ArticleGenetics2000
Functional interaction between the PKC1 pathway and CDC31 network of SPB duplication genes.
Article in Genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 30 citations in OpenAlex.
- The role of gene dosage in budding yeast centrosome scaling and spontaneous diploidization.PLoS genetics · 2020Article
- Centrin/Cdc31 is a novel regulator of protein degradation.Molecular and cellular biology · 2008Article
- Centrin1 is required for organelle segregation and cytokinesis in Trypanosoma brucei.Molecular biology of the cell · 2007Article
- Cell wall integrity signaling in Saccharomyces cerevisiae.Microbiology and molecular biology reviews : MMBR · 2005Review
- Molecular analysis reveals localization of Saccharomyces cerevisiae protein kinase C to sites of polarized growth and Pkc1p targeting to the nucleus and mitotic spindle.Eukaryotic cell · 2005Article
- Fission yeast cdc31p is a component of the half-bridge and controls SPB duplication.Molecular biology of the cell · 2003Article
- Article
- Yeast RSC function is required for organization of the cellular cytoskeleton via an alternative PKC1 pathway.Genetics · 2002Article
- Nnf1p, Dsn1p, Mtw1p, and Nsl1p: a new group of proteins important for chromosome segregation in Saccharomyces cerevisiae.Eukaryotic cell · 2002Article
- Requirement of the spindle pole body for targeting and/or tethering proteins to the inner nuclear membrane.Nucleus (Austin, Tex.)Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The earliest known step in yeast spindle pole body (SPB) duplication requires Cdc31p and Kar1p, two physically interacting SPB components, and Dsk2p and Rad23p, a pair of ubiquitin-like proteins. Components of the PKC1 pathway were found to interact with these SPB duplication genes in two independent genetic screens. Initially, SLG1 and PKC1 were obtained as high-copy suppressors of dsk2Delta rad23Delta and a mutation in MPK1 was synthetically lethal with kar1-Delta17. Subsequently, we demonstrated extensive genetic interactions between the PKC1 pathway and the SPB duplication mutants that affect Cdc31p function. The genetic interactions are unlikely to be related to the cell-wall integrity function of the PKC1 pathway because the SPB mutants did not exhibit cell-wall defects. Overexpression of multiple PKC1 pathway components suppressed the G2/M arrest of the SPB duplication mutants and mutations in MPK1 exacerbated the cell cycle arrest of kar1-Delta17, suggesting a role for the PKC1 pathway in SPB duplication. We also found that mutations in SPC110, which encodes a major SPB component, showed genetic interactions with both CDC31 and the PKC1 pathway. In support of the model that the PKC1 pathway regulates SPB duplication, one of the phosphorylated forms of Spc110p was absent in pkc1 and mpk1Delta mutants.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.