{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["218(12)"],"submitter":["Stamos DB"],"pubmed_abstract":["Analysis of the transcriptional profiles of developing thymocytes has shown that T lineage commitment is associated with loss of stem cell and early progenitor gene signatures and the acquisition of T cell gene signatures. Less well understood are the epigenetic alterations that accompany or enable these transcriptional changes. Here, we show that the histone demethylase Lsd1 (Kdm1a) performs a key role in extinguishing stem/progenitor transcriptional programs in addition to key repressive gene programs during thymocyte maturation. Deletion of Lsd1 caused a block in late T cell development and resulted in overexpression of interferon response genes as well as genes regulated by the Gfi1, Bcl6, and, most prominently, Bcl11b transcriptional repressors in CD4+CD8+ thymocytes. Transcriptional overexpression in Lsd1-deficient thymocytes was not always associated with increased H3K4 trimethylation at gene promoters, indicating that Lsd1 indirectly affects the expression of many genes. Together, these results identify a critical function for Lsd1 in the epigenetic regulation of multiple repressive gene signatures during T cell development."],"journal":["The Journal of experimental medicine"],"pagination":["e20202012"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8570297"],"repository":["biostudies-literature"],"pubmed_title":["The histone demethylase Lsd1 regulates multiple repressive gene programs during T cell development."],"pmcid":["PMC8570297"],"pubmed_authors":["El-Khoury D","Bhandoola A","Stamos DB","Nie J","Lee J","Mitra A","Li L","Chopp LB","Ding Y","Love PE","Bosselut R","Das A","Clubb LM","Venkataganesh H"],"additional_accession":[]},"is_claimable":false,"name":"The histone demethylase Lsd1 regulates multiple repressive gene programs during T cell development.","description":"Analysis of the transcriptional profiles of developing thymocytes has shown that T lineage commitment is associated with loss of stem cell and early progenitor gene signatures and the acquisition of T cell gene signatures. Less well understood are the epigenetic alterations that accompany or enable these transcriptional changes. Here, we show that the histone demethylase Lsd1 (Kdm1a) performs a key role in extinguishing stem/progenitor transcriptional programs in addition to key repressive gene programs during thymocyte maturation. Deletion of Lsd1 caused a block in late T cell development and resulted in overexpression of interferon response genes as well as genes regulated by the Gfi1, Bcl6, and, most prominently, Bcl11b transcriptional repressors in CD4+CD8+ thymocytes. Transcriptional overexpression in Lsd1-deficient thymocytes was not always associated with increased H3K4 trimethylation at gene promoters, indicating that Lsd1 indirectly affects the expression of many genes. Together, these results identify a critical function for Lsd1 in the epigenetic regulation of multiple repressive gene signatures during T cell development.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Dec","modification":"2025-04-21T23:39:08.784Z","creation":"2025-02-18T23:32:16.308Z"},"accession":"S-EPMC8570297","cross_references":{"pubmed":["34726730"],"doi":["10.1084/jem.20202012"]}}