<HashMap><database>GEO</database><scores/><additional><omics_type>Genomics</omics_type><species>Homo sapiens</species><gds_type>Genome binding/occupancy profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334084</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Arginine methylationof BAF155 regualtes interactions with RNA processing machinery [CUT&amp;RUN]</name><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&amp;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.</description><dates><publication>2026/06/03</publication></dates><accession>GSE334084</accession><cross_references><GSM>GSM9780180</GSM><GSM>GSM9780181</GSM><GSM>GSM9780184</GSM><GSM>GSM9780185</GSM><GSM>GSM9780182</GSM><GSM>GSM9780183</GSM><GSM>GSM9780188</GSM><GSM>GSM9780189</GSM><GSM>GSM9780186</GSM><GSM>GSM9780187</GSM><GSM>GSM9780148</GSM><GSM>GSM9780149</GSM><GSM>GSM9780146</GSM><GSM>GSM9780147</GSM><GSM>GSM9780191</GSM><GSM>GSM9780192</GSM><GSM>GSM9780190</GSM><GSM>GSM9780195</GSM><GSM>GSM9780151</GSM><GSM>GSM9780196</GSM><GSM>GSM9780152</GSM><GSM>GSM9780193</GSM><GSM>GSM9780150</GSM><GSM>GSM9780194</GSM><GSM>GSM9780155</GSM><GSM>GSM9780156</GSM><GSM>GSM9780153</GSM><GSM>GSM9780197</GSM><GSM>GSM9780198</GSM><GSM>GSM9780154</GSM><GSM>GSM9780159</GSM><GSM>GSM9780157</GSM><GSM>GSM9780158</GSM><GSM>GSM9780162</GSM><GSM>GSM9780163</GSM><GSM>GSM9780160</GSM><GSM>GSM9780161</GSM><GSM>GSM9780166</GSM><GSM>GSM9780167</GSM><GSM>GSM9780164</GSM><GSM>GSM9780165</GSM><GSM>GSM9780168</GSM><GSM>GSM9780169</GSM><GSM>GSM9780170</GSM><GSM>GSM9780173</GSM><GSM>GSM9780174</GSM><GSM>GSM9780171</GSM><GSM>GSM9780172</GSM><GSM>GSM9780177</GSM><GSM>GSM9780178</GSM><GSM>GSM9780175</GSM><GSM>GSM9780176</GSM><GSM>GSM9780179</GSM><GPL>34284</GPL><GSE>334084</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>