Myt1 inhibition of Cyclin A/Cdk1 is essential for fusome integrity and premeiotic centriole engagement in Drosophila spermatocytes

Autor: Joseph O. Ayeni, Ellen Homola, Ramya Varadarajan, Shelagh D. Campbell, Zhigang Jin
Rok vydání: 2016
Předmět:
Zdroj: Molecular Biology of the Cell
ISSN: 1939-4586
Popis: Drosophila Myt1 is essential for male fertility. Loss of Myt1 activity causes defective fusomes and premature centriole disengagement during premeiotic G2 phase due to lack of Myt1 inhibition of Cyclin A/Cdk1. These functions are distinct from known roles for Myt1 inhibition of Cyclin B/Cdk1 used to regulate G2/MI timing.
Regulation of cell cycle arrest in premeiotic G2 phase coordinates germ cell maturation and meiotic cell division with hormonal and developmental signals by mechanisms that control Cyclin B synthesis and inhibitory phosphorylation of the M-phase kinase, Cdk1. In this study, we investigated how inhibitory phosphorylation of Cdk1 by Myt1 kinase regulates premeiotic G2 phase of Drosophila male meiosis. Immature spermatocytes lacking Myt1 activity exhibit two distinct defects: disrupted intercellular bridges (fusomes) and premature centriole disengagement. As a result, the myt1 mutant spermatocytes enter meiosis with multipolar spindles. These myt1 defects can be suppressed by depletion of Cyclin A activity or ectopic expression of Wee1 (a partially redundant Cdk1 inhibitory kinase) and phenocopied by expression of a Cdk1F mutant defective for inhibitory phosphorylation. We therefore conclude that Myt1 inhibition of Cyclin A/Cdk1 is essential for normal fusome behavior and centriole engagement during premeiotic G2 arrest of Drosophila male meiosis. The novel meiotic functions we discovered for Myt1 kinase are spatially and temporally distinct from previously described functions of Myt1 as an inhibitor of Cyclin B/Cdk1 to regulate G2/MI timing.
Databáze: OpenAIRE