Evidence map›Paper›PMID 8744945›Full record

ArticleMolecular biology of the cell1996

Distinct roles of yeast MEC and RAD checkpoint genes in transcriptional induction after DNA damage and implications for function.

G L Kiser, T A Weinert

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

2 authors at 1 institution in 1 country.

G L KiserMolecular and Cellular Biology Department, University of Arizona, Tucson 85721, USA.
T A Weinert
University of Arizona · US

Funding

GENETIC CONTROL OF CELL CYCLE ARREST AFTER DNA DAMAGER01GM045276 · NIGMS · UNIVERSITY OF ARIZONA · PI WEINERT, TED A. · 1991 to 2000
$219k
NIGMS NIH HHS R01-GM45276-05
6 · The paper itself

Abstract

In eukaryotic cells, checkpoint genes cause arrest of cell division when DNA is damaged or when DNA replication is blocked. In this study of budding yeast checkpoint genes, we identify and characterize another role for these checkpoint genes after DNA damage-transcriptional induction of genes. We found that three checkpoint genes (of six genes tested) have strong and distinct roles in transcriptional induction in four distinct pathways of regulation (each defined by induction of specific genes). MEC1 mediates the response in three transcriptional pathways, RAD53 mediates two of these pathways, and RAD17 mediates but a single pathway. The three other checkpoint genes (including RAD9) have small (twofold) but significant roles in transcriptional induction in all pathways. One of the pathways that we identify here leads to induction of MEC1 and RAD53 checkpoint genes themselves. This suggests a positive feedback circuit that may increase the cell's ability to respond to DNA damage. We make two primary conclusions from these studies. First, MEC1 appears to be the key regulator because it is required for all responses (both transcriptional and cell cycle arrest), while other genes serve only a subset of these responses. Second, the two types of responses, transcriptional induction and cell cycle arrest, appear distinct because both require MEC1 yet only cell cycle arrest requires RAD9. These and other results were used to formulate a working model of checkpoint gene function that accounts for roles of different checkpoint genes in different responses and after different types of damage. The conclusion that the yeast MEC1 gene is a key regulator also has implications for the role of a putative human homologue, the ATM gene.

Indexed as

Cell Cycle ProteinsDNA DamageGene Expression RegulationGenes, FungalProtein Serine-Threonine KinasesSaccharomyces cerevisiae ProteinsCDC28 Protein Kinase, S cerevisiaeCell CycleCheckpoint Kinase 2DNA-Binding ProteinsFeedbackFungal ProteinsGene DeletionGenes, cdcIntracellular Signaling Peptides and ProteinsModels, GeneticCDC28 Protein Kinase, S cerevisiaeCell Cycle ProteinsCheckpoint Kinase 2DNA-Binding ProteinsFungal ProteinsIntracellular Signaling Peptides and ProteinsMEC1 protein, S cerevisiaeNuclear ProteinsProtein KinasesProtein Serine-Threonine KinasesRAD17 protein, S cerevisiaeRAD53 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID8744945
PMCPMC275924
OpenAlexW2071037207

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.