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δEF1和Sip1对鸡胚躯干神经嵴脱层的调控

Regulation of trunk neural crest delamination by δEF1 and Sip1 in the chicken embryo.

作者信息

Yasumi Takahiro, Inoue Masashi, Maruhashi Mitsuji, Kamachi Yusuke, Higashi Yujiro, Kondoh Hisato, Uchikawa Masanori

机构信息

Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka, Suita, Osaka, 565-0871, Japan.

School of Environmental Science and Engineering, Kochi University of Technology, 185 Miyanokuchi, Tosayamada-cho, Kami-shi, Kochi, 782-8502, Japan.

出版信息

Dev Growth Differ. 2016 Feb;58(2):205-14. doi: 10.1111/dgd.12256. Epub 2015 Dec 22.

Abstract

The vertebrate Zfhx1 transcription factor family comprises δEF1 and Sip1, which bind to CACCT-containing sequences and act as transcriptional repressors. It has been a longstanding question whether these transcription factors share the same regulatory functions in vivo. It has been shown that neural crest (NC) delamination depends on the Sip1 activity at the cranial level in mouse and chicken embryos, and it remained unclear how NC delamination is regulated at the trunk level. We observed that the expression of δEF1 and Sip1 overlaps in many tissues in chicken embryos, including NC cells at the trunk level. To clarify the above questions, we separately knocked down δEF1 and Sip1 or in combination in NC cells by electroporation of vectors expressing short hairpin RNAs (shRNAs) against respective mRNAs on the dorsal side of neural tubes that generate NC cells. In all cases, the migrating NC cell population was significantly reduced, paralleled by the decreased expression of δEF1 or Sip1 targeted by shRNAs. Expression of Sox10, the major transcription factor that regulates NC development, was also decreased by the shRNAs against δEF1 or Sip1. We conclude that the trunk NC delamination is regulated by both δEF1 and Sip1 in an analogous manner, and that these transcription factors can share equivalent regulatory functions in embryonic tissues.

摘要

脊椎动物Zfhx1转录因子家族由δEF1和Sip1组成,它们与含有CACCT的序列结合并作为转录抑制因子发挥作用。这些转录因子在体内是否具有相同的调节功能一直是个长期存在的问题。研究表明,神经嵴(NC)脱层依赖于小鼠和鸡胚胎中颅部水平的Sip1活性,而躯干水平的NC脱层如何调节仍不清楚。我们观察到,δEF1和Sip1在鸡胚胎的许多组织中表达重叠,包括躯干水平的NC细胞。为了阐明上述问题,我们通过在产生NC细胞的神经管背侧电穿孔表达针对各自mRNA的短发夹RNA(shRNA)的载体,分别或联合敲低NC细胞中的δEF1和Sip1。在所有情况下,迁移的NC细胞群体显著减少,同时shRNA靶向的δEF1或Sip1表达降低。针对δEF1或Sip1的shRNA也降低了调节NC发育的主要转录因子Sox10的表达。我们得出结论,躯干NC脱层由δEF1和Sip1以类似方式调节,并且这些转录因子在胚胎组织中可共享等效的调节功能。

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