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Resources » Paper

J Apfeld et al. (1999) International C. elegans Meeting "Multiple Layers of Cell Non-autonomy in the Control of C. elegans Lifespan"

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00022918

    J Apfeld, & C Kenyon (1999). Multiple Layers of Cell Non-autonomy in the Control of C. elegans Lifespan presented in International C. elegans Meeting. Unpublished information; cite only with author permission.

    The insulin/IGF-receptor homologue daf-2 regulates 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. The lifespan extension and dauer formation phenotypes observed in daf-2 mutants are dependent on the activity of daf-16 , a transcription factor of the HNF-3/winged-helix family. 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-2 functions cell non-autonomously in both processes. Our findings imply that the lifespan of C. elegans is determined by a signaling cascade in which daf-2 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. C. elegans obtains information about its external environment through sensory cilia. We have found that animals with defective sensory cilia live longer than animals with intact sensory cilia. This lifespan extension is dependent on the activity of daf-16 , and mutations that disrupt cilium structure do not further increase the lifespan of daf-2 mutants. The long-lived cilium structure mutants feed normally, suggesting that sensory perception itself, rather than an associated effect on food intake, influences lifespan. The lifespan of C. elegans is also under the control of signals from the germline; laser ablation of the germline precursors leads to a lifespan extension that is dependent on the activity of daf-16 (1). We have found that a number of mutations that interfere in different ways with the development of the germline also extend lifespan. Together, our results indicate that the C. elegans insulin/IGF-1 like signaling pathway may integrate two different types of information in setting the lifespan of the animal: internal signals that reflect the state of the germline, and external signals that may convey information about the animal's surrounding environment. (1) Hsin and Kenyon, Nature, in press.


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