Evidence map›Paper›PMID 27590805›Full record

ArticleBMC genomics2016

Copy number variation contributes to cryptic genetic variation in outbreak lineages of Cryptococcus gattii from the North American Pacific Northwest.

Jacob L Steenwyk, John S Soghigian, John R Perfect, John G Gibbons

Abstract read
In one paragraph

Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Intra-Species Genomic Variation in the Pine PathogenJournal of fungi (Basel, Switzerland) · 2022
    Article
  8. Gene, virulence and related regulatory mechanisms inActa biochimica et biophysica Sinica · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Microevolution in the pansecondary metabolome ofProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors.

Jacob L SteenwykBiology Department, Clark University, 950 Main Street, Worcester, MA, USA.
John S SoghigianBiology Department, Clark University, 950 Main Street, Worcester, MA, USA.
John R PerfectDivision of Infectious Diseases, Department of Medicine, Duke University Medical Center, Durham, NC, USA.
John G GibbonsBiology Department, Clark University, 950 Main Street, Worcester, MA, USA. jgibbons@clarku.edu.

Funding

Pathobiology of C. neoformans in the Central Nervous SystemR01AI073896 · NIAID · DUKE UNIVERSITY · PI PERFECT, JOHN R. · 2008 to 2018
$4.4M
Evolution of Cryptococcus neoformans Strains from Patients with HIV/AIDSR01AI093257 · NIAID · DUKE UNIVERSITY · PI PERFECT, JOHN R. · 2011 to 2022
$3.8M
NIAID NIH HHS R01 AI073896NIAID NIH HHS R01 AI093257
6 · The paper itself

Abstract

backgroundCopy number variants (CNVs) are a class of structural variants (SVs) and are defined as fragments of DNA that are present at variable copy number in comparison with a reference genome. Recent advances in bioinformatics methodologies and sequencing technologies have enabled the high-resolution quantification of genome-wide CNVs. In pathogenic fungi SVs have been shown to alter gene expression, influence host specificity, and drive fungicide resistance, but little attention has focused specifically on CNVs. Using publicly available sequencing data, we identified 90 isolates across 212 Cryptococcus gattii genomes that belong to the VGII subgroups responsible for the recent deadly outbreaks in the North American Pacific Northwest. We generated CNV profiles for each sample to investigate the prevalence and function of CNV in C. gattii.

resultsWe identified eight genetic clusters among publicly available Illumina whole genome sequence data from 212 C. gattii isolates through population structure analysis. Three clusters represent the VGIIa, VGIIb, and VGIIc subgroups from the North American Pacific Northwest. CNV was bioinformatically predicted and affected ~300-400 Kilobases (Kb) of the C. gattii VGII subgroup genomes. Sixty-seven loci, encompassing 58 genes, showed highly divergent patterns of copy number variation between VGII subgroups. Analysis of PFam domains within divergent CN variable genes revealed enrichment of protein domains associated with transport, cell wall organization and external encapsulating structure.

conclusionsCNVs may contribute to pathological and phenotypic differences observed between the C. gattii VGIIa, VGIIb, and VGIIc subpopulations. Genes overlapping with population differentiated CNVs were enriched for several virulence related functional terms. These results uncover novel candidate genes to examine the genetic and functional underpinnings of C. gattii pathogenicity.

Indexed as

DNA Copy Number VariationsGenetic VariationGenome, BacterialComputational BiologyCryptococcosisCryptococcus gattiiDatabases, Nucleic AcidDisease OutbreaksGene OntologyGenetic LociGenomicsHigh-Throughput Nucleotide SequencingHumansNorthwestern United StatesCopy number variationCryptococcus gattiiPathogenPathogenicityPopulation genomics

Identifiers

PMID27590805
PMCPMC5009542

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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.