인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
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Citeasy
크롬 서지관리 다운로드
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
CK1 enzymes are conserved regulators of diverse cellular processes. In Schizosaccharomyces pombe, the CK1 orthologs of CK1δ and CK1ε, Hhp1 and Hhp2, are required for a mitotic checkpoint that delays cytokinesis when the mitotic spindle is disrupted. Here, we show that Hhp2, but not Hhp1, undergoes transient hyperphosphorylation during mitosis. Hhp2 autophosphorylates at four residues and is phosphorylated by the cyclin-dependent kinase Cdk1 at three additional sites. Functionally, these phosphorylation events inhibit Hhp2 catalytic activity, as phospho-ablating mutants exhibited enhanced in vitro kinase activity. In vivo, a mutant combining all seven sites (hhp2-7A) behaved as a gain-of-function mutant in the mitotic checkpoint and also had the unexpected phenotype of accelerating mitosis and cytokinesis in unperturbed conditions. Further genetic analyses indicated that Hhp2 likely promotes mitotic progression in parallel with the Polo-like kinase, Plo1. These findings establish that mitotic phosphorylation of Hhp2 serves as a negative regulatory mechanism that silences checkpoint activity and modulates cell cycle timing. Because mitotic phosphorylation of human CK1δ has been observed, our results suggest that Cdk1-mediated inhibition of CK1 enzymes is a conserved mechanism coupling the core cell cycle control machinery to CK1-dependent signaling pathways.
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오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
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