A phosphatidylinositol-3-OH kinase family member regulating longevity and diapause in Caenorhabditis elegans
A phosphatidylinositol-3-OH kinase family member regulating longevity and diapause in Caenorhabditis elegans
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DOI：
10.1038/382536a0
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发表时间：
1996-08-08
期刊：
影响因子：
64.8
通讯作者：
Ruvkun, G
中科院分区：
文献类型：
--
作者：
Morris, JZ;Tissenbaum, HA;Ruvkun, G
信息素诱导的线虫神经分泌途径在达尔滞育阶段触发发育停滞和延长寿命。AGE-1基因是非Dauer发育和正常衰老所必需的。AGE-1编码哺乳动物磷脂酰肌醇-3-羟基激酶(PI(3)K)催化亚基的同源物。缺乏母体和合子AGE-1活性会导致Dauer的形成，而具有母体AGE-1活性但没有合子AGE-1活性的动物会发展为非Dauer，寿命是正常的两倍以上。这些数据表明，由AGE-1蛋白介导的磷脂酰肌醇信号控制着寿命和达尔滞育决定。
A PHEROMONE-INDUCED neurosecretory pathway in Caenorhabditis elegans triggers developmental arrest and an increase in longevity at the dauer diapause stage. The gene age-1 is required for non-dauer development and normal senescence. age-1 encodes a homologue of mammalian phosphatidylinositol-3-OH kinase (PI(3)K) catalytic subunits. Lack of both maternal and zygotic age-1 activity causes dauer formation, whereas animals with maternal but not zygotic age-1 activity develop as non-dauers that live more than twice as long as normal. These data suggest that phosphatidylinositol signalling mediated by AGE-1 protein controls lifespan and the dauer diapause decision.