The Genetic Basis of Natural Variation in Caenorhabditis elegans Telomere Length
Daniel E. Cook, Stefan Zdraljevic, Robyn E. Tanny, Beomseok Seo, David D. Riccardi, Luke M. Noble, Matthew V. Rockman, Mark J. Alkema, Christian Braendle, Jan E. Kammenga, John Wang, Leonid Kruglyak, Marie-Anne Félix,Junho Lee, Erik C. Andersen
GENETICS September 1, 2016 vol. 204 no. 1 371-383;
Telomeres are involved in the maintenance of chromosomes and the prevention of genome instability. Despite this central importance, significant variation in telomere length has been observed in a variety of organisms. The genetic determinants of telomere-length variation and their effects on organismal fitness are largely unexplored. Here, we describe natural variation in telomere length across theCaenorhabditis elegans species. We identify a large-effect variant that contributes to differences in telomere length. The variant alters the conserved oligonucleotide/oligosaccharide-binding fold of protection of telomeres 2 (POT-2), a homolog of a human telomere-capping shelterin complex subunit. Mutations within this domain likely reduce the ability of POT-2 to bind telomeric DNA, thereby increasing telomere length. We find that telomere-length variation does not correlate with offspring production or longevity in C. elegans wild isolates, suggesting that naturally long telomeres play a limited role in modifying fitness phenotypes in C. elegans.
CAENORHABDITIS ELEGANS QTL SHELTERIN TELOMERE LENGTH
We thank Joshua Bloom and members of the Andersen laboratory for critical comments on this manuscript. We also thank M. Barkoulas, T. Bélicard, D. Bourc’his, N. Callemeyn-Torre, S. Carvalho, J. Dumont, L. Frézal, C.-Y. Kao, L. Lokmane, I. Ly, K. Ly, A. Paaby, J. Riksen, and G. Wang for isolating new wild C. elegans strains. The National Bioresource Project provided the FX1400 strain, and Wormbase data made a variety of analyses possible. This work was supported by a National Institutes of Health R01 subcontract to E.C.A. (GM-107227), the Chicago Biomedical Consortium with support from the Searle Funds at the Chicago Community Trust, and an American Cancer Society Research Scholar grant to E.C.A. (127313-RSG-15-135-01-DD), along with support from the Cell and Molecular Basis of Disease training grant (T32GM008061) to S.Z. and from the National Science Foundation Graduate Research Fellowship (DGE-1324585) to D.E.C.
Supplemental material is available online at www.genetics.org/lookup/suppl/doi:10.1534/genetics.116.191148/-/DC1.
Communicating editor: V. Reinke
Received May 1, 2016 Accepted July 14, 2016
Copyright © 2016 by the Genetics Society of America
Available freely online through the author-supported open access option.