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Lacefield, S.

Publications and source records attributed to Lacefield, S..

2 recordsLinked to original sources

The 14-3-3 Proteins Bmh1 and Bmh2 Are Key Regulators of Meiotic Commitment

Induction of meiosis requires exogenous signals that activate internal gene regulatory networks. Meiotic commitment ensures the irreversible continuation of meiosis, even upon withdrawal of the meiosis inducing signals. Budding yeast cells have a unique property in that cells enter meiosis when starved, but if given nutrient-rich medium prior to the commitment point, they exit meiosis and enter mitosis. After the meiotic commitment point in prometaphase I, cells remain in meiosis even with addition of nutrients. Despite the importance of meiotic commitment in ensuring the production of gametes, only a few genes involved in the commitment process are known. We performed a genome-scale screen in budding yeast and discovered new regulators of meiotic commitment including Bcy1, which is involved in nutrient sensing, the meiosis-specific kinase Ime2, Polo kinase Cdc5, and the 14-3-3 proteins Bmh1 and Bmh2. Importantly, we found that Bmh1 and Bmh2 are involved in multiple processes throughout meiosis including the maintenance of the middle meiosis transcription factor Ndt80, activation of Cdc5, and interaction with an RNA-binding protein Pes4, which is important for regulating the timing of translation of several mRNAs in meiosis II. This study identifies a meiotic commitment regulatory network with the 14-3-3 proteins functioning as central regulators.

cell biology↗

Bub3 and Bub1 maintain the balance of kinetochore-localized Aurora B Kinase and Protein Phosphatase I to Regulate Chromosome Segregation and Anaphase Onset in Meiosis

Accurate chromosome segregation depends on proper attachment of kinetochores to spindle microtubules prior to anaphase onset. The Ipl1/Aurora B kinase corrects improper attachments by phosphorylating kinetochore components and so releasing aberrant kinetochore-microtubule interactions. The localization of Ipl1 to kinetochores in budding yeast depends upon multiple pathways, including the Bub1/Bub3 pathway. We show here that in meiosis, Bub3 is crucial for correction of attachment errors. Depletion of Bub3 results in reduced levels of kinetochore-localized Ipl1, and concomitant massive chromosome mis-segregation caused by incorrect chromosome-spindle attachments. Depletion of Bub3 also results in shorter metaphase I and metaphase II due to premature localization of protein phosphatase 1 (PP1) to kinetochores, which antagonizes Ipl1-mediated phosphorylation. We propose a new role for the Bub1-Bub3 pathway in maintaining the balance between kinetochore-localization of Ipl1 and PP1, a balance that is essential for accurate meiotic chromosome segregation and timely anaphase onset.\n\nSummaryCairo et al show that in S. cerevisiae meiosis, spindle checkpoint proteins Bub1 and Bub3 have an essential role in preventing chromosome mis-segregation and setting the normal duration of anaphase I and anaphase II onset by regulating the kinetochore-localization of Ipl1 and PP1.

cell biology↗