| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2005: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2004: ¥3,100,000 (Direct Cost: ¥3,100,000)
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| Research Abstract |
We visualized the spindle and the chromosome using GFP-tagging systems in living fission yeast cells and observed their dynamics at meiosis. At both meiotic divisions, chromosomes attach to the spindle in a bi-polar fashion during spindle formation, and then undergo anaphase A and anaphase B. Sister chromatid cohesion is resolved first at arms at meiosis I, and then at centromeres at meiosis II around anaphase onset. At meiosis II, however, arm cohesion is still retained at centromere-proximal regions. This suggests that arm cohesion is not resolved near the centromere at meiosis I or that arm cohesion is re-established around centromeres at meiosis II. We then examined roles of the spindle assembly checkpoint (SAC) factor Mad2 in the progression of meiosis by analyzing mutant cells defective in either homolog association at meiosis I or sister chromatid cohesion at meiosis II. We found that as in mitosis, Mad2 delays anaphase onset by sensing improper spindle attachment of chromosomes at meiosis by inhibiting an essential activator of the anaphase-promoting complex (APC), Slp1. Interestingly, we found that when anaphase onset is delayed by the SAC at meiosis I, anaphase onset is conversely advanced at meiosis II. We found that a meiosis-specific APC activator Fzr1 also participates in anaphase regulation, and that anaphase II advancement which is caused by meiosis I-delay was eliminated by Fzr1 depletion. Therefore, there is Fzr1-dependent, meiosis-specific anaphase regulation, and this causes anaphase advancement at meiosis II when meiosis I is delayed by the SAC.
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