| Literature DB >> 31515253 |
Daniel Sasca1,2,3, Haiyang Yun1,2, George Giotopoulos1,2, Jakub Szybinski3, Theo Evan1,2, Nicola K Wilson1,2, Moritz Gerstung4, Paolo Gallipoli1,2, Anthony R Green1,2, Robert Hills5, Nigel Russell6, Cameron S Osborne7, Elli Papaemmanuil8, Berthold Göttgens1,2, Peter Campbell9, Brian J P Huntly1,2.
Abstract
Cohesin complex disruption alters gene expression, and cohesin mutations are common in myeloid neoplasia, suggesting a critical role in hematopoiesis. Here, we explore cohesin dynamics and regulation of hematopoietic stem cell homeostasis and differentiation. Cohesin binding increases at active regulatory elements only during erythroid differentiation. Prior binding of the repressive Ets transcription factor Etv6 predicts cohesin binding at these elements and Etv6 interacts with cohesin at chromatin. Depletion of cohesin severely impairs erythroid differentiation, particularly at Etv6-prebound loci, but augments self-renewal programs. Together with corroborative findings in acute myeloid leukemia and myelodysplastic syndrome patient samples, these data suggest cohesin-mediated alleviation of Etv6 repression is required for dynamic expression at critical erythroid genes during differentiation and how this may be perturbed in myeloid malignancies.Entities:
Mesh:
Substances:
Year: 2019 PMID: 31515253 PMCID: PMC7484777 DOI: 10.1182/blood.2019001553
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113