Evidence map›Paper›PMID 26889705›Full record

ArticleNucleus (Austin, Tex.)2016

Priming for tolerance and cohesion at replication forks.

Dana Branzei, Barnabas Szakal

Open access · goldAbstract read
In one paragraph

Article in Nucleus (Austin, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. 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.

Dana Branzeia IFOM, the FIRC Institute of Molecular Oncology , Milan , Italy.
Barnabas Szakala IFOM, the FIRC Institute of Molecular Oncology , Milan , Italy.
FIRC Institute of Molecular Oncology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome duplication is coupled with DNA damage tolerance (DDT) and chromatin structural changes. Recently we reported that mutations in Primase subunits or factors that bridge Polα/Primase with the replicative helicase, Ctf4, caused abnormal usage of DDT pathways, negatively influenced sister chromatid cohesion (SCC), and associated with increased fork reversal. (1) We also found that cohesin, which is paradigmatic for SCC, facilitates recombination-mediated DDT. However, only the recombination defects of cohesin, but not of cohesion-defective Polα/Primase/Ctf4 mutants, were rescued by artificial tethering of sister chromatids. Genetic tests and electron microscopy analysis of replication intermediates made us propose that management of single-stranded DNA forming proximal to the fork is a critical determinant of chromosome and replication fork structure, and influences DDT pathway choice. Here we discuss the implications of our findings for understanding DDT regulation and cohesion establishment during replication, and outline directions to rationalize the relationship between these chromosome metabolism processes.

Indexed as

DNA-Binding ProteinsDNA, FungalDNA Polymerase IDNA PrimaseDNA ReplicationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCTF4 protein, S cerevisiaeDNA-Binding ProteinsDNA, FungalDNA Polymerase IDNA PrimaseSaccharomyces cerevisiae ProteinsChromosome replicationDNA damage tolerancefork reversal recombinationreprimingsister chromatid cohesion

Identifiers

PMID26889705
PMCPMC4916891
OpenAlexW2327962154

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.