NDLI: CDK1-dependent inhibition of the E3 ubiquitin ligase CRL4CDT2 ensures robust transition from S Phase to Mitosis.

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CDK1-dependent inhibition of the E3 ubiquitin ligase CRL4CDT2 ensures robust transition from S Phase to Mitosis.

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CDK1-dependent inhibition of the E3 ubiquitin ligase CRL4CDT2 ensures robust transition from S Phase to Mitosis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Oh, Seeun Cook, Jeanette Gowen Varma, Dileep Rizzardi, Lindsay F. Coleman, Kate E. Matson, Jacob P.
Description	Author Affiliation: Rizzardi LF ( From the Curriculum in Genetics and Molecular Biology and.); Coleman KE ( From the Curriculum in Genetics and Molecular Biology and.); Varma D ( the Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599.); Matson JP ( the Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599.); Oh S ( the Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599.); Cook JG ( From the Curriculum in Genetics and Molecular Biology and the Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599 jgcook@email.unc.edu.)
Abstract	Replication-coupled destruction of a cohort of cell cycle proteins ensures efficient and precise genome duplication. Three proteins destroyed during replication via the CRL4(CDT2) ubiquitin E3 ligase, CDT1, p21, and SET8 (PR-SET7), are also essential or important during mitosis, making their reaccumulation after S phase a critical cell cycle event. During early and mid-S phase and during DNA repair, proliferating cell nuclear antigen (PCNA) loading onto DNA (PCNA(DNA)) triggers the interaction between CRL4(CDT2) and its substrates, resulting in their degradation. We have discovered that, beginning in late S phase, PCNA(DNA) is no longer sufficient to trigger CRL4(CDT2)-mediated degradation. A CDK1-dependent mechanism that blocks CRL4(CDT2) activity by interfering with CDT2 recruitment to chromatin actively protects CRL4(CDT2) substrates. We postulate that deliberate override of replication-coupled destruction allows anticipatory accumulation in late S phase. We further show that (as for CDT1) de novo SET8 reaccumulation is important for normal mitotic progression. In this manner, CDK1-dependent CRL4(CDT2) inactivation contributes to efficient transition from S phase to mitosis.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	1
Volume Number	290
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2015-01-02
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Chromatin Metabolism Cyclin-Dependent Kinases Genetics Mitosis Nuclear Proteins S Phase Ubiquitin-Protein Ligases Cell Cycle Proteins Chemistry Cyclin-Dependent Kinase Inhibitor P21 Gene Expression Regulation HCT116 Cells HEK293 Cells HeLa Cells Histone-Lysine N-Methyltransferase Proliferating Cell Nuclear Antigen Proteolysis Signal Transduction Ubiquitination Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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