Evidence map›Paper›PMID 14595109›Full record

ArticleMolecular biology of the cell2004

Mek1 kinase activity functions downstream of RED1 in the regulation of meiotic double strand break repair in budding yeast.

Lihong Wan, Teresa de los Santos, Chao Zhang, Kevan Shokat, Nancy M Hollingsworth

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

83 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
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  4. bioRxiv : the preprint server for biology · 2026
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  14. Review
  15. Derived alleles of two axis proteins affect meiotic traits in autotetraploidProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

23 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Lihong WanInstitute for Cell and Developmental Biology, Department of Biochemistry and Cell Biology, SUNY Stony Brook, Stony Brook, New York 11794-5215, USA.
Teresa de los Santos
Chao Zhang
Kevan Shokat
Nancy M Hollingsworth
Stony Brook University · USUniversity of California, San Francisco · US

Funding

ANALYSIS OF MEIOTIC CHROMOSOME SYNAPSIS IN YEASTR01GM050717 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI HOLLINGSWORTH, NANCY M. · 1995 to 2020
$8.0M
SPECIFIC INHIBITOR OF LCK TO PROBE T CELL SIGNALINGR01AI044009 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHOKAT, KEVAN M. · 1998 to 2006
$2.1M
NIAID NIH HHS AI44009NIAID NIH HHS R01 AI044009NIGMS NIH HHS GM-50717NIGMS NIH HHS R01 GM050717
6 · The paper itself

Abstract

Three meiosis-specific chromosomal components in budding yeast, Mek1, Red1, and Hop1, are required for recombination, proper segregation of homologs, and the meiotic recombination checkpoint. Mek1 is a protein kinase. Mutations that increase the size of the ATP binding pocket of Mek1 (mek1-as1) sensitize the kinase to specific small molecule inhibitors. Experiments using mek1-as1 demonstrate that the requirement for Mek1 kinase activity coincides with the formation of double strand breaks (DSBs) and that this activity is necessary after DSB formation to prevent repair by DMC1-independent pathways. Contrary to previous reports, Red1 is not a substrate for Mek1. Instead, RED1 is required for wild-type levels of Mek1 kinase activity. In addition, activation of Mek1 requires HOP1, the formation of Red1/Hop1 complexes and a functional Mek1 FHA domain. The requirement for RED1 to produce active kinase can be bypassed by a mek1 mutation that creates a constitutively active Mek1 kinase. We propose that Red1 is phosphorylated by a kinase other than MEK1 and that phosphothreonines on Red1 then interact with the Mek1 FHA domain to recruit the kinase to sites of DSBs where Mek1 is activated to prevent DMC1-independent DSB repair.

Indexed as

MAP Kinase Kinase 1Adenosine TriphosphateCell Cycle ProteinsDNA-Binding ProteinsDNA DamageEnzyme ActivationEnzyme InhibitorsMeiosisMitogen-Activated Protein Kinase KinasesModels, MolecularMutationPhosphorylationProtein BindingProtein Structure, TertiaryRecombination, GeneticSaccharomyces cerevisiaeAdenosine TriphosphateCell Cycle ProteinsDMC1 protein, S cerevisiaeDNA-Binding ProteinsEnzyme InhibitorsHOP1 protein, S cerevisiaeMAP Kinase Kinase 1Mek1 protein, S pombeMitogen-Activated Protein Kinase KinasesRED1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSchizosaccharomyces pombe Proteins

Identifiers

PMID14595109
PMCPMC307523
OpenAlexW2101380023

What OpenQuestion holds

Textmetadata
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.