Evidence map›Paper›PMID 27206717›Full record

ArticleGenetics2016

Phenotypic Consequences of a Spontaneous Loss of Heterozygosity in a Common Laboratory Strain of Candida albicans.

Toni Ciudad, Meleah Hickman, Alberto Bellido, Judith Berman, Germán Larriba

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.7field-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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  9. Review
  10. Mechanisms of genome evolution in Candida albicans.Current opinion in microbiology · 2019
    Review
  11. Article
  12. Article
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  15. Diverse Lineages ofGenetics · 2019
    Article
  16. Article
  17. Article
  18. Ploidy dynamics and evolvability in fungi.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016
    Review
  19. 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 3 countries.

Toni CiudadDepartamento de Ciencias Biomédicas, Área Microbiología, Facultad de Ciencias, Universidad de Extremadura, 06006 Badajoz, Spain.ORCID 0000-0002-9303-1628
Meleah HickmanDepartment of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, Minnesota 55455.
Alberto BellidoDepartamento de Ciencias Biomédicas, Área Microbiología, Facultad de Ciencias, Universidad de Extremadura, 06006 Badajoz, Spain.ORCID 0000-0002-9050-8339
Judith BermanDepartment of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, Minnesota 55455 Department of Microbiology and Biotechnology, George S. Wise Faculty of Life Sciences, Tel Aviv University, Ramat Aviv 69978, Israel.ORCID 0000-0002-8577-0084
Germán LarribaDepartamento de Ciencias Biomédicas, Área Microbiología, Facultad de Ciencias, Universidad de Extremadura, 06006 Badajoz, Spain glarriba@unex.es.ORCID 0000-0001-6262-233X
Universidad de Extremadura · ESUniversity of Minnesota · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

By testing the susceptibility to DNA damaging agents of several Candida albicans mutant strains derived from the commonly used laboratory strain, CAI4, we uncovered sensitivity to methyl methanesulfonate (MMS) in CAI4 and its derivatives, but not in CAF2-1. This sensitivity is not a result of URA3 disruption because the phenotype was not restored after URA3 reintroduction. Rather, we found that homozygosis of a short region of chromosome 3R (Chr3R), which is naturally heterozygous in the MMS-resistant-related strains CAF4-2 and CAF2-1, confers MMS sensitivity and modulates growth polarization in response to MMS. Furthermore, induction of homozygosity in this region in CAF2-1 or CAF4-2 resulted in MMS sensitivity. We identified 11 genes by SNP/comparative genomic hybridization containing only the a alleles in all the MMS-sensitive strains. Four candidate genes, SNF5, POL1, orf19.5854.1, and MBP1, were analyzed by generating hemizygous configurations in CAF2-1 and CAF4-2 for each allele of all four genes. Only hemizygous MBP1a/mbp1b::SAT1-FLIP strains became MMS sensitive, indicating that MBP1a in the homo- or hemizygosis state was sufficient to account for the MMS-sensitive phenotype. In yeast, Mbp1 regulates G1/S genes involved in DNA repair. A second region of homozygosis on Chr2L increased MMS sensitivity in CAI4 (Chr3R homozygous) but not CAF4-2 (Chr3R heterozygous). This is the first example of sign epistasis in C. albicans.

Indexed as

Epistasis, GeneticAllelesAntifungal AgentsCandida albicansComparative Genomic HybridizationDNA DamageDNA RepairFungal ProteinsGene Expression Regulation, FungalLoss of HeterozygosityMethyl MethanesulfonatePolymorphism, Single NucleotideAntifungal AgentsFungal ProteinsMethyl MethanesulfonateCandida albicansgrowth polarizationLOHMBP1MMS susceptibility

Identifiers

PMID27206717
PMCPMC4937476
OpenAlexW2403782941

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.