ArticleGenetics2025
Analysis of combinatorial cohesin subunit gene deletions in budding yeast.
Article in Genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Aberrant cohesin function in Saccharomyces cerevisiae activates Mcd1 degradation to promote cell lethality.PLoS genetics · 2025Article
- Aberrant cohesin function inbioRxiv : the preprint server for biology · 2025Article
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.
Funding
Abstract
Throughout the cell cycle, DNA molecules convert between hierarchical intramolecular (cis) and intermolecular (trans) associations. Cohesin ATPase complexes produce both types of DNA associations which collectively are required for sister chromatid segregation, chromatin condensation, genomic architecture, gene transcription, and DNA repair. The mechanisms that regulate cohesin cis- and trans-activities, however, remain controversial. A popular model is that a regulatory complex (Pds5, Irr1/Scc3, and Rad61) sits atop a core ring-like complex (Mcd1/Scc1, Smc1, and Smc3), the latter of which exhibits the inherent ATPase activities responsible for producing cis- and trans-DNA conformations. Additional proteins transiently interact with cohesins to promote cohesin deposition onto DNA (Scc2 and Scc4) or stabilize cohesin-DNA binding (Eco1/Ctf7). Of these 9 components, only RAD61 is nonessential. Recent findings, however, identified pairs of suppressor mutations that support the viability of cells individually deleted for either PDS5 or ECO1/CTF7 (herein ECO1). Intriguingly, CLN2 deletion is common in both suppressor pairs, suggesting that combined suppressor mutations may support the viability of cells co-deleted for both ECO1 and PDS5. These results further suggest that the addition of other suppressor mutations (such as ELG1 and RAD61) may support the viability of cells deleted of all auxiliary subunits-including IRR1/SCC3 (herein SCC3). Here, we test these predictions and report on novel gene deletion combinations required for cell cycle progression and cell viability.
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Registered trials
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