ArticleMolecular biology of the cell2010
Cell type-dependent requirement for PIP box-regulated Cdt1 destruction during S phase.
Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- The Crk4-Cyc4 complex regulates GThe EMBO journal · 2024Article
- PCR cloning Intermediated Gibson assembly (PIG) for Constructing DNA Repair Templates in CRISPR-Cas9 Based Gene Editing.microPublication biology · 2023Article
- Article
- Regulation of Smoothened ubiquitylation and cell surface expression through a Cul4-DDB1-Gβ E3 ubiquitin ligase complex.Journal of cell science · 2018Article
- Temporal remodeling of the cell cycle accompanies differentiation in the Drosophila germline.Developmental biology · 2017Article
- DNA Replication Control DuringGenetics · 2017Review
- Re-replication induced by geminin depletion occurs from G2 and is enhanced by checkpoint activation.Journal of cell science · 2012Article
- MicroRNA transgene overexpression complements deficiency-based modifier screens in Drosophila.Genetics · 2012Article
- Dynamic interactions of high Cdt1 and geminin levels regulate S phase in early Xenopus embryos.Development (Cambridge, England) · 2012Article
- Mechanism of CRL4(Cdt2), a PCNA-dependent E3 ubiquitin ligase.Genes & development · 2011Review
- Cdt1 proteolysis is promoted by dual PIP degrons and is modulated by PCNA ubiquitylation.Nucleic acids research · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 3 countries.
Funding
Abstract
DNA synthesis-coupled proteolysis of the prereplicative complex component Cdt1 by the CRL4(Cdt2) E3 ubiquitin ligase is thought to help prevent rereplication of the genome during S phase. To directly test whether CRL4(Cdt2)-triggered destruction of Cdt1 is required for normal cell cycle progression in vivo, we expressed a mutant version of Drosophila Cdt1 (Dup), which lacks the PCNA-binding PIP box (Dup(ΔPIP)) and which cannot be regulated by CRL4(Cdt2). Dup(ΔPIP) is inappropriately stabilized during S phase and causes developmental defects when ectopically expressed. Dup(ΔPIP) restores DNA synthesis to dup null mutant embryonic epidermal cells, but S phase is abnormal, and these cells do not progress into mitosis. In contrast, Dup(ΔPIP) accumulation during S phase did not adversely affect progression through follicle cell endocycles in the ovary. In this tissue the combination of Dup(ΔPIP) expression and a 50% reduction in Geminin gene dose resulted in egg chamber degeneration. We could not detect Dup hyperaccumulation using mutations in the CRL4(Cdt2) components Cul4 and Ddb1, likely because these cause pleiotropic effects that block cell proliferation. These data indicate that PIP box-mediated destruction of Dup is necessary for the cell division cycle and suggest that Geminin inhibition can restrain Dup(ΔPIP) activity in some endocycling cell types.
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