Evidence map›Paper›PMID 32571205›Full record

ArticleBMC genomics2020

Replication origin location might contribute to genetic variability in Trypanosoma cruzi.

Christiane Bezerra de Araujo, Julia Pinheiro Chagas da Cunha, Davi Toshio Inada, Jeziel Damasceno, Alex Ranieri Jerônimo Lima, Priscila Hiraiwa, Catarina Marques, Evonnildo Gonçalves, Milton Yutaka Nishiyama-Junior, Richard McCulloch and 1 more

Abstract read
In one paragraph

Article in BMC genomics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Pathogens (Basel, Switzerland) · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. The ElusivePathogens (Basel, Switzerland) · 2023
    Review
  8. An induced population ofFrontiers in cellular and infection microbiology · 2022
    Article
  9. Article
  10. Article
  11. Genes · 2020
    Review
  12. 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

11 authors.

Christiane Bezerra de AraujoLaboratório de Ciclo Celular, Instituto Butantan, São Paulo, Brazil.
Julia Pinheiro Chagas da CunhaLaboratório de Ciclo Celular, Instituto Butantan, São Paulo, Brazil. julia.cunha@butantan.gov.br.
Davi Toshio InadaLaboratório de Ciclo Celular, Instituto Butantan, São Paulo, Brazil.
Jeziel DamascenoThe Wellcome Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Alex Ranieri Jerônimo LimaLaboratório de Tecnologia Biomolecular - Bioinformática, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, Brazil.
Priscila HiraiwaFundação Oswaldo Cruz, Instituto Carlos Chagas, Paraná, Brazil.
Catarina MarquesThe Wellcome Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Evonnildo GonçalvesLaboratório de Tecnologia Biomolecular - Bioinformática, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, Brazil.
Milton Yutaka Nishiyama-JuniorCenter of Toxins, Immune Response and Cell Signaling (CeTICS), Instituto Butantan, São Paulo, Brazil.
Richard McCullochThe Wellcome Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Maria Carolina EliasLaboratório de Ciclo Celular, Instituto Butantan, São Paulo, Brazil. carolina.eliassabbaga@butantan.gov.br.ORCID http://orcid.org/0000-0002-0501-8280

Funding

BBSRC BB/N016165/1Fundação de Amparo à Pesquisa do Estado de São Paulo 2013/07467-1Fundação de Amparo à Pesquisa do Estado de São Paulo 2014/13375-5Fundação de Amparo à Pesquisa do Estado de São Paulo 2016/50050-2Fundação de Amparo à Pesquisa do Estado de São Paulo 2017/10853-1Fundação para a Ciência e Tecnologia SFRH/BD/68784/2010Marie Curie fellowship 750259, RECREPEMLEMedical Research Council G0401553National Council for Scientific and Technological Development (CNPq) 304329/2015-0Wellcome Trust 083485Wellcome Trust 104111
6 · The paper itself

Abstract

backgroundDNA replication in trypanosomatids operates in a uniquely challenging environment, since most of their genomes are constitutively transcribed. Trypanosoma cruzi, the etiological agent of Chagas disease, presents high variability in both chromosomes size and copy number among strains, though the underlying mechanisms are unknown.

resultsHere we have mapped sites of DNA replication initiation across the T. cruzi genome using Marker Frequency Analysis, which has previously only been deployed in two related trypanosomatids. The putative origins identified in T. cruzi show a notable enrichment of GC content, a preferential position at subtelomeric regions, coinciding with genes transcribed towards the telomeres, and a pronounced enrichment within coding DNA sequences, most notably in genes from the Dispersed Gene Family 1 (DGF-1).

conclusionsThese findings suggest a scenario where collisions between DNA replication and transcription are frequent, leading to increased genetic variability, as seen by the increase SNP levels at chromosome subtelomeres and in DGF-1 genes containing putative origins.

Indexed as

Polymorphism, Single NucleotideReplication OriginAnimalsBase CompositionDNA, ProtozoanDNA ReplicationHigh-Throughput Nucleotide SequencingTriatomaTrypanosoma cruziWhole Genome SequencingDNA, ProtozoanDGF-1Genetic variabilityReplication originsTrypanosoma cruzi

Identifiers

PMID32571205
PMCPMC7310030

What Socratic 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 Socratic graph.