Evidence map›Paper›PMID 22038252›Full record

ArticleGenome research2011

Chromosome and gene copy number variation allow major structural change between species and strains of Leishmania.

Matthew B Rogers, James D Hilley, Nicholas J Dickens, Jon Wilkes, Paul A Bates, Daniel P Depledge, David Harris, Yerim Her, Pawel Herzyk, Hideo Imamura and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Genome research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 268 papers.

0numbers the graph read from it
0cells of the map it votes in
268citing 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

268 citing papers in PubMed, 454 citations in OpenAlex.

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  13. Unraveling the Genome Diversity ofLife (Basel, Switzerland) · 2025
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208 more citing papers are in PubMed but not listed here.

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

18 authors at 6 institutions in 2 countries.

Matthew B RogersWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge CB10 1SA, United Kingdom.
James D Hilley
Nicholas J Dickens
Jon Wilkes
Paul A Bates
Daniel P Depledge
David Harris
Yerim Her
Pawel Herzyk
Hideo Imamura
Thomas D Otto
Mandy Sanders
Kathy Seeger
Jean-Claude Dujardin
Matthew Berriman
Deborah F Smith
Christiane Hertz-Fowler
Jeremy C Mottram
Wellcome Sanger Institute · GBWellcome Centre for Molecular Parasitology · GBUniversity of York · GBLancaster University · GBUniversity of Antwerp · BEUniversity of Glasgow · GB

Funding

Wellcome TrustWellcome Trust 076355Wellcome Trust 085775Wellcome Trust 085822
6 · The paper itself

Abstract

Leishmania parasites cause a spectrum of clinical pathology in humans ranging from disfiguring cutaneous lesions to fatal visceral leishmaniasis. We have generated a reference genome for Leishmania mexicana and refined the reference genomes for Leishmania major, Leishmania infantum, and Leishmania braziliensis. This has allowed the identification of a remarkably low number of genes or paralog groups (2, 14, 19, and 67, respectively) unique to one species. These were found to be conserved in additional isolates of the same species. We have predicted allelic variation and find that in these isolates, L. major and L. infantum have a surprisingly low number of predicted heterozygous SNPs compared with L. braziliensis and L. mexicana. We used short read coverage to infer ploidy and gene copy numbers, identifying large copy number variations between species, with 200 tandem gene arrays in L. major and 132 in L. mexicana. Chromosome copy number also varied significantly between species, with nine supernumerary chromosomes in L. infantum, four in L. mexicana, two in L. braziliensis, and one in L. major. A significant bias against gene arrays on supernumerary chromosomes was shown to exist, indicating that duplication events occur more frequently on disomic chromosomes. Taken together, our data demonstrate that there is little variation in unique gene content across Leishmania species, but large-scale genetic heterogeneity can result through gene amplification on disomic chromosomes and variation in chromosome number. Increased gene copy number due to chromosome amplification may contribute to alterations in gene expression in response to environmental conditions in the host, providing a genetic basis for disease tropism.

Indexed as

Polymorphism, Single NucleotideBase SequenceChromosomesGene DosageGene Expression RegulationGenes, ProtozoanLeishmaniaMolecular Sequence DataSpecies Specificity

Identifiers

PMID22038252
PMCPMC3227102
OpenAlexW2171530398

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.