Suppr超能文献

依赖于Dpp/TGFβ的共抑制因子施努里蛋白在果蝇胚胎中保护上皮细胞免受JNK诱导的凋亡。

The Dpp/TGFβ-dependent corepressor Schnurri protects epithelial cells from JNK-induced apoptosis in drosophila embryos.

作者信息

Beira Jorge V, Springhorn Alexander, Gunther Stefan, Hufnagel Lars, Pyrowolakis Giorgos, Vincent Jean-Paul

机构信息

Medical Research Council National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK; Department of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK.

BIOSS Centre for Biological Signalling Studies and Institute for Biology I, University of Freiburg, Schänzlestrasse 18, 79104 Freiburg, Germany; Spemann Graduate School of Biology and Medicine, Research Training Program GRK 1104, Albert Ludwigs University, 79104 Freiburg, Germany.

出版信息

Dev Cell. 2014 Oct 27;31(2):240-7. doi: 10.1016/j.devcel.2014.08.015. Epub 2014 Oct 9.

Abstract

Jun N-terminal kinase (JNK) often mediates apoptosis in response to cellular stress. However, during normal development, JNK signaling controls a variety of live cell behaviors, such as during dorsal closure in Drosophila embryos. During this process, the latent proapoptotic activity of JNK becomes apparent following Dpp signaling suppression, which leads to JNK-dependent transcriptional activation of the proapoptotic gene reaper. Dpp signaling also protects cells from JNK-dependent apoptosis caused by epithelial disruption. We find that repression of reaper transcription by Dpp is mediated by Schnurri. Moreover, reporter gene analysis shows that a transcriptional regulatory module comprising AP-1 and Schnurri binding sites located upstream of reaper integrate the activities of JNK and Dpp. This arrangement allows JNK to control a migratory behavior without triggering apoptosis. Dpp plays a dual role during dorsal closure. It cooperates with JNK in stimulating cell migration and also prevents JNK from inducing apoptosis.

摘要

JNK氨基末端激酶(JNK)通常在细胞应激反应中介导细胞凋亡。然而,在正常发育过程中,JNK信号传导控制着多种活细胞行为,例如在果蝇胚胎背侧闭合过程中。在此过程中,JNK潜在的促凋亡活性在Dpp信号传导被抑制后变得明显,这导致促凋亡基因收割者(reaper)的JNK依赖性转录激活。Dpp信号传导还保护细胞免受上皮破坏引起的JNK依赖性细胞凋亡。我们发现Dpp对收割者转录的抑制是由施努里(Schnurri)介导的。此外,报告基因分析表明,一个由位于收割者上游的AP-1和施努里结合位点组成的转录调节模块整合了JNK和Dpp的活性。这种安排使JNK能够控制迁移行为而不触发细胞凋亡。Dpp在背侧闭合过程中发挥双重作用。它与JNK协同刺激细胞迁移,同时也防止JNK诱导细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f238/4220000/a258c55b22ff/fx1.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验