ArticleMolecular biology of the cell2009
Regulation of cell polarity through phosphorylation of Bni4 by Pho85 G1 cyclin-dependent kinases in Saccharomyces cerevisiae.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Mutation-induced filaments of folded proteins are inert and non-toxic in a cellular system.Molecular systems biology · 2025Article
- Stage-Specific Genetic Interaction betweenInternational journal of molecular sciences · 2022Article
- Transcriptomic and metabolomic analysis reveals genes related to stress tolerance in high gravity brewing.World journal of microbiology & biotechnology · 2022Article
- Retention of duplicated genes in evolution.Trends in genetics : TIG · 2022Review
- The Role of the Cell Integrity Pathway in Septum Assembly in Yeast.Journal of fungi (Basel, Switzerland) · 2021Review
- Article
- Exploring whole-genome duplicate gene retention with complex genetic interaction analysis.Science (New York, N.Y.) · 2020Article
- Regulation of small GTPase activity by G1 cyclins.Small GTPases · 2019Review
- Systematic analysis of complex genetic interactions.Science (New York, N.Y.) · 2018Article
- Redundancy or specificity? The role of the CDK Pho85 in cell cycle control.International journal of biochemistry and molecular biology · 2013Review
- Systematic triple-mutant analysis uncovers functional connectivity between pathways involved in chromosome regulation.Cell reports · 2013Article
- Functional genomics in the study of yeast cell polarity: moving in the right direction.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013Review
- Impaired manganese metabolism causes mitotic misregulation.The Journal of biological chemistry · 2012Article
- Article
- Functional wiring of the yeast kinome revealed by global analysis of genetic network motifs.Genome research · 2012Article
- Morphogenesis and the cell cycle.Genetics · 2012Review
- A chemical-genetic screen to unravel the genetic network of CDC28/CDK1 links ubiquitin and Rad6-Bre1 to cell cycle progression.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Cryptococcal titan cell formation is regulated by G-protein signaling in response to multiple stimuli.Eukaryotic cell · 2011Article
- Regulation of septin dynamics by the Saccharomyces cerevisiae lysine acetyltransferase NuA4.PloS one · 2011Article
- Acid phosphatases of budding yeast as a model of choice for transcription regulation research.Enzyme research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the budding yeast Saccharomyces cerevisiae, the G1-specific cyclin-dependent kinases (Cdks) Cln1,2-Cdc28 and Pcl1,2-Pho85 are essential for ensuring that DNA replication and cell division are properly linked to cell polarity and bud morphogenesis. However, the redundancy of Cdks and cyclins means that identification of relevant Cdk substrates remains a significant challenge. We used array-based genetic screens (synthetic genetic array or SGA analysis) to dissect redundant pathways associated with G1 cyclins and identified Bni4 as a substrate of the Pcl1- and Pcl2-Pho85 kinases. BNI4 encodes an adaptor protein that targets several proteins to the bud neck. Deletion of BNI4 results in severe growth defects in the absence of the Cdc28 cyclins Cln1 and Cln2, and overexpression of BNI4 is toxic in yeast cells lacking the Pho85 cyclins Pcl1 and Pcl2. Phosphorylation of Bni4 by Pcl-Pho85 is necessary for its localization to the bud neck, and the bud neck structure can be disrupted by overexpressing BNI4 in pcl1Deltapcl2Delta mutant cells. Our data suggest that misregulated Bni4 may bind in an uncontrolled manner to an essential component that resides at the bud neck, causing catastrophic morphogenesis defects.
Indexed as
Identifiers
What OpenQuestion holds
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.