During gonadogenesis, somatic gonadal blast cells undergo an essentially invariant pattern of cell divisions, migrations and differentiation. We have isolated four recessive, loss-of-function alleles of the
gon-4 locus. All
gon-4 mutants are sterile with variable defects in gonad formation. In most
gon-4 adults, the gonad is smaller than normal and gonadal structures are not properly organized. By cell lineage analysis, we found that the initial defect in
gon-4 mutants is a dramatic delay in the timing of somatic gonadal cell divisions. For example in
gon-4 mutants, Z1 or Z4 often divide in L2 instead of L1. Furthermore, the synchrony of Z1 and Z4 cell divisions is lost, resulting in a loss of symmetry in the hermaphrodite gonad. Although fewer cells are made than normal, GFP reporters for specific somatic gonadal tissues are expressed at the correct times in
gon-4 mutants, suggesting that delayed divisions and an incomplete lineage do not block cell differentiation. By contrast, the germ line precursor cells divided normally in L1 and L2 (later germ line defects might reflect DTC defects), the M and B lineages were normal during L1 and L2 (they were not followed further), and the timing of larval molts was unaffected. Therefore, the cell division defects appear to be specific to the somatic gonadal lineage. The
gon-4 locus maps to linkage group IV near
unc-43 . Using transformation rescue, RNAi, and sequence analysis, we have established that
gon-4 encodes a novel protein (transcript K04D7.5). All four
gon-4 alleles have nonsense mutations in the coding region. Developmental Northern blots suggest that
gon-4 mRNA is expressed mainly in the germ line. A
gon-4 ::GFP transgene rescued
gon-4(
q519) and expressed GFP in somatic gonadal cells and in the germ line. Preliminary results indicate that a GON-4 antibodies co-localize with a marker of mitotic cells (phosphohistone H3) in the germ line, consistent with the idea that
gon-4 is required for normal progression through the cell cycle.