Evidence map›Paper›PMID 21951709›Full record

ArticleBMC microbiology2011

The role of Candida albicans homologous recombination factors Rad54 and Rdh54 in DNA damage sensitivity.

Samantha J Hoot, Xiuzhong Zheng, Catherine J Potenski, Theodore C White, Hannah L Klein

Open access · goldAbstract read
In one paragraph

Article in BMC microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. DNA damage checkpoint and repair: From the budding yeastComputational and structural biotechnology journal · 2021
    Review
  4. Article
  5. Review
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.

Samantha J HootDepartment of Biochemistry, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.
Xiuzhong Zheng
Catherine J Potenski
Theodore C White
Hannah L Klein
New York University · USUniversity of Missouri–Kansas City · US

Funding

INFECTIOUS DISEASES &BASIC MICROBIOLOGICAL MECHANISMST32AI007180 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WEISER, JEFFREY NEAL · 1985 to 2022
$8.9M
DNA HELICASES IN RECOMBINATION AND REPAIRR01GM053738 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI KLEIN, HANNAH L. · 1997 to 2010
$2.4M
AIDS Related Oral Candidiasis: Drugs, Sterols, and Fungal CellsR01DE017078 · NIDCR · SEATTLE BIOMEDICAL RESEARCH INSTITUTE · PI WHITE, THEODORE C. · 2006 to 2010
$2.1M
NIAID NIH HHS T32AI007180NIDCR NIH HHS DE17078NIGMS NIH HHS GM53738NIGMS NIH HHS R01 GM053738
6 · The paper itself

Abstract

backgroundThe fungal pathogen Candida albicans is frequently seen in immune suppressed patients, and resistance to one of the most widely used antifungals, fluconazole (FLC), can evolve rapidly. In recent years it has become clear that plasticity of the Candida albicans genome contributes to drug resistance through loss of heterozygosity (LOH) at resistance genes and gross chromosomal rearrangements that amplify gene copy number of resistance associated genes. This study addresses the role of the homologous recombination factors Rad54 and Rdh54 in cell growth, DNA damage and FLC resistance in Candida albicans.

resultsThe data presented here support a role for homologous recombination in cell growth and DNA damage sensitivity, as Candida albicans rad54Δ/rad54Δ mutants were hypersensitive to MMS and menadione, and had an aberrant cell and nuclear morphology. The Candida albicans rad54Δ/rad54Δ mutant was defective in invasion of Spider agar, presumably due to the altered cellular morphology. In contrast, mutation of the related gene RDH54 did not contribute significantly to DNA damage resistance and cell growth, and deletion of either Candida albicans RAD54 or Candida albicans RDH54 did not alter FLC susceptibility.

conclusionsTogether, these results support a role for homologous recombination in genome stability under nondamaging conditions. The nuclear morphology defects in the rad54Δ/rad54Δ mutants show that Rad54 performs an essential role during mitotic growth and that in its absence, cells arrest in G2. The viability of the single mutant rad54Δ/rad54Δ and the inability to construct the double mutant rad54Δ/rad54Δ rdh54Δ/rdh54Δ suggests that Rdh54 can partially compensate for Rad54 during mitotic growth.

Indexed as

DNA DamageAntifungal AgentsCandida albicansDNA HelicasesDNA RepairFungal ProteinsHomologous RecombinationMethyl MethanesulfonateMutagensAntifungal AgentsDNA HelicasesFungal ProteinsMethyl MethanesulfonateMutagens

Identifiers

PMID21951709
PMCPMC3197502
OpenAlexW2167285496

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.