ArticleGenetics1997
Allele-specific suppression by formation of new protein-protein interactions in yeast.
Article in Genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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Who cites it
14 citing papers in PubMed, 32 citations in OpenAlex.
- Suppressor Mutants: History and Today's Applications.EcoSal Plus · 2021Review
- High-throughput synthetic rescue for exhaustive characterization of suppressor mutations in human genes.Cellular and molecular life sciences : CMLS · 2020Review
- Detection of functional protein domains by unbiased genome-wide forward genetic screening.Scientific reports · 2018Article
- Genetic suppression: Extending our knowledge from lab experiments to natural populations.BioEssays : news and reviews in molecular, cellular and developmental biology · 2017Review
- ER-associated retrograde SNAREs and the Dsl1 complex mediate an alternative, Sey1p-independent homotypic ER fusion pathway.Molecular biology of the cell · 2014Article
- A point mutation in the cargo-binding domain of myosin V affects its interaction with multiple cargoes.Eukaryotic cell · 2005Article
- The Saccharomyces cerevisiae calponin/transgelin homolog Scp1 functions with fimbrin to regulate stability and organization of the actin cytoskeleton.Molecular biology of the cell · 2003Article
- Stu1p is physically associated with beta-tubulin and is required for structural integrity of the mitotic spindle.Molecular biology of the cell · 2002Article
- A molecular genetic analysis of the interaction between the cytoplasmic dynein intermediate chain and the glued (dynactin) complex.Molecular biology of the cell · 2000Article
- Sorting of yeast membrane proteins into an endosome-to-Golgi pathway involves direct interaction of their cytosolic domains with Vps35p.The Journal of cell biology · 2000Article
- Dominant mutations in three different subunits of replication factor C suppress replication defects in yeast PCNA mutants.Genetics · 1999Article
- Article
- Coronin promotes the rapid assembly and cross-linking of actin filaments and may link the actin and microtubule cytoskeletons in yeast.The Journal of cell biology · 1999Article
- Multiple functions for actin during filamentous growth of Saccharomyces cerevisiae.Molecular biology of the cell · 1998Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Yeast fimbrin is encoded by the SAC6 gene, mutations of which suppress temperature-sensitive mutations in the actin gene (ACT1). To examine the mechanism of suppression, we have conducted a biochemical analysis of the interaction between various combinations of wild-type and mutant actin and Sac6 proteins. Previously, we showed that actin mutations that are suppressed by sac6 mutations encode proteins with a reduced affinity for wild-type Sac6p. In the present study, we have found that mutant Sac6 proteins bind more tightly to mutant actin than does wild-type Sac6p, and thus compensate for weakened interactions caused by the mutant actin. Remarkably, we have also found that mutant Sac6 proteins bind more tightly to wild-type actin than does wild-type Sac6p. This result indicates that suppression does not occur through the restoration of the original contact site, but rather through the formation of a novel contact site. This finding argues against suppression occurring through a "lock-and-key" mechanism and suggests a mechanism involving more global increases in affinity between the two proteins. We propose that the most common kind of suppressors involving interacting proteins will likely occur through this less specific mechanism.
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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.