Beta-arrestin1 regulates zebrafish hematopoiesis through binding to YY1 and relieving polycomb group repression.

Abstract:

:Beta-arrestin1 is a multifunctional protein critically involved in signal transduction. Recently, it is also identified as a nuclear transcriptional regulator, but the underlying mechanisms and physiological significance remain to be explored. Here, we identified beta-arrestin1 as an evolutionarily conserved protein essential for zebrafish development. Zebrafish embryos depleted of beta-arrestin1 displayed severe posterior defects and especially failed to undergo hematopoiesis. In addition, the expression of cdx4, a critical regulator of embryonic blood formation, and its downstream hox genes were downregulated by depletion of beta-arrestin1, while injection of cdx4, hoxa9a or hoxb4a mRNA rescued the hematopoietic defects. Further mechanistic studies revealed that beta-arrestin1 bound to and sequestered the polycomb group (PcG) recruiter YY1, and relieved PcG-mediated repression of cdx4-hox pathway, thus regulating hematopoietic lineage specification. Taken together, this study demonstrated a critical role of beta-arrestin1 during zebrafish primitive hematopoiesis, as well as an important regulator of PcG proteins and cdx4-hox pathway.

journal_name

Cell

journal_title

Cell

authors

Yue R,Kang J,Zhao C,Hu W,Tang Y,Liu X,Pei G

doi

10.1016/j.cell.2009.08.038

subject

Has Abstract

pub_date

2009-10-30 00:00:00

pages

535-46

issue

3

eissn

0092-8674

issn

1097-4172

pii

S0092-8674(09)01112-X

journal_volume

139

pub_type

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