OrganismSaccharomyces cerevisiae (replicative)
Aging PhenotypeShortened life-span
Allele TypeDeletion
DescriptionDeletion of HDF2 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 PhenotypesHDF2 mutants are defective for NHEJ (Milne et al., 1996).
Null mutant is defective for telomere silencing (Boulton and Jackson, 1998; Laroche et al., 1998)
HomologsS.p. Spbc543.03cp
M.m. 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 ReferencesBoulton, S. J., and Jackson, S. P. (1998). Components of the Ku-dependent non-homologous end-joining pathway are involved in telomeric length maintenance and telomeric silencing. Embo J 17, 1819-28. [Abstract]
Laroche, 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, DNA damage, silencing, yeast, replicative senescence, Saccharomyces cerevisiae, Ku, NHEJ