gon-2 encodes a predicted cation channel belonging to the TRP superfamily. Loss-of-function mutations in
gon-2 severely impair the mitotic divisions of the gonadal precursors. Our working hypothesis is that
gon-2 functions within Z1 and Z4 to allow the influx of cations (probably Ca 2+ ), which then stimulate G1 progression. In order to identify genes that act in conjunction with
gon-2 , we have screened for extragenic revertants of the temperature sensitive allele,
gon-2(
q388) . To date, we have identified four distinct gem loci ( g on-2 e xtragenic m odifier) that can mutate to suppress
gon-2(
q388) .
gem-1 X and
gem-4 IV are represented by multiple alleles, whereas
gem-2 II and
gem-3 III are represented by a single allele each. We are currently performing SNP mapping and transformation rescue assays to determine the molecular identities of the gem loci. As another means of identifying genes that interact with
gon-2 , we screened for mutations that cause similar gonadogenesis defects.
gon-11(
dx5) is a recessive, temperature sensitive allele that produces a phenotype similar to that of
gon-2(
q388) .
dx5 has relatively low penetrance, so it is only marginally useful. Therefore, we used non-complementation screening to search for more robust alleles of
gon-11 . This resulted in the identification of
gon-11(
dx106) , which causes fully penetrant late embryonic lethality. We are currently using
dx106 for SNP mapping and transformation rescue assays. This work is supported by NIH RO1 GM49785