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NF-
B and Snail1a coordinate the cell cycle with gastrulation
Correspondence to Lingfei Luo: lluo{at}swu.edu.cn
The cell cycle needs to strictly coordinate with developmental processes to ensure correct generation of the body plan and different tissues. However, the molecular mechanism underlying the coordination remains largely unknown. In this study, we investigate how the cell cycle coordinates gastrulation cell movements in zebrafish. We present a system to modulate the cell cycle in early zebrafish embryos by manipulating the geminin-Cdt1 balance. Alterations of the cell cycle change the apoptotic level during gastrulation, which correlates with the nuclear level of antiapoptotic nuclear factor
B (NF-
B). NF-
B associates with the Snail1a promoter region on the chromatin and directly activates Snail1a, an important factor controlling cell delamination, which is the initial step of mesendodermal cell movements during gastrulation. In effect, the cell cycle coordinates the delamination of mesendodermal cells through the transcription of Snail1a. Our results suggest a molecular mechanism by which NF-
B and Snail1a coordinate the cell cycle through gastrulation.
B, nuclear factor
B; ntl, no tail; Sn1-CAT, Snail1a promoter driving chloramphenicol acetyl transferase construct.
© 2009 Liu et al.
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
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