Cell nonautonomy of C-elegans daf-2 function in the regulation of diapause and life span

被引:267
作者
Apfeld, J [1 ]
Kenyon, C [1 ]
机构
[1] Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94143 USA
关键词
D O I
10.1016/S0092-8674(00)81751-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:199 / 210
页数:12
相关论文
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