zyg-1 mutations disrupt cell divisions in the early C. elegans embryo as well as in the vulval lineage. Mutant embryos show two types of spindle formation defects. In two alleles, many embryos have multipolar first divisions. Tubulin staining has shown extra centrosomes around the male pronucleus as early as the midpronuclear stage. After the first division however, all
zyg-1 embryos show essentially the opposite phenotype; the divisions for approximately the next hour are largely monopolar. The abnormal nuclei in these cells continue to break down at regular intervals however, suggesting that at least some aspects of the normal cell cycle are still functioning in
zyg-1 embryos. Embryos arrest with fewer than 50 cells. In addition to this embryonic phenotype, four out of five of the
zyg-1 alleles show a weak egg laying defective (Egl) phenotype at 25 C. All five alleles show an increased penetrance of this Egl phenotype when heterozygous with ccDf5, a deficiency which deletes
zyg-1. Adult
zyg-1 mutant animals often have abnormal vulval morphology. The six vulval precursor cells appear normal in
zyg-1 mutant animals, but they often fail to divide. Both the
zyg-1(
it25ts) and
zyg-1(
b1ts) alleles have temperature sensitive periods for this phenotype around the L2/L3 boundary. This is before the vulval precursor cells divide; thus
zyg-1 may act at this time to prepare these cells for the subsequent divisions. Our current hypothesis is that
zyg-1 regulates centrosome function and/or replication in the early embryo, the vulval precursor cells, and possibly the developing sperm. I have also initiated a molecular analysis to clarify the role of
zyg-1.
zyg-1 is between
clr-1 and
lin-4 on chromosome II, and is deleted by ccDf5. The
zyg-1 phenotype is rescued by the cosmid C08D10.