Analysis of meiotic chromosome dynamics and its regulation in fission yeast

2005 Fiscal Year Final Research Report Summary

• Project/Area Number: 16570169
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Cell biology
• Research Institution: The National Institute of Information and Communications Technology
• Principal Investigator: YAMAMOTO Ayumu The National Institute of Information and Communications Technology, Basic and Advanced Research Department Cell Biology Group, Senior Researcher, 基礎先端部門生物情報グループ, 主任研究員 (70359082)
• Project Period (FY): 2004 – 2005
• Keywords: Cell Biology / Molecular Biology / Meiosis / Fission yeast / Chromosome segregation / Spindle assembly checkpoint / Anaphase promoting complex / Spindle

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.