Pax3和TGFbeta2信号的转录调控:神经嵴发育的潜在基因调控网络。

H. Nakazaki, Yueh-wei Shen, B. Yun, Anvesh C. Reddy, Anvesh C. Reddy, Varun Khanna, B. Mania‐Farnell, S. Ichi, David G. McLone, T. Tomita, C. Mayanil
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引用次数: 14

摘要

Pax3调节神经嵴细胞迁移,在神经嵴发育过程中起关键作用。TGFbs改变神经嵴细胞的迁移和分化。TGFbeta2无合子胚胎(TGFbeta2(-/-)Pax3(+/+))显示开放的神经管和双裂脊柱,而野生型胚胎的神经管是闭合的。在之前的工作中,我们已经证明Pax3通过直接结合其启动子上的顺式调控元件来调控TGFbeta2。在本研究中,我们发现通过下调一个Pax3等位基因,TGFbeta2(-/-)Pax3(+/-)小鼠育种获得的TGFbeta2(-/-)Pax3(+/-)胚胎可以逆转TGFbeta2的失合表型为野生型表型。本文的数据表明,Pax3和TGFbeta2在一个协调的基因调控网络中相互作用,由共同的下游效应基因连接,从而导致这种表型逆转。下游效应物可能包括Hes1、Ngn2和Sox9,以及其他参与神经元分化的基因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Transcriptional regulation by Pax3 and TGFbeta2 signaling: a potential gene regulatory network in neural crest development.
Pax3 regulates neural crest cell migration and is critical during neural crest development. TGFbs modify neural crest cell migration and differentiation. TGFbeta2 nullizygous embryos (TGFbeta2(-/-)Pax3(+/+)) display open neural tube and bifid spine, whereas in wild type embryos, the neural tube is closed. In previous work, we have demonstrated that Pax3 regulates TGFbeta2 by directly binding to cis-regulatory elements on its promoter. In this study, we found that the TGFbeta2 nullizygous phenotype can be reversed to the wild type phenotype by down-regulating one allele of Pax3, as in TGFbeta2(-/-)Pax3(+/-) embryos obtained through breeding TGFb2(+/-)Pax3(+/-) mice. The data in this paper suggest that Pax3 and TGFbeta2 interact in a coordinated gene regulatory network, linked by common downstream effector genes, to bring about this phenotypic reversal. Downstream effectors may include Hes1, Ngn2 and Sox9, as well as other genes involved in neuronal differentiation.
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