Insulin-like signalling to the maternal germline controls progeny response to osmotic stress.
Insulin-like signalling to the maternal germline controls progeny response to osmotic stress.
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DOI：
10.1038/ncb3470
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发表时间：
2017-03
影响因子：
21.3
通讯作者：
Horvitz HR
中科院分区：
文献类型：
--
作者：
Burton NO;Furuta T;Webster AK;Kaplan RE;Baugh LR;Arur S;Horvitz HR
1893年，魏斯曼提出，关于环境的信息不能从体细胞传递到生殖细胞，这一假说现在被称为魏斯曼屏障。然而，最近的研究表明，父母暴露于环境压力可以修改后代的生理和父母的压力可以有助于后代疾病。调节这些现象的机制知之甚少。本文报道了线虫C.秀丽线虫可以通过进入发育停滞状态来保护自身免受渗透胁迫，并且可以通过增加后代中甘油生物合成酶GPDH-2的表达来保护其后代免受渗透胁迫。这两种保护机制都受到胰岛素样信号的调节：肠道的胰岛素样信号调节发育停滞，而母体生殖系的胰岛素样信号调节后代的甘油代谢。因此，在母体生殖系的胰岛素样信号传导与子代代谢和基因表达之间存在可遗传的联系。我们推测，胰岛素样信号传导到生殖细胞的类似调节是负责母体环境对涉及胰岛素信号传导的人类疾病（如肥胖症和2型糖尿病）的影响。
In 1893 August Weismann proposed that information about the environment could not pass from somatic cells to germ cells, a hypothesis now known as the Weismann barrier. However, recent studies have indicated that parental exposure to environmental stress can modify progeny physiology and that parental stress can contribute to progeny disorders. The mechanisms regulating these phenomena are poorly understood. We report that the nematode C. elegans can protect itself from osmotic stress by entering a state of arrested development and can protect its progeny from osmotic stress by increasing the expression of the glycerol biosynthetic enzyme GPDH-2 in progeny. Both of these protective mechanisms are regulated by insulin-like signalling: insulin-like signalling to the intestine regulates developmental arrest, while insulin-like signalling to the maternal germline regulates glycerol metabolism in progeny. Thus, there is a heritable link between insulin-like signalling to the maternal germline and progeny metabolism and gene expression. We speculate that analogous modulation of insulin-like signalling to the germline is responsible for effects of the maternal environment on human diseases that involve insulin signalling, such as obesity and type-2 diabetes.