ArticleGenetics1999
Genetic analysis of the shared role of CLN3 and BCK2 at the G(1)-S transition in Saccharomyces cerevisiae.
Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 76 citations in OpenAlex.
- Single-cell imaging reveals a key role of Bck2 in yeast cell size adaptation to nutrient challenges.The Journal of cell biology · 2026Article
- A Fkh1/2 binding site array in the WHI5 promoter drives sub-scaling transcription.Cell reports · 2026Article
- A Fkh1/2 binding site array in thebioRxiv : the preprint server for biology · 2025Article
- Impact of inter-species hybridisation on antifungal drug response in the Saccharomyces genus.BMC genomics · 2024Article
- Modeling the START transition in the budding yeast cell cycle.PLoS computational biology · 2024Article
- The microprotein Nrs1 rewires the G1/S transcriptional machinery during nitrogen limitation in budding yeast.PLoS biology · 2022Article
- Cell-size regulation in budding yeast does not depend on linear accumulation of Whi5.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- A hybrid stochastic model of the budding yeast cell cycle.NPJ systems biology and applications · 2020Article
- The p38/HOG stress-activated protein kinase network couples growth to division in Candida albicans.PLoS genetics · 2019Article
- A Stochastic Model of the Yeast Cell Cycle Reveals Roles for Feedback Regulation in Limiting Cellular Variability.PLoS computational biology · 2016Article
- A Model of Yeast Cell-Cycle Regulation Based on a Standard Component Modeling Strategy for Protein Regulatory Networks.PloS one · 2016Article
- Experimental testing of a new integrated model of the budding yeast Start transition.Molecular biology of the cell · 2015Article
- Article
- From START to FINISH: computational analysis of cell cycle control in budding yeast.NPJ systems biology and applications · 2015Article
- Functional overlap among distinct G1/S inhibitory pathways allows robust G1 arrest by yeast mating pheromones.Molecular biology of the cell · 2013Article
- Bck2 acts through the MADS box protein Mcm1 to activate cell-cycle-regulated genes in budding yeast.PLoS genetics · 2013Article
- CDK-dependent Hsp70 Phosphorylation controls G1 cyclin abundance and cell-cycle progression.Cell · 2012Article
- Cbk1 kinase and Bck2 control MAP kinase activation and inactivation during heat shock.Molecular biology of the cell · 2011Article
- The transcriptional network activated by Cln3 cyclin at the G1-to-S transition of the yeast cell cycle.Genome biology · 2010Article
- The Rts1 regulatory subunit of protein phosphatase 2A is required for control of G1 cyclin transcription and nutrient modulation of cell size.PLoS genetics · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The transcription complexes SBF and MBF mediate the G(1)-S transition in the cell cycle of Saccharomyces cerevisiae. In late G(1), SBF and MBF induce a burst of transcription in a number of genes, including G(1)- and S-phase cyclins. Activation of SBF and MBF depends on the G(1) cyclin Cln3 and a largely uncharacterized protein called Bck2. We show here that the induction of SBF/MBF target genes by Bck2 depends partly, but not wholly, on SBF and MBF. Unlike Cln3, Bck2 is capable of inducing its transcriptional targets in the absence of functional Cdc28. Our results revealed promoter-specific mechanisms of regulation by Cln3, Bck2, SBF, and MBF. We isolated high-copy suppressors of the cln3 bck2 growth defect; all of these had the ability to increase CLN2 expression. One of these suppressors was the negative regulator of meiosis RME1. Rme1 induces CLN2, and we show that it has a haploid-specific role in regulating cell size and pheromone sensitivity. Genetic analysis of the cln3 bck2 defect showed that CLN1, CLN2, and other SBF/MBF target genes have an essential role in addition to the degradation of Sic1.
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.