期刊
MOLECULAR BIOLOGY OF THE CELL
卷 29, 期 15, 页码 1798-1810出版社
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E18-03-0163
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资金
- Stowers Institute for Medical Research of the National Institutes of Health (NIH) [R01 GM121443]
- National Institute of General Medicine of the National Institutes of Health (NIH) [R01 GM121443]
- NIH [GM117102]
- National Science Foundation [MCB1121771]
The budding yeast centrosome, often called the spindle pole body (SPB), nudeates microtubules for chromosome segregation during cell division. An appendage, called the half bridge, attaches to one side of the SPB and regulates SPB duplication and separation. Like DNA, the SPB is duplicated only once per cell cycle. During meiosis, however, after one round of DNA replication, two rounds of SPB duplication and separation are coupled with homologue segregation in meiosis I and sister-chromatid segregation in meiosis II. How SPB duplication and separation are regulated during meiosis remains to be elucidated, and whether regulation in meiosis differs from that in mitosis is unclear. Here we show that overproduction of the half-bridge component Kar1 leads to premature SPB separation during meiosis. Furthermore, excessive Kar1 induces SPB overduplication to form supernumerary SPBs, leading to chromosome missegregation and erroneous ascospore formation. Kar1-mediated SPB duplication bypasses the requirement of dephosphorylation of Sfi1, another half-bridge component previously identified as a licensing factor. Our results therefore reveal an unexpected role of Kar1 in licensing meiotic SPB duplication and suggest a unique mechanism of SPB regulation during budding yeast meiosis.
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