TORC2 signaling antagonizes SKN-1 to induce C. elegans mesendodermal embryonic development.
TORC2 signaling antagonizes SKN-1 to induce C. elegans mesendodermal embryonic development.
复制标题
DOI：
10.1016/j.ydbio.2013.08.011
复制
发表时间：
2013-12-15
影响因子：
2.7
通讯作者：
Neumann-Haefelin, Elke
中科院分区：
文献类型：
--
作者：
Ruf, Vanessa;Holzem, Christina;Peyman, Tobias;Walz, Gerd;Blackwell, T. Keith;Neumann-Haefelin, Elke
进化上保守的雷帕霉素（TOR）激酶的目标控制基本的代谢过程，以支持细胞和组织的生长。TOR在两种不同的复合物TORC 1和TORC 2的背景下发挥作用。TORC 2及其特异性组分Rictor最近被认为与衰老以及生长和代谢的调节有关。在这里，我们确定rict-1/Rictor作为C.优雅的转录因子skn-1在胚胎中建立中内胚层的发育，并且是成体细胞稳态和长寿所必需的。母体skn-1功能的丧失导致中内胚层前体的错误指定以及肠和咽的形成失败。我们发现rict-1基因失活通过恢复skn-1缺陷胚胎中的中内胚层特化抑制skn-1相关致死性。其他TORC 2而不是TORC 1组分的失活也部分挽救了skn-1胚胎致死性。SGK-1激酶在rict-1/TORC 2下游介导这些功能，因为sgk-1功能获得性突变体抑制rict-1突变体表型。这些数据表明TORC 2和SGK-1在胚胎发育期间拮抗SKN-1。
The evolutionarily conserved target of rapamycin (TOR) kinase controls fundamental metabolic processes to support cell and tissue growth. TOR functions within the context of two distinct complexes, TORC1 and TORC2. TORC2, with its specific component Rictor, has been recently implicated in aging and regulation of growth and metabolism. Here, we identify rict-1/Rictor as a regulator of embryonic development in C. elegans. The transcription factor skn-1 establishes development of the mesendoderm in embryos, and is required for cellular homeostasis and longevity in adults. Loss of maternal skn-1 function leads to misspecification of the mesendodermal precursor and failure to form intestine and pharynx. We found that genetic inactivation of rict-1 suppressed skn-1-associated lethality by restoring mesendodermal specification in skn-1 deficient embryos. Inactivation of other TORC2 but not TORC1 components also partially rescued skn-1 embryonic lethality. The SGK-1 kinase mediated these functions downstream of rict-1/TORC2, as a sgk-1 gain-of-function mutant suppressed the rict-1 mutant phenotype. These data indicate that TORC2 and SGK-1 antagonize SKN-1 during embryonic development.
登录
查看更多内容
影响因子：
3.7
作者：
Hasegawa K;Miwa J
通讯作者：
Miwa J
影响因子：
2.7
作者：
Fukushige, T;Hawkins, MG;McGhee, JD
通讯作者：
McGhee, JD
影响因子：
5.3
作者：
Kamada, Y;Fujioka, Y;Ohsumi, Y
通讯作者：
Ohsumi, Y
影响因子：
64.8
作者：
Honjoh, Sakiko;Yamamoto, Takuya;Nishida, Eisuke
通讯作者：
Nishida, Eisuke
影响因子：
12.3
作者：
通讯作者：
--