A ubiquitin ligase toggles red cell differentiation

التفاصيل البيبلوغرافية
العنوان: A ubiquitin ligase toggles red cell differentiation
المؤلفون: Thijs C. J. Verheul, Sjaak Philipsen
المساهمون: Cell biology
المصدر: Blood
Blood, 137(2), 143-144. American Society of Hematology
سنة النشر: 2021
مصطلحات موضوعية: 0301 basic medicine, Red Cell, Ubiquitin, Ubiquitin-Protein Ligases, Immunology, Regulator, Ubiquitination, Plenary Paper, Repressor, Cell Biology, Hematology, macromolecular substances, Biology, Biochemistry, Homology (biology), Ubiquitin ligase, Cell biology, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Proteolysis, biology.protein, Erythropoiesis, Gene, 030215 immunology
الوصف: The histone mark H3K27me3 and its reader/writer polycomb repressive complex 2 (PRC2) mediate widespread transcriptional repression in stem and progenitor cells. Mechanisms that regulate this activity are critical for hematopoietic development but are poorly understood. Here we show that the E3 ubiquitin ligase F-box only protein 11 (FBXO11) relieves PRC2-mediated repression during erythroid maturation by targeting its newly identified substrate bromo adjacent homology domain–containing 1 (BAHD1), an H3K27me3 reader that recruits transcriptional corepressors. Erythroblasts lacking FBXO11 are developmentally delayed, with reduced expression of maturation-associated genes, most of which harbor bivalent histone marks at their promoters. In FBXO11(−/−) erythroblasts, these gene promoters bind BAHD1 and fail to recruit the erythroid transcription factor GATA1. The BAHD1 complex interacts physically with PRC2, and depletion of either component restores FBXO11-deficient erythroid gene expression. Our studies identify BAHD1 as a novel effector of PRC2-mediated repression and reveal how a single E3 ubiquitin ligase eliminates PRC2 repression at many developmentally poised bivalent genes during erythropoiesis.
وصف الملف: application/pdf
تدمد: 1528-0020
0006-4971
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::56daafcf6a3e2a4f1efe5d8c6299733f
https://pubmed.ncbi.nlm.nih.gov/33156908
Rights: OPEN
رقم الانضمام: edsair.doi.dedup.....56daafcf6a3e2a4f1efe5d8c6299733f
قاعدة البيانات: OpenAIRE