Evidence map›Paper›PMID 19805819›Full record

ArticleGenetics2009

Centromere replication timing determines different forms of genomic instability in Saccharomyces cerevisiae checkpoint mutants during replication stress.

Wenyi Feng, Jeff Bachant, David Collingwood, M K Raghuraman, Bonita J Brewer

Open access · greenAbstract read
In one paragraph

Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

33 citing papers in PubMed, 41 citations in OpenAlex.

  1. The yeast Dbf4 ZnCurrent genetics · 2022
    Article
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  6. The regulation of chromosome segregation via centromere loops.Critical reviews in biochemistry and molecular biology · 2019
    Review
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  8. Article
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  11. Article
  12. Review
  13. Article
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  15. Article
  16. Article
  17. Article
  18. Analysis of replication timing using synchronized budding yeast cultures.Methods in molecular biology (Clifton, N.J.) · 2014
    Article
  19. The CINs of the centromere.Biochemical Society transactions · 2013
    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

5 authors at 2 institutions in 1 country.

Wenyi FengDepartment of Genome Sciences, University of Washington, Box 355065 Foege Bldg., Room S041, 1705 NE Pacific St., Seattle, Washington 98195, USA.
Jeff Bachant
David Collingwood
M K Raghuraman
Bonita J Brewer
University of California, Riverside · USUniversity of Washington · US

Funding

Single Stranded DNA: The Genome's Achilles HeelK99GM081378 · NIGMS · UNIVERSITY OF WASHINGTON · PI FENG, WENYI · 2007 to 2009
$248k
NIGMS NIH HHS 1K99GM081378-01NIGMS NIH HHS K99 GM081378PHS HHS 18926
6 · The paper itself

Abstract

Yeast replication checkpoint mutants lose viability following transient exposure to hydroxyurea, a replication-impeding drug. In an effort to understand the basis for this lethality, we discovered that different events are responsible for inviability in checkpoint-deficient cells harboring mutations in the mec1 and rad53 genes. By monitoring genomewide replication dynamics of cells exposed to hydroxyurea, we show that cells with a checkpoint deficient allele of RAD53, rad53K227A, fail to duplicate centromeres. Following removal of the drug, however, rad53K227A cells recover substantial DNA replication, including replication through centromeres. Despite this recovery, the rad53K227A mutant fails to achieve biorientation of sister centromeres during recovery from hydroxyurea, leading to secondary activation of the spindle assembly checkpoint (SAC), aneuploidy, and lethal chromosome segregation errors. We demonstrate that cell lethality from this segregation defect could be partially remedied by reinforcing bipolar attachment. In contrast, cells with the mec1-1 sml1-1 mutations suffer from severely impaired replication resumption upon removal of hydroxyurea. mec1-1 sml1-1 cells can, however, duplicate at least some of their centromeres and achieve bipolar attachment, leading to abortive segregation and fragmentation of incompletely replicated chromosomes. Our results highlight the importance of replicating yeast centromeres early and reveal different mechanisms of cell death due to differences in replication fork progression.

Indexed as

DNA ReplicationGenomic InstabilityMutationAllelesCell Cycle ProteinsCell SurvivalCentromereCheckpoint Kinase 2Chromosome BreakageChromosome SegregationChromosomes, FungalDNA, FungalDNA, Single-StrandedHydroxyureaIntracellular Signaling Peptides and ProteinsPhenotypeCell Cycle ProteinsCheckpoint Kinase 2DNA, FungalDNA, Single-StrandedHydroxyureaIntracellular Signaling Peptides and ProteinsMEC1 protein, S cerevisiaeProtein Serine-Threonine KinasesRAD53 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSML1 protein, S cerevisiae

Identifiers

PMID19805819
PMCPMC2787418
OpenAlexW2110904385

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.