OrganismSaccharomyces cerevisiae (replicative)
Aging PhenotypeShortened life-span
Allele TypeDeletion
DescriptionDeletion of HDF1 shortens life span, but does not accelerate the normal aging process (Kaeberlein et al., 1999).
Gene FunctionRequired for non-homologous end-joining (NHEJ) and telomere maintenance (Milne et al., 1996; Laroche et al., 1998).
Other PhenotypesHDF1 mutants are defective for NHEJ (Milne et al., 1996).
Null mutant is defective for telomeric silencing (Laroche et al., 1998)
HomologsS.p. pku70
M.m. G22P1
H.s. G22P1
Primary ReferenceKaeberlein, M., McVey, M., and Guarente, L. (1999). The SIR2/3/4 complex and SIR2 alone promote longevity in Saccharomyces cerevisiae by two different mechanisms. Genes Dev 13, 2570-80. [Abstract]
Other ReferencesLaroche, T., Martin, S. G., Gotta, M., Gorham, H. C., Pryde, F. E., Louis, E. J., and Gasser, S. M. (1998). Mutation of yeast Ku genes disrupts the subnuclear organization of telomeres. Curr Biol 8, 653-6. [Abstract]
Milne, G. T., Jin, S., Shannon, K. B., and Weaver, D. T. (1996). Mutations in two Ku homologs define a DNA end-joining repair pathway in Saccharomyces cerevisiae. Mol Cell Biol 16, 4189-98. [Abstract]
Relevant LinksSGD:
Keywordstelomeres, silencing, DNA damage, yeast, replicative senescence, Saccharomyces cerevisiae, non-homologous end-joining, Ku, NHEJ