OrganismCaenorhabditis elegans
Aging PhenotypeLife-span extension
Allele TypeRecessive
StrainBristol N2
DescriptionLoss of function can increase life span 100-150% (Apfeld and Kenyon, 1999).
Gene FunctionMember of the TPR family. Required for dauer formation and recovery (Vowels and Thomas, 1992; Malone et al., 1996)
Other PhenotypesIn addition to being dauer defective, loss of function mutants are chemotaxis defective (Bargmann et al., 1993). and dye filling defective (Starich et al., 1995). Dauer defective phenotype is suppressed by daf-2. (Vowels and Thomas, 1992).
HomologsS.c. CDC23, CDC16, CDC27
S.p. Spbc23e6.09p, nuc2
C.e. K04G7.3, F38B6.6, B0464.2, F32D1.3
D. m. CG12548, CG15190, CG4137, BcDNA, CG2469, anon-DM192
R.n. OGT
H.s. D13S1056E , OGT, GTF3C3
Primary ReferenceApfeld, J., and Kenyon, C. (1999). Regulation of lifespan by sensory perception in Caenorhabditis elegans. Nature 402, 804-9. [Abstract]
Other ReferencesBargmann, C. I., Hartwieg, E., and Horvitz, H. R. (1993). Odorant-selective genes and neurons mediate olfaction in C. elegans. Cell 74, 515-27. [Abstract]
Vowels, J. J., and Thomas, J. H. (1992). Genetic analysis of chemosensory control of dauer formation in Caenorhabditis elegans. Genetics 130, 105-23. [Abstract]
Relevant LinksWormBase:
KeywordsCaenorhabditis, elegans, worm, neurons, dauer