clk-1, mitochondria, and physiological rates

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Abstract
Mutations in the C. elegans maternal‐effect gene clk‐1 are highly pleiotropic, affecting the duration of diverse developmental and behavioral processes. They result in an average slowing of embryonic and post‐embryonic development, adult rhythmic behaviors, reproduction, and aging.(1) CLK‐1 is a highly conserved mitochondrial protein,(2,3) but even severe clk‐1 mutations affect mitochondrial respiration only slightly.(3) Here, we review the evidence supporting the regulatory role of clk‐1 in physiological timing. We also discuss possible models for the action of CLK‐1, in particular, one proposing that CLK‐1 is involved in the coordination of mitochondrial and nuclear function. BioEssays 22:48–56, 2000. ©2000 John Wiley & Sons, Inc.