Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 7-Day Trial for You or Your Team.

Learn More →

REREa/Atrophin‐2 interacts with histone deacetylase and Fgf8 signaling to regulate multiple processes of zebrafish development

REREa/Atrophin‐2 interacts with histone deacetylase and Fgf8 signaling to regulate multiple... The transcriptional regulator RERE/Atrophin‐2 (RERE) is required for the normal patterning of the early vertebrate embryo, including the central nervous system, pharyngeal arches, and limbs. Consistent with a role as a transcriptional corepressor, RERE binds histone deacetylase 1 and 2 (HDAC1/2), and orphan nuclear receptors such as Tlx. Here, we identify the zebrafish babyface (bab) as a mutant in rerea and show that it interacts genetically with fibroblast growth factor 8 (fgf8). We suggest that this finding is largely due to its interactions with HDAC, because genetic or pharmacological disruptions of HDAC phenocopy many features of the bab mutant. Furthermore, removing the functions of either REREa or HDAC synergizes with loss of Fgf8 function to disrupt posterior mesoderm formation during somitogenesis, midbrain–hindbrain boundary maintenance, and pharyngeal cartilage development. Together, these results reveal novel in vivo roles for REREa in HDAC‐mediated regulation of Fgf signaling. We present a model for RERE‐dependent patterning in which tissue‐specific transcriptional repression, by means of an REREa‐HDAC complex, modulates growth factor signaling during embryogenesis. Developmental Dynamics 236:1891–1904, 2007. © 2007 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Developmental Dynamics Wiley

REREa/Atrophin‐2 interacts with histone deacetylase and Fgf8 signaling to regulate multiple processes of zebrafish development

Loading next page...
 
/lp/wiley/rerea-atrophin-2-interacts-with-histone-deacetylase-and-fgf8-signaling-ANe8cox9yQ

References (59)

Publisher
Wiley
Copyright
Copyright © 2007 Wiley‐Liss, Inc.
ISSN
1058-8388
eISSN
1097-0177
DOI
10.1002/dvdy.21196
pmid
17576618
Publisher site
See Article on Publisher Site

Abstract

The transcriptional regulator RERE/Atrophin‐2 (RERE) is required for the normal patterning of the early vertebrate embryo, including the central nervous system, pharyngeal arches, and limbs. Consistent with a role as a transcriptional corepressor, RERE binds histone deacetylase 1 and 2 (HDAC1/2), and orphan nuclear receptors such as Tlx. Here, we identify the zebrafish babyface (bab) as a mutant in rerea and show that it interacts genetically with fibroblast growth factor 8 (fgf8). We suggest that this finding is largely due to its interactions with HDAC, because genetic or pharmacological disruptions of HDAC phenocopy many features of the bab mutant. Furthermore, removing the functions of either REREa or HDAC synergizes with loss of Fgf8 function to disrupt posterior mesoderm formation during somitogenesis, midbrain–hindbrain boundary maintenance, and pharyngeal cartilage development. Together, these results reveal novel in vivo roles for REREa in HDAC‐mediated regulation of Fgf signaling. We present a model for RERE‐dependent patterning in which tissue‐specific transcriptional repression, by means of an REREa‐HDAC complex, modulates growth factor signaling during embryogenesis. Developmental Dynamics 236:1891–1904, 2007. © 2007 Wiley‐Liss, Inc.

Journal

Developmental DynamicsWiley

Published: Jul 1, 2007

There are no references for this article.