{"title":"Inactivation of the Catalytic Activity of Mps1 Kinase Prevents Its Own Degradation at Centrosomes.","authors":"Shrabani Halder, Arpita Dutta, Rupsa Mondal, Banhi Chowdhury, Benu Brata Das, Shubhra Majumder","doi":"10.1002/cm.22032","DOIUrl":null,"url":null,"abstract":"<p><p>Mps1 kinase plays important roles in regulating centriole assembly, apart from its essential role in spindle assembly checkpoint. Here we report a novel mode of regulating centrosomal Mps1 level, which is governed by its own catalytic activity that promotes its degradation at centrosomes. A kinase-dead mutant of Mps1 or catalytically inactive Mps1 due to treatment with a specific kinase inhibitor is protected from degradation at centrosomes. This autoregulatory mode of controlling Mps1 activity at centrosomes likely restricts excess centriole production in a dividing cell.</p>","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cytoskeleton (Hoboken, N.J.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/cm.22032","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Mps1 kinase plays important roles in regulating centriole assembly, apart from its essential role in spindle assembly checkpoint. Here we report a novel mode of regulating centrosomal Mps1 level, which is governed by its own catalytic activity that promotes its degradation at centrosomes. A kinase-dead mutant of Mps1 or catalytically inactive Mps1 due to treatment with a specific kinase inhibitor is protected from degradation at centrosomes. This autoregulatory mode of controlling Mps1 activity at centrosomes likely restricts excess centriole production in a dividing cell.