{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE334nnn/GSE334084/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334084"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Arginine methylationof BAF155 regualtes interactions with RNA processing machinery [CUT&RUN]","description":"Post-translational modifications (PTMs) of chromatin remodelers are abundant but functionally understudied. Here we investigate the role of asymmetric dimethylation of arginine 1064 (BAF155me2a) on the SWI/SNF core subunit BAF155, a mark deposited by CARM1/PRMT4 that has been linked to tumor progression but whose molecular function remains unclear. Using immunoprecipitation–mass spectrometry with a dimethyl-specific antibody, we found that R1064me2 selectively enhances BAF155 interactions with RNA processing factors, including the anti-termination protein SCAF4, splicing factors, and the transcription factor RFX5. CUT&RUN profiling showed that BAF155me2a, SCAF4, and RFX5 co-occupy promoter regions, and reciprocal immunoprecipitations confirmed that the SCAF4–BAF155 interaction depends on R1064 methylation. To test the functional consequences of this modification, we generated cells expressing either wild-type BAF155 or a methylation-deficient BAF155-R1064K mutant. Loss of methylation did not alter chromatin accessibility, BAF155 genomic occupancy, or SCAF4 recruitment. However, nascent transcription measured by TT-seq revealed a coordinated reduction in 5′ sense transcripts and upstream antisense transcripts (PROMPTs) at BAF155-bound promoters, with a quantitatively larger decrease in PROMPTs at SCAF4 co-bound sites. The effect was restricted to the promoter-proximal region and resolved toward the gene end, consistent with a defect in productive elongation downstream of RNA polymerase II recruitment. These data support a model in which BAF155 dimethylation provides a co-transcriptional interface coupling SWI/SNF to RNA processing machinery, and identify regulation of nascent transcription as a non-canonical function of SWI/SNF PTMs.","dates":{"publication":"2026/06/03"},"accession":"GSE334084","cross_references":{"GSM":["GSM9780180","GSM9780181","GSM9780184","GSM9780185","GSM9780182","GSM9780183","GSM9780188","GSM9780189","GSM9780186","GSM9780187","GSM9780148","GSM9780149","GSM9780146","GSM9780147","GSM9780191","GSM9780192","GSM9780190","GSM9780195","GSM9780151","GSM9780196","GSM9780152","GSM9780193","GSM9780150","GSM9780194","GSM9780155","GSM9780156","GSM9780153","GSM9780197","GSM9780198","GSM9780154","GSM9780159","GSM9780157","GSM9780158","GSM9780162","GSM9780163","GSM9780160","GSM9780161","GSM9780166","GSM9780167","GSM9780164","GSM9780165","GSM9780168","GSM9780169","GSM9780170","GSM9780173","GSM9780174","GSM9780171","GSM9780172","GSM9780177","GSM9780178","GSM9780175","GSM9780176","GSM9780179"],"GPL":["34284"],"GSE":["334084"],"taxon":["Homo sapiens"]}}