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The C. elegans maternal-effect gene clk-2 is essential for embryonic development, encodes a protein homologous to yeast Tel2p and affects telomere length

Claire Bénard, Brent McCright^*,, Yue Zhang, Stephanie Felkai, Bernard Lakowski and Siegfried Hekimi^¶

Department of Biology, McGill University, 1205 Avenue Dr Penfield, H3A 1B1, Montréal, Québec, Canada
^* Present address: The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609, USA
Present address: Genzentrum, Ludwig-Maximilians Universitaet, Feodor-Lynen-Str. 25, D-81377, Munich, Germany
These authors contributed equally to this work

¶Author for correspondence (e-mail: Siegfried.Hekimi{at}mcgill.ca)

Accepted July 20, 2001

The Caenorhabditis elegans maternal-effect clk genes are involved in the temporal control of development and behavior. We report the genetic and molecular characterization of clk-2. A temperature-sensitive mutation in the gene clk-2 affects embryonic and post-embryonic development, reproduction, and rhythmic behaviors. Yet, virtually all phenotypes are fully maternally rescued. Embryonic development strictly requires the activity of maternal clk-2 during a narrow time window between oocyte maturation and the two- to four-cell embryonic stage. Positional cloning of clk-2 reveals that it encodes a protein homologous to S. cerevisiae Tel2p. In yeast, the gene TEL2 regulates telomere length and participates in gene silencing at subtelomeric regions. In C. elegans, clk-2 mutants have elongated telomeres, and clk-2 overexpression can lead to telomere shortening. Tel2p has been reported to bind to telomeric DNA repeats in vitro. However, we find that a functional CLK-2::GFP fusion protein is cytoplasmic in worms. We discuss how the phenotype of clk-2 mutants could be the result of altered patterns of gene expression.

Key words: clk-2, TEL2, Caenorhabditis elegans, Maternal effect, Telomere length, Lifespan