Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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-pre-bound loci, but augments self-renewal programmes. 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.

Original publication

DOI

10.1182/blood.2019001553

Type

Journal article

Journal

Blood

Publication Date

12/09/2019