ArticleMolecular biology of the cell2018
The half-bridge component Kar1 promotes centrosome separation and duplication during budding yeast meiosis.
Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Using Yeast Two-Hybrid Screening and Structural Modeling to Identify Candidate Hrr25 Kinase Interactors at the Meiotic Kinetochore inInternational journal of molecular sciences · 2026Article
- Unveiling the cultivable yeast endophyte diversity in muscadine grape berries and their known functional prospects.BMC microbiology · 2025Article
- The Spo13/Meikin pathway confines the onset of gamete differentiation to meiosis II in yeast.The EMBO journal · 2022Article
- Tell the Difference Between Mitosis and Meiosis: Interplay Between Chromosomes, Cytoskeleton, and Cell Cycle Regulation.Frontiers in cell and developmental biology · 2021Review
- The role of gene dosage in budding yeast centrosome scaling and spontaneous diploidization.PLoS genetics · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The budding yeast centrosome, often called the spindle pole body (SPB), nucleates 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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