The Caenorhabditis elegans misc-1 gene encodes a mitochondrial carrier with a role in oxidative stress response. The knock-out mutant has no lifespan phenotype and fails to upregulate the gei-7-mediated glyoxylate shunt, an extra-mitochondrial pathway of energy production. We show that gei-7 is required for the longevity of the mitochondrial mutant clk-1. Our data suggest that only mitochondrial mutants that upregulate gei-7 can achieve longevity.
Bibliographical noteFunding Information:
The authors would like to thank Christine Spurgeon for important technical assistance. This work was supported by a Canadian Institutes of Health Research grant ( MOP 79458 ) to DLR and a Natural Sciences and Engineering Research Council of Canada Alexander Graham Bell Canada Graduate Scholarship, Michael Smith Foundation for Health Research Senior Graduate Studentship , Izaak Walton Killam Memorial Pre-Doctoral Fellowship and a William and Dorothy Gilbert Graduate Scholarship in Bio-Medical Sciences to MG. SAGE data were obtained from the Genome BC C. elegans Gene Expression Consortium ( http://elegans.bcgsc.bc.ca/ ). Some nematode strains used in this work were provided by the Caenorhabditis Genetics Center, which is funded by the NIH National Center for Research Resources (NCRR). The misc-1 knock-out allele was generated by the knock-out project directed by Dr. Mitani. The gei-7 knock-out allele was obtained from the C. elegans knock-out consortium.
All Science Journal Classification (ASJC) codes
- Developmental Biology