clk-1, mitochondria, and physiological rates

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

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Biological Clocks
  • Caenorhabditis / genetics
  • Caenorhabditis / physiology
  • Caenorhabditis elegans Proteins*
  • Conserved Sequence
  • Helminth Proteins / chemistry
  • Helminth Proteins / genetics
  • Helminth Proteins / physiology*
  • Humans
  • Mitochondria / physiology*
  • Molecular Sequence Data
  • Rickettsia / genetics
  • Saccharomyces cerevisiae / genetics
  • Sequence Alignment
  • Sequence Homology, Amino Acid

Substances

  • CLK-1 protein, C elegans
  • Caenorhabditis elegans Proteins
  • Helminth Proteins