Figure 6.

lab-1(tm1791) partially suppresses the mitotic defects of air-2(or207ts). (A) Embryonic lethality, larval lethality, and incidence of males among the progeny of hermaphrodites of the indicated genotypes. Error bars represent standard deviation of the mean. Asterisks indicate statistically significant reduction in embryonic lethality in air-2(or207); lab-1(tm1791) (P < 0.0001) and air-2(or207); sgo-1(RNAi) (P = 0.0005 by the two-tailed Mann-Whitney test, 95% C.I.) when compared with air-2(or207). (B) air-2(or207ts) mitotic defects at 25°C. Failure in chromosome segregation and cytokinesis in air-2(or207ts) embryos leading to polyploid cells. Bar, 5 μm. (C) Histone H3 phosphorylation is abolished in air-2(or207) embryos, but not in the germline. A GFP∷AIR-2 transgene or lab-1(tm1791) can independently restore embryonic phosphorylation of Histone H3 in air-2(or207) mutants. Bars: premeiotic tip, 5 μm; diakinesis and metaphase I, 2 μm; late prophase and anaphase, 5 μm. (D) AIR-2 and LAB-1 localization on prometaphase I bivalents in air-2(or207ts) worms grown at the restrictive temperature. Bar, 0.5 μm. (E) Quantification of Histone H3 phosphorylation in the gonad and embryo. The sample sizes are shown above each bar. Phosphorylation is significantly reduced in −1 diakinesis oocytes and embryos (P < 0.0001, respectively, by the two-sided Fisher’s Exact Test, 95% C.I.), but not at the premeiotic tip (histone H3 phosphorylation was observed in 100% of the examined premeiotic tips) of air-2(or207) worms when compared with the wild type. Phosphorylation is significantly improved in −1 oocytes (one asterisk) and embryos (two asterisks) of air-2(or207) lab-1(tm1791) (P < 0.0019 and P < 0.0001, respectively) and air-2; sgo-1(RNAi) mutants (P < 0.0004 and P < 0.0001, by the two-sided Fisher’s Exact Test, 95% C.I.) when compared with air-2(or207).