β-TrCP- and Casein Kinase II-Mediated Degradation of Cyclin F Controls Timely Mitotic Progression.
β-TrCP- and Casein Kinase II-Mediated Degradation of Cyclin F Controls Timely Mitotic Progression.
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DOI:
10.1016/j.celrep.2018.08.076
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发表时间:
2018-09-25
期刊:
影响因子:
8.8
通讯作者:
D'Angiolella V
中科院分区:
文献类型:
--
作者:
Mavrommati I;Faedda R;Galasso G;Li J;Burdova K;Fischer R;Kessler BM;Carrero ZI;Guardavaccaro D;Pagano M;D'Angiolella V
Orderly progressions of events in the cell division cycle are necessary to ensure the replication of DNA and cell division. Checkpoint systems allow the accurate execution of each cell-cycle phase. The precise regulation of the levels of cyclin proteins is fundamental to coordinate cell division with checkpoints, avoiding genome instability. Cyclin F has important functions in regulating the cell cycle during the G2 checkpoint; however, the mechanisms underlying the regulation of cyclin F are poorly understood. Here, we observe that cyclin F is regulated by proteolysis through β-TrCP. β-TrCP recognizes cyclin F through a non-canonical degron site (TSGXXS) after its phosphorylation by casein kinase II. The degradation of cyclin F mediated by β-TrCP occurs at the G2/M transition. This event is required to promote mitotic progression and favors the activation of a transcriptional program required for mitosis. β-TrCP1 and β-TrCP2 interact with cyclin F and control cyclin F levels during mitosis A TSGXXS motif is necessary for β-TrCP1 and β-TrCP2 binding to cyclin F CKIIα phosphorylates cyclin F at S704 within the TSGXXS motif β-TrCP-mediated degradation of cyclin F promotes mitotic progression via B-Myb Mavrommati et al. identify how cyclin F is regulated during mitosis by proteolysis. Cyclin F is ubiquitylated by β-TrCP after phosphorylation by CKII on S704 within a TSGXXS degron. β-TrCP-mediated degradation of cyclin F favors timely mitotic progression through the control of a B-Myb transcriptional program.
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影响因子:
16
作者:
Elia AE;Boardman AP;Wang DC;Huttlin EL;Everley RA;Dephoure N;Zhou C;Koren I;Gygi SP;Elledge SJ
通讯作者:
Elledge SJ
DOI:
10.1073/pnas.0307700101
发表时间:
2004-03-30
影响因子:
11.1
作者:
Watanabe, N;Arai, H;Osada, H
通讯作者:
Osada, H
影响因子:
16
作者:
Dankert, John F.;Rona, Gergely;Clijsters, Linda;Geter, Phillip;Skaar, Jeffrey R.;Bermudez-Hernandez, Keria;Sassani, Elizabeth;Fenyo, David;Ueberheide, Beatrix;Schneider, Robert;Pagano, Michele
通讯作者:
Pagano, Michele
DOI:
10.15252/embj.201593374
发表时间:
2016-07-01
期刊:
The EMBO journal
影响因子:
--
作者:
Raducu M;Fung E;Serres S;Infante P;Barberis A;Fischer R;Bristow C;Thézénas ML;Finta C;Christianson JC;Buffa FM;Kessler BM;Sibson NR;Di Marcotullio L;Toftgård R;D'Angiolella V
通讯作者:
D'Angiolella V
影响因子:
16.6
作者:
Walter D;Hoffmann S;Komseli ES;Rappsilber J;Gorgoulis V;Sørensen CS
通讯作者:
Sørensen CS