ArticleMolecular and cellular biology2003
Two ubiquitin-conjugating enzymes, UbcP1/Ubc4 and UbcP4/Ubc11, have distinct functions for ubiquitination of mitotic cyclin.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Cdc13 (cyclin B) is degraded by autophagy under sulfur depletion in fission yeast.Autophagy reports · 2022Article
- Fission yeast Rad8/HLTF facilitates Rad52-dependent chromosomal rearrangements through PCNA lysine 107 ubiquitination.PLoS genetics · 2021Article
- UBE2C overexpression in melanoma and its essential role in G2/M transition.Journal of Cancer · 2019Article
- A Golgi rhomboid protease Rbd2 recruits Cdc48 to cleave yeast SREBP.The EMBO journal · 2016Article
- Endoplasmic Reticulum Exit of Golgi-resident Defective for SREBP Cleavage (Dsc) E3 Ligase Complex Requires Its Activity.The Journal of biological chemistry · 2015Article
- E3 ubiquitin ligase Pub1 is implicated in endocytosis of a GPI-anchored protein Ecm33 in fission yeast.PloS one · 2014Article
- An E2 enzyme Ubc11 is required for ubiquitination of Slp1/Cdc20 and spindle checkpoint silencing in fission yeast.Cell cycle (Georgetown, Tex.) · 2013Article
- Fission yeast 26S proteasome mutants are multi-drug resistant due to stabilization of the Pap1 transcription factor.PloS one · 2012Article
- Processive ubiquitin chain formation by the anaphase-promoting complex.Seminars in cell & developmental biology · 2011Review
- Cubism and the cell cycle: the many faces of the APC/C.Nature reviews. Molecular cell biology · 2011Review
- Yeast SREBP cleavage activation requires the Golgi Dsc E3 ligase complex.Molecular cell · 2011Article
- Nuclear protein quality is regulated by the ubiquitin-proteasome system through the activity of Ubc4 and San1 in fission yeast.The Journal of biological chemistry · 2011Article
- State of the APC/C: organization, function, and structure.Critical reviews in biochemistry and molecular biology · 2011Review
- UBE2S elongates ubiquitin chains on APC/C substrates to promote mitotic exit.Nature cell biology · 2009Article
- Mapping epigenetic mutations in fission yeast using whole-genome next-generation sequencing.Genome research · 2009Article
- The unique N terminus of the UbcH10 E2 enzyme controls the threshold for APC activation and enhances checkpoint regulation of the APC.Molecular cell · 2008Article
- Genomic expression patterns in cell separation mutants of Schizosaccharomyces pombe defective in the genes sep10 ( + ) and sep15 ( + ) coding for the Mediator subunits Med31 and Med8.Molecular genetics and genomics : MGG · 2008Article
- Structural organization of the anaphase-promoting complex bound to the mitotic activator Slp1.Molecular cell · 2007Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell cycle events are regulated by sequential activation and inactivation of Cdk kinases. Mitotic exit is accomplished by the inactivation of mitotic Cdk kinase, which is mainly achieved by degradation of cyclins. The ubiquitin-proteasome system is involved in this process, requiring APC/C (anaphase-promoting complex/cyclosome) as a ubiquitin ligase. In Xenopus and clam oocytes, the ubiquitin-conjugating enzymes that function with APC/C have been identified as two proteins, UBC4 and UBCx/E2-C. Previously we reported that the fission yeast ubiquitin-conjugating enzyme UbcP4/Ubc11, a homologue of UBCx/E2-C, is required for mitotic transition. Here we show that the other fission yeast ubiquitin-conjugating enzyme, UbcP1/Ubc4, which is homologous to UBC4, is also required for mitotic transition in the same manner as UbcP4/Ubc11. Both ubiquitin-conjugating enzymes are essential for cell division and directly required for the degradation of mitotic cyclin Cdc13. They function nonredundantly in the ubiquitination of CDC13 because a defect in ubcP1/ubc4+ cannot be suppressed by high expression of UbcP4/Ubc11 and a defect in ubcP4/ubc11+ cannot be suppressed by high expression of UbcP1/Ubc4. In vivo analysis of the ubiquitinated state of Cdc13 shows that the ubiquitin chains on Cdc13 were short in ubcP1/ubc4 mutant cells while ubiquitinated Cdc13 was totally reduced in ubcP4/ubc11 mutant cells. Taken together, these results indicate that the two ubiquitin-conjugating enzymes play distinct and essential roles in the degradation of mitotic cyclin Cdc13, with the UbcP4/Ubc11-pathway initiating ubiquitination of Cdc13 and the UbcP1/Ubc4-pathway elongating the short ubiquitin chains on Cdc13.
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