We combine classical, quantitative, and molecular genetic analyses in determining whether the
age-1 gene, which is involved in the specification of life span, is also involved in the specification of hermaphrodite fertility. In the nematode Caenorhabditis elegans the mutant form of the
age-1 gene lengthens life span up to 70% (Age). This gene has been mapped to the center of chromosome 11. The
age-1 mutation cosegregates with a temperature-sensitive mutant allele of
fer-15 and is also associated with a four-fold reduction in hermaphrodite self fertility (Brd). Deficiencies on chromosome 11 have been used to map these three characters. One class of deficiencies (mnDf92, mnDf94, mnDf98) has a genetic end point to the left of
fer-15 and complements
fer-15,
emb-27, and Brd; a second class of eleven deficiencies (mnDf91, etc.) has a nominal end point to the right of
fer-15 and fails to complement
fer-15,
emb-27, and Brd. Thus, these two classes of deficiencies define a genetic region containing
fer-15,
emb-27, and the Brd phenotype. Both deficiency classes complement
age1 in 11 of 15 possible tests. Complementation mapping with other chromosome 11 deficiencies suggest that
age-1 is under mnDf63 and mnDf89, near
unc-4. This position agrees with multipoint mapping of Hutchinson et al.
fer-15,
emb-27, and Brd are also positioned to the physical map by identifying DNA polymorphisms associated with the end points of the first two classes of deficiencies. We have identified the right-hand end point of 10 of 11 deficiencies and the lefthand end point of 5 of 6 deficiencies examined and have mapped the positions of these end points using cosmids from the Rol-6 contig which covers much of chromosome 11. We have also discovered a RFLP that cosegregates with the
fer-15(
b26ts) mutant allele and presumably results from an alteration other than a single base-pair change. The Brd phenotype in deficiency heterozygotes behaves as a complete recessive at 25 but as an additive or semi-dominant trait at 20 .