emb-5 encodes a nuclear protein that is required maternally for the correct timing of gut precursor E cell division and zygotically for the proliferation of germ cells. We have isolated suppressor mutations of the temperature-sensitive allele
hc61 and found that about 20% of them were dpy mutations including
dpy-7, 8 and 10. Surveys of commonly used dpy markers revealed that
dpy-2, 3, 7, 8 and 10 suppressed
emb-5, whereas
dpy-5, 6, 11, 13, 17 and 18 did not. The very same suppression pattern as observed with
emb-5 were obtained with
glp-1. Of the dpy markers examined above,
dpy-2, 7, and 10 are known to encode collagens, extracellular matrix proteins. Since unc- 52, which codes for a proteoglycan, another matrix protein, is reported to suppress
mup-1, we tested and observed the suppression of
emb-5 and
glp-1 by
unc-52. These results suggest that some common mechanisms are operative in the suppression of
emb-5 and
glp-1 by mutations in genes encoding those extracellular matrix proteins. Two isolated suppressor
dpy-10 alleles showed ts morphology; that is, they were Dpy or wild type when grown at 25 or 16C, respectively. Interestingly in this respect, these alleles suppressed
hc61 and rescued embryos only when the embryos were born of the morphologically Dpy parent hermaphrodites that were grown at 25C. With the
hc61 mutation, the two E cells divide prematurely at the 26-cell stage instead of the normal 44- cell stage; however, the overall cell division rate is somewhat slower in the
hc61 mutant than in the wild type. We have investigated how dpy suppressors counteracted the abnormal cell division timing of
hc61 embryos and found that they did so by correcting not the cell division rate but the cell division sequence in embryogenesis. In fact, the overall division rate was slower in
hc61 and dpy suppressor doubles than in
hc61 alone. The non-suppressor
dpy-5 did not show these phenotypes. Possible suppression mechanisms will be discussed.