The dauer-like phenotype identifies genes with interesting roles in dauer function. Wild-type pathways provide C. elegans with the choice of reproductive development, when the conditions are favorable or dauer when the environment is not conducive to survival. Most dauer mutants simply increase or decrease the proportion of animals that enter dauer under given conditions. Thus, these genes presumably act by affecting signal transduction events that promote or repress dauer in all tissues. Dauer-like mutants are different. Two dauer-like mutations that have been isolated and studied by Albert and Riddle are
daf-9 and
daf-15 . In these mutants some tissues enter dauer, some do not, and many exhibit intermediate traits. Thus, the same dauer-like individual worm will have some Daf-d (dauer defective) tissues and some Daf-c (dauer-constitutive) tissues, indicating that the same gene can promote dauer in one cell type but repress it in another. The difference between
daf-9 and
daf-15 mutants is which tissues are Daf-c or Daf-d. Both
daf-9 and
daf-15 are sterile, have a life span around three weeks versus dauers two months and can not withstand the SDS selection as well as full dauer. They also differ;
daf-9 has more dauer characteristics than
daf-15. For example, the
daf-9 mutants body shrinks more radially and it has a dispersal pattern that is more like a dauer, i.e.
daf-9 mutants disperse at a greater rate than
daf-15 mutants.Two recent papers on
daf-9 (K. Jia et al, 2002 and B. Gerisch et al, 2001) identify DAF-9 as a cytochrome
p450 upstream of
daf-12 and propose it functions in metabolism of a steroid ligand for DAF-12. We are studying
daf-15 to identify its role in the pathway, as well as to see if there are any functional connections or parallels between DAF-15 and DAF-9. We are mapping
daf-15 from the left boundary, which has been defined as
fem-3. The right boundary has been mapped by our lab, narrowing the interval to 250 kb region. We are screening progeny from
daf-15 (
m81)/CB4856 heterozygotes for recombinants and subsequently SNP testing. We will narrow the
daf-15 interval suitable for cloning. We would also like to categorize
daf-15 phenotype. We plan to study the epistatic relationships that
daf-15 has with other genes, in order to determine where in the pathway
daf-15 is acting, as well as to look at progression of
daf-15 mutants through larval development to understand the pathway better.