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Review
. 2000 Jan;22(1):48-56.
doi: 10.1002/(SICI)1521-1878(200001)22:1<48::AID-BIES9>3.0.CO;2-F.

clk-1, mitochondria, and physiological rates

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Review

clk-1, mitochondria, and physiological rates

R Branicky et al. Bioessays. 2000 Jan.

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.

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