Cell nonautonomy of C-elegans daf-2 function in the regulation of diapause and life span
Cell nonautonomy of C-elegans daf-2 function in the regulation of diapause and life span
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DOI：
10.1016/s0092-8674(00)81751-1
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发表时间：
1998-10-16
期刊：
影响因子：
64.5
通讯作者：
Kenyon, C
中科院分区：
文献类型：
--
作者：
Apfeld, J;Kenyon, C
胰岛素/IGF受体同系物DAF-2调节线虫的衰老。DAF-2活性的降低会导致有生育能力的成虫保持活动的时间比正常长得多，寿命也是正常的两倍以上。更严重的daf-2功能下降会导致幼虫进入滞育状态，而不是进入成年期。我们询问了哪些细胞需要daf-2基因的活性，才能使动物发育到成年并正常衰老。我们发现，daf-a在这两个过程中都非自主地发挥细胞功能。我们的发现表明，线虫的寿命是由一个信号级联决定的，在这个信号级联中，DAF-2受体在多个细胞系中作用，调节一个或多个次级信号的产生或活动，而次级信号又控制着动物个体组织的生长和寿命。
The insulin/IGF receptor homolog DAF-2 regulates the aging in C. elegans. Decreasing daf-2 activity causes fertile adults to remain active much longer than normal and to live more than twice as long. A more severe decrease in daf-2 function causes young larvae to enter a state of diapause rather than progressing to adulthood. We have asked which cells require daf-2 gene activity in order for the animal to develop to adulthood and to age normally. We found that daf-a functions cell nonautonomously in both processes. Our findings imply that the life span of C. elegans is determined by a signaling cascade in which the DAF-2 receptor acts in multiple cell lineages to regulate the production or activity of a secondary signal (or signals), which, in turn, controls the growth and longevity of individual tissues in the animal.