Evidence map›Paper›PMID 22496671›Full record

ArticlePLoS genetics2012

Regulation of budding yeast mating-type switching donor preference by the FHA domain of Fkh1.

Jin Li, Eric Coïc, Kihoon Lee, Cheng-Sheng Lee, Jung-Ae Kim, Qiuqin Wu, James E Haber

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  11. Dissecting quantitative trait nucleotides by saturation genome editing.bioRxiv : the preprint server for biology · 2024
    Article
  12. Broadly Applicable Control Approaches Improve Accuracy of ChIP-Seq Data.International journal of molecular sciences · 2023
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Yeast ATM and ATR kinases use different mechanisms to spread histone H2A phosphorylation around a DNA double-strand break.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  19. Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Jin LiDepartment of Biology and Rosenstiel Center, Brandeis University, Waltham, Massachusetts, USA.
Eric Coïc
Kihoon Lee
Cheng-Sheng Lee
Jung-Ae Kim
Qiuqin Wu
James E Haber
Brandeis University · USCellectis (United States) · USRockefeller University · US

Funding

Recombination Mechanisms in Yeast Cell DifferentiationR37GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2007 to 2016
$5.5M
Arrest, Recovery, and Adaptation from DNA DamageR01GM061766 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2001 to 2016
$4.6M
RECOMBINATION MECHANISMS IN YEAST CELL DIFFERENTIATIONR01GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 1985 to 2006
$3.4M
NIGMS NIH HHS GM20056NIGMS NIH HHS GM61766NIGMS NIH HHS R01 GM020056NIGMS NIH HHS R01 GM061766NIGMS NIH HHS R37 GM020056
6 · The paper itself

Abstract

During Saccharomyces cerevisiae mating-type switching, an HO endonuclease-induced double-strand break (DSB) at MAT is repaired by recombining with one of two donors, HMLα or HMRa, located at opposite ends of chromosome III. MATa cells preferentially recombine with HMLα; this decision depends on the Recombination Enhancer (RE), located about 17 kb to the right of HML. In MATα cells, HML is rarely used and RE is bound by the MATα2-Mcm1 corepressor, which prevents the binding of other proteins to RE. In contrast, in MATa cells, RE is bound by multiple copies of Fkh1 and a single copy of Swi4/Swi6. We report here that, when RE is replaced with four LexA operators in MATa cells, 95% of cells use HMR for repair, but expression of a LexA-Fkh1 fusion protein strongly increases HML usage. A LexA-Fkh1 truncation, containing only Fkh1's phosphothreonine-binding FHA domain, restores HML usage to 90%. A LexA-FHA-R80A mutant lacking phosphothreonine binding fails to increase HML usage. The LexA-FHA fusion protein associates with chromatin in a 10-kb interval surrounding the HO cleavage site at MAT, but only after DSB induction. This association occurs even in a donorless strain lacking HML. We propose that the FHA domain of Fkh1 regulates donor preference by physically interacting with phosphorylated threonine residues created on proteins bound near the DSB, thus positioning HML close to the DSB at MAT. Donor preference is independent of Mec1/ATR and Tel1/ATM checkpoint protein kinases but partially depends on casein kinase II. RE stimulates the strand invasion step of interchromosomal recombination even for non-MAT sequences. We also find that when RE binds to the region near the DSB at MATa then Mec1 and Tel1 checkpoint kinases are not only able to phosphorylate histone H2A (γ-H2AX) around the DSB but can also promote γ-H2AX spreading around the RE region.

Indexed as

Cell Cycle ProteinsEnhancer Elements, GeneticForkhead Transcription FactorsGenes, Mating Type, FungalRecombination, GeneticSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsBacterial ProteinsCell Cycle CheckpointsChromatinDNA Breaks, Double-StrandedGene Expression Regulation, FungalHistonesIntracellular Signaling Peptides and ProteinsLexA Repressor ProteinPhosphorylationBacterial ProteinsCell Cycle ProteinsChromatinFkh1 protein, S cerevisiaeForkhead Transcription FactorsHistonesIntracellular Signaling Peptides and ProteinsLexA Repressor ProteinMEC1 protein, S cerevisiaePhosphothreonineProtein Serine-Threonine KinasesSaccharomyces cerevisiae ProteinsSerine EndopeptidasesTEL1 protein, S cerevisiae

Identifiers

PMID22496671
PMCPMC3320585
OpenAlexW2066837662

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.