SHC-3: a previously unidentified C. elegans Shc family member functions in the insulin-like signaling pathway to enhance survival during L1 arrest.

IF 3.3 3区生物学 Q2 GENETICS & HEREDITY

Genetics Pub Date : 2024-10-07 DOI:10.1093/genetics/iyae093

Mercedes Di Bernardo, Victoria L León Guerrero, Jacob C Sutoski, William Rod Hardy, Lesley T MacNeil

引用次数: 0

Abstract

Shc (Src homologous and collagen) proteins function in many different signaling pathways where they mediate phosphorylation-dependent protein-protein interactions. These proteins are characterized by the presence of two phosphotyrosine-binding domains, an N-terminal PTB and a C-terminal SH2. We describe a previously unrecognized Caenorhabditis elegans Shc gene, shc-3 and characterize its role in stress response. Both shc-3 and shc-1 are required for long-term survival in L1 arrest and survival in heat stress, however, they do not act redundantly but rather play distinct roles in these processes. Loss of shc-3 did not further decrease survival of daf-16 mutants in L1 arrest, suggesting that like SHC-1, SHC-3 functions in the insulin-like signaling pathway. In the absence of SHC-3, DAF-16 nuclear entry and exit are slowed, suggesting that SHC-3 is required for rapid changes in DAF-16 signaling.

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SHC-3：一种之前尚未发现的秀丽隐杆线虫 Shc 家族成员，在 L1 停滞期间通过胰岛素样信号通路提高存活率。

Shc 蛋白在许多不同的信号通路中发挥作用，介导依赖磷酸化的蛋白质-蛋白质相互作用。这些蛋白的特点是存在两个磷酸化酪氨酸结合域，即 N 端 PTB 和 C 端 SH2。我们描述了一种以前未被发现的秀丽隐杆线虫 Shc 基因 shc-3，并描述了它在应激反应中的作用。shc-3和shc-1都是在L1停滞期长期存活和在热应激中存活所必需的，但它们在这些过程中并不是多余的，而是扮演着不同的角色。缺失shc-3不会进一步降低daf-16突变体在L1停滞期的存活率，这表明与SHC-1一样，SHC-3也在类胰岛素信号通路中发挥作用。在 SHC-3 缺失的情况下，DAF-16 核进入和退出的速度减慢，这表明 DAF-16 信号的快速变化需要 SHC-3。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Genetics GENETICS & HEREDITY-

CiteScore

6.90

自引率

6.10%

发文量

177

审稿时长

1.5 months

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