4-cell embryos exposed to anoxia contain detectable SAN-1 localized to the kinetochore and in lateral projections from the metaphase plate. There is less detectable SAN-1 in the nucleoplasm in metaphase blastomeres of embryos exposed to 30 minutes or 6 hours of anoxia in comparison to normoxic embryos. The lateral projections were not as easily detected in 8-cell embryos exposed to 6 hours or more of anoxia suggesting that either the kinetochore projections are only a characteristic of 4-cell embryos or the projections are more difficult to detect in embryos developed beyond the 4-cell stage. Embryos exposed to 12 hours or more of anoxia contains SAN-1 localized in punctate form in the nucleoplasm surrounding the metaphase plate. Embryos exposed to at least 24 hours of anoxia display a reduction in the detection of SAN-1 at the kinetochore. Taken together, it is concluded that SAN-1 localization changes are dependent upon anoxia exposure time.
4-cell embryos exposed to anoxia contain detectable SAN-1 localized to the kinetochore and in lateral projections from the metaphase plate. There is less detectable SAN-1 in the nucleoplasm in metaphase blastomeres of embryos exposed to 30 minutes or 6 hours of anoxia in comparison to normoxic embryos. The lateral projections were not as easily detected in 8-cell embryos exposed to 6 hours or more of anoxia suggesting that either the kinetochore projections are only a characteristic of 4-cell embryos or the projections are more difficult to detect in embryos developed beyond the 4-cell stage. Embryos exposed to 12 hours or more of anoxia contains SAN-1 localized in punctate form in the nucleoplasm surrounding the metaphase plate. Embryos exposed to at least 24 hours of anoxia display a reduction in the detection of SAN-1 at the kinetochore. Taken together, it is concluded that SAN-1 localization changes are dependent upon anoxia exposure time.
"In 72% of lin-15(rf) (n = 18) and 68% of let-60(gf) animals (n = 34), LIP-1::GFP was up-regulated in P3.p, P4.p, or P8.p in addition to P5.p and P7.p (Fig. 2F)."
In most animals only P5.p or P7.p descendants showed migration defect, but in 45 percent both P5.p and P7.p descendants showed Mig defects. Many cells that should have divided along the transverse axis in P6.p and P7.p descendants instead divided along the longitudinal axis.