The gon-4 gene is required for gonadogenesis in the nematode Caenorhabditis
elegans. Normally, two precursor cells, Z1 and Z4, follow a reproducible p
attern of cell divisions to generate the mature somatic gonadal structures
(e.g., uterus in hermaphrodites, vas deferens in males). In contrast, in go
n-4 mutants, the Z1/Z4 cell lineages are variably aborted in both hermaphro
dites and males: Z1 and Z4 divide much later than normal and subsequent div
isions are either absent or severely delayed. In gon-4 adults, normal somat
ic gonadal structures are never observed, and germ-line and vulval tissues,
which depend on somatic gonadal cues for their development, are also aberr
ant. In contrast, nongonadal tissues and the timing of other developmental
events (e.g., molts) appear to be normal in gon-4 mutants. The gon-4 allele
s are predicted to be strong loss-of-function or null alleles by both genet
ic and molecular criteria. We have cloned gon-4 in an attempt to learn how
it regulates gonadogenesis. The gon-4 gene encodes a novel, acidic protein.
A GON-4::GFP fusion protein, which rescues a gon-4 mutant to fertility, is
expressed in somatic gonadal cells during early gonadal development. Furth
ermore, this fusion protein is nuclear. We conclude that gon-4 is a regulat
or of the early lineage of Z1 and Z4 and suggest that it is a part of a gen
etic program common to the regulation of both hermaphrodite and male gonado
genesis. (C) 2000 Academic Press.