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. 2003 Nov 21;4(12):1175–1181. doi: 10.1038/sj.embor.7400029

Figure 3.

Figure 3

mbk-2 microtubule defects result from persistence of MEI-1/katanin during mitosis. (A) Images from time-lapse movies of wild-type (WT), mel-26(RNAi), mbk-2(dd5ts) and mbk-2(dd5ts); mei-1(RNAi) anaphase embryos expressing histone::GFP and β-tubulin::GFP. Note the similarity between mel-26(RNAi) and mbk-2(dd5ts) embryos, which both exhibit abnormal spindle positioning and lagging chromosomes. These defects are entirely suppressed in mei-1(RNAi); mbk-2(dd5ts) embryos (bottom, right panel in A). Enlargement of the polar body indicates a meiosis failure in these embryos (left arrow), characteristic of mei-1(RNAi). The arrow at the right points to meiotic chromosomes that have been abnormally captured by the microtubules. (B) WT and mbk-2(dd5ts) early-anaphase embryos expressing MEI-1::GFP. The corresponding differential interference contrast (DIC) images are shown to the left. Note the presence of ectopic MEI-1::GFP on the spindle in the mutant.