The gonad of the Caenorhabditis elegans hermaphrodite is generated by
the postembryonic divisions of two somatic precursors, Z1 and Z4, and
two germline precursors, Z2 and Z3. These cells begin division midway
through the first larval stage. By the end of the fourth larval stage,
Z1 and Z4 produce 143 descendants, while Z2 and Z3 give rise to simil
ar to 1000 descendants. The divisions of Z2 and Z3 are dependent on si
gnals produced by ZI and Z4, but not vice versa. We have characterized
the properties of five loss-of-function alleles of a newly described
gene, which we call gon-2. In gon-2 mutants, gonadogenesis is severely
impaired; in some animals, none of the gonad progenitors undergo any
postembryonic divisions. Mutations in gon-2 have a partial maternal ef
fect: either maternal or zygotic expression is sufficient to prevent t
he severe gonadogenesis defects, By cell lineage analysis, we found th
at the primary defect in gon-2 mutants is a delay (sometimes a complet
e block) in the onset and continuation of gonadal divisions. The resul
ts of upshift experiments using a temperature-sensitive allele suggest
that zygotic expression of gon-2 begins early in embryogenesis, befor
e the birth of Z1 and Z4. The results of downshift experiments suggest
that Z1 and Z4 can generate the full complement of gonadal tissues ev
en even gon-2 function is inhibited until the end of the second larval
stage. Thus, gon-2 activity is probably not required for the specific
ation of gonadal cell fates, but appears to he generally required for
gonadal cell divisions.