Determination of Life-Span in <b> <i>Caenorhabditis elegans</i> </b> by Four Clock Genes

TLDR

Caenorhabditis elegans is a genetic model for aging, and maternal‑effect mutations in clk‑1, clk‑2, clk‑3, and gro‑1 jointly control development length and lifespan, with clock‑mutant longevity independent of dauer‑related pathways. Mutant analysis indicates a general physiological clock, and worms carrying daf‑2(e1370) and clk‑1(e2519) mutations live almost five times longer than wild‑type.

Abstract

The nematode worm Caenorhabditis elegans is a model system for the study of the genetic basis of aging. Maternal-effect mutations in four genes— clk-1, clk-2 , clk-3, and gro-1 — interact genetically to determine both the duration of development and life-span. Analysis of the phenotypes of these mutants suggests the existence of a general physiological clock in the worm. Mutations in certain genes involved in dauer formation (an alternative larval stage induced by adverse conditions in which development is arrested) can also extend life-span, but the life extension of Clock mutants appears to be independent of these genes. The daf-2(e1370) clk-1(e2519) worms, which carry life-span-extending mutations from two different pathways, live nearly five times as long as wild-type worms.