{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Johnson K"],"funding":["NIAID NIH HHS","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["853-61"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1635547"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5(8)"],"pubmed_abstract":["Immunoglobulin heavy chain rearrangement (V(H)-to-DJ(H)) occurs only in B cells, suggesting it is inhibited in other lineages. Here we found that in the mouse V(H) locus, methylation of lysine 9 on histone H3 (H3-K9), a mark of inactive chromatin, was present in non-B lineage cells but was absent in B cells. As others have shown that H3-K9 methylation can inhibit V(D)J recombination on engineered substrates, our data support the idea that H3-K9 methylation inhibits endogenous V(H)-to-DJ(H) recombination. We also show that Pax5, a transcription factor required for B cell commitment, is necessary and sufficient for the removal of H3-K9 methylation in the V(H) locus and provide evidence that one function of Pax5 is to remove this inhibitory modification by a mechanism of histone exchange, thu"],"journal":["Nature immunology"],"pubmed_title":["B cell-specific loss of histone 3 lysine 9 methylation in the V(H) locus depends on Pax5."],"pmcid":["PMC1635547"],"funding_grant_id":["R01 AI43576","R01 AI32524","R01 GM040924","R01 AI032524","GM40924","R01 CA102709","R01 AI043576"],"pubmed_authors":["Bothwell AL","Johnson K","Thomas-Tikhonenko A","Pflugh DL","Calame K","Lin KI","Schatz DG","Yu D","Hesslein DG"],"additional_accession":[]},"is_claimable":false,"name":"B cell-specific loss of histone 3 lysine 9 methylation in the V(H) locus depends on Pax5.","description":"Immunoglobulin heavy chain rearrangement (V(H)-to-DJ(H)) occurs only in B cells, suggesting it is inhibited in other lineages. Here we found that in the mouse V(H) locus, methylation of lysine 9 on histone H3 (H3-K9), a mark of inactive chromatin, was present in non-B lineage cells but was absent in B cells. As others have shown that H3-K9 methylation can inhibit V(D)J recombination on engineered substrates, our data support the idea that H3-K9 methylation inhibits endogenous V(H)-to-DJ(H) recombination. We also show that Pax5, a transcription factor required for B cell commitment, is necessary and sufficient for the removal of H3-K9 methylation in the V(H) locus and provide evidence that one function of Pax5 is to remove this inhibitory modification by a mechanism of histone exchange, thu","dates":{"release":"2004-01-01T00:00:00Z","publication":"2004 Aug","modification":"2025-04-04T13:41:36.081Z","creation":"2019-03-27T01:46:13Z"},"accession":"S-EPMC1635547","cross_references":{"pubmed":["15258579"],"doi":["10.1038/ni1099"]}}