elsewhere on the genome. We targeted Srsf11, which was both alternatively spliced and H3"],"journal":["Neuron"],"pubmed_title":["Chromatin-mediated alternative splicing regulates cocaine-reward behavior."],"pmcid":["PMC8454057"],"funding_grant_id":["T32 GM008076","T32 DA028874","DP1 DA044250","R00 DA045795","R36 DA050877","R01 DA033641","R01 DA015214","K01 DA039308"],"pubmed_authors":["Wimmer ME","Pierce RC","Xu SJ","Fischer DK","Heller EA","Hamilton PJ","Neve RL","Marchione DM","Garcia BA","Lim CJ","Lombroso SI","Carpenter MD"],"additional_accession":[]},"is_claimable":false,"name":"Chromatin-mediated alternative splicing regulates cocaine-reward behavior.","description":"Neuronal alternative splicing is a key gene regulatory mechanism in the brain. However, the spliceosome machinery is insufficient to fully specify splicing complexity. In considering the role of the epigenome in activity-dependent alternative splicing, we and others find the histone modification H3K36me3 to be a putative splicing regulator. In this study, we found that mouse cocaine self-administration caused widespread differential alternative splicing, concomitant with the enrichment of H3K36me3 at differentially spliced junctions. Importantly, only targeted epigenetic editing can distinguish between a direct role of H3K36me3 in splicing and an indirect role via regulation of splice factor expression elsewhere on the genome. We targeted Srsf11, which was both alternatively spliced and H3","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2026-05-08T11:19:26.955Z","creation":"2025-04-05T23:24:30.223Z"},"accession":"S-EPMC8454057","cross_references":{"pubmed":["34480866"],"doi":["10.1016/j.neuron.2021.08.008"]}}