Evidence map›Paper›PMID 27845384›Full record

ArticleScientific reports2016

Mutation tendency of mutator Plasmodium berghei with proofreading-deficient DNA polymerase δ.

Hajime Honma, Mamoru Niikura, Fumie Kobayashi, Toshihiro Horii, Toshihiro Mita, Hiroyoshi Endo, Makoto Hirai

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Microbiology spectrum · 2025
    Article
  3. Deletion of theAntimicrobial agents and chemotherapy · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Proteome size reduction in Apicomplexans is linked with loss of DNA repair and host redundant pathways.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2021
    Article
  11. ApiAP2 Transcription Factors in Apicomplexan Parasites.Pathogens (Basel, Switzerland) · 2019
    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

7 authors.

Hajime HonmaDepartment of International Affairs and Tropical Medicine, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku, Tokyo, Japan.
Mamoru NiikuraDepartment of Infectious Diseases, Kyorin University School of Medicine, 20-2, Shinkawa 6, Mitaka City, Tokyo, Japan.
Fumie KobayashiDepartment of Infectious Diseases, Kyorin University School of Medicine, 20-2, Shinkawa 6, Mitaka City, Tokyo, Japan.
Toshihiro HoriiDepartment of Molecular Protozoology, Research Institute for Microbial Diseases, Osaka University, 3-1 Suita, Osaka, Japan.
Toshihiro MitaDepartment of Molecular and Cellular Parasitology, Juntendo University, 2-1-1 Hongo, Bunkyo, Tokyo, Japan.
Hiroyoshi EndoDepartment of International Affairs and Tropical Medicine, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku, Tokyo, Japan.
Makoto HiraiDepartment of Molecular and Cellular Parasitology, Juntendo University, 2-1-1 Hongo, Bunkyo, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we investigated the mutation tendency of a mutator rodent malaria parasite, Plasmodium berghei, with proofreading-deficient DNA polymerase δ. Wild-type and mutator parasites were maintained in mice for over 24 weeks, and the genome-wide accumulated mutations were determined by high-throughput sequencing. The mutator P. berghei had a significant preference for C/G to A/T substitutions; thus, its genome had a trend towards a higher AT content. The mutation rate was influenced by the sequence context, and mutations were markedly elevated at TCT. Some genes mutated repeatedly in replicate passage lines. In particular, knockout mutations of the AP2-G gene were frequent, which conferred strong growth advantages on parasites during the blood stage but at the cost of losing the ability to form gametocytes. This is the first report to demonstrate a biased mutation tendency in malaria parasites, and its results help to promote our basic understanding of Plasmodium genetics.

Indexed as

AnimalsDiscriminant AnalysisDNA Polymerase IIIDNA, ProtozoanErythrocytesHigh-Throughput Nucleotide SequencingMiceMutationPlasmodium bergheiProtozoan ProteinsSequence Analysis, DNADNA Polymerase IIIDNA, ProtozoanProtozoan Proteins

Identifiers

PMID27845384
PMCPMC5109483

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Registered trials

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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.