ist-1/IRS1以daf-16/FoxO依赖和独立的方式影响L1的饥饿抗性。

microPublication biology Pub Date : 2025-06-13 eCollection Date: 2025-01-01 DOI:10.17912/micropub.biology.001648
Jingxian Chen, Ainsley R Scheiner, Ivan B Falsztyn, L Ryan Baugh
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引用次数: 0

摘要

哺乳动物IRS1基因是胰岛素和胰岛素样生长因子受体的重要受体,但其在线虫线虫中的唯一同源物ist-1受到的关注相对较少。我们发现ist-1 /IRS1对L1饥饿抗性有适度的影响,两个无效突变体在L1长时间停滞后恢复后增加了幼虫的生长和繁殖。在饥饿L1幼虫中,ist-1 /IRS1突变体增加了胰岛素/IGF信号的关键效应因子DAF-16 /FoxO的核定位,这与ist-1 /IRS1转导DAF-2 /IGFR信号一致。然而,上位分析表明,ist-1 /IRS1也独立于daf-16 /FoxO发挥作用,这表明它具有额外的新功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
ist-1/IRS1 affects L1 starvation resistance in daf-16/FoxO- dependent and independent fashion.

The mammalian IRS1 gene is an important adaptor for the insulin and insulin-like growth factor receptors, but its sole homolog in the nematode C. elegans , ist-1 , has received relatively little attention. We show that ist-1 /IRS1 has modest effects on L1 starvation resistance, with two null mutants increasing larval growth and reproduction after recovery from extended L1 arrest. ist-1 /IRS1 mutants increase nuclear localization of DAF-16 /FoxO, a critical effector of insulin/IGF signaling, in starved L1 larvae, consistent with IST-1 /IRS1 transducing DAF-2 /IGFR signaling. However, epistasis analysis suggests that ist-1 /IRS1 also functions independently of daf-16 /FoxO , suggesting additional, novel function.

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