Evidence map›Paper›PMID 35804459›Full record

ArticleParasites & vectors2022

Plasmodium berghei Brca2 is required for normal development and differentiation in mice and mosquitoes.

Yasunaga Yoshikawa, Shunta Kimura, Akira Soga, Makoto Sugiyama, Aki Ueno, Hiroki Kondo, Zida Zhu, Kazuhiko Ochiai, Kazuhiko Nakayama, Jun Hakozaki and 6 more

Abstract read
In one paragraph

Article in Parasites & vectors, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Microorganisms · 2023
    Review
  2. 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

16 authors.

Yasunaga YoshikawaLaboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan. yyoshika@vmas.kitasato-u.ac.jp.ORCID http://orcid.org/0000-0003-4257-3088
Shunta KimuraLaboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Akira SogaNational Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada, Obihiro, 080-8555, Japan.
Makoto SugiyamaLaboratory of Veterinary Anatomy, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Aki UenoLaboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Hiroki KondoLaboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Zida ZhuLaboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Kazuhiko OchiaiLaboratory of Veterinary Hygiene, School of Veterinary Medicine, Nippon Veterinary and Life Science University, Musashino, Tokyo, 180-8602, Japan.
Kazuhiko NakayamaLaboratory of Veterinary Parasitology, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Jun HakozakiLaboratory of Veterinary Parasitology, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Kodai KusakisakoLaboratory of Veterinary Parasitology, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Asako HaraguchiLaboratory of Veterinary Parasitology, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Taisuke KitanoLaboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Koichi OrinoLaboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.
Shinya FukumotoNational Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada, Obihiro, 080-8555, Japan.
Hiromi IkadaiLaboratory of Veterinary Parasitology, School of Veterinary Medicine, Kitasato University, Towada, Aomori, 034-8628, Japan.

Funding

Resource for Biocomputing Visualization and InformaticsP41GM103311 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FERRIN, THOMAS E · 2012 to 2017
$8.2M
Japan Society for the Promotion of Science 17H04073Japan Society for the Promotion of Science 20K06417National Research Center for Protozoan Diseases of Obihiro University of Agriculture and Veterinary Medicine 2020-joint-15National Research Center for Protozoan Diseases of Obihiro University of Agriculture and Veterinary Medicine 2021-joint-14NIGMS NIH HHS P41 GM103311
6 · The paper itself

Abstract

backgroundMalaria is a major global parasitic disease caused by species of the genus Plasmodium. Zygotes of Plasmodium spp. undergo meiosis and develop into tetraploid ookinetes, which differentiate into oocysts that undergo sporogony. Homologous recombination (HR) occurs during meiosis and introduces genetic variation. However, the mechanisms of HR in Plasmodium are unclear. In humans, the recombinases DNA repair protein Rad51 homolog 1 (Rad51) and DNA meiotic recombinase 1 (Dmc1) are required for HR and are regulated by breast cancer susceptibility protein 2 (BRCA2). Most eukaryotes harbor BRCA2 homologs. Nevertheless, these have not been reported for Plasmodium.

methodsA Brca2 candidate was salvaged from a database to identify Brca2 homologs in Plasmodium. To confirm that the candidate protein was Brca2, interaction activity between Plasmodium berghei (Pb) Brca2 (PbBrca2) and Rad51 (PbRad51) was investigated using a mammalian two-hybrid assay. To elucidate the functions of PbBrca2, PbBrca2 was knocked out and parasite proliferation and differentiation were assessed in mice and mosquitoes. Transmission electron microscopy was used to identify sporogony.

resultsThe candidate protein was conserved among Plasmodium species, and it was indicated that it harbors critical BRCA2 domains including BRC repeats, tower, and oligonucleotide/oligosaccharide-binding-fold domains. The P. berghei BRC repeats interacted with PbRad51. Hence, the candidate was considered a Brca2 homolog. PbBrca2 knockout parasites were associated with reduced parasitemia with increased ring stage and decreased trophozoite stage counts, gametocytemia, female gametocyte ratio, oocyst number, and ookinete development in both mice and mosquitoes. Nevertheless, the morphology of the blood stages in mice and the ookinete stage was comparable to those of the wild type parasites. Transmission electron microscopy results showed that sporogony never progressed in Brca2-knockout parasites.

conclusionsBrca2 is implicated in nearly all Plasmodium life cycle stages, and especially in sporogony. PbBrca2 contributes to HR during meiosis.

Indexed as

CulicidaeMalariaParasitesAnimalsFemaleHomologous RecombinationLife Cycle StagesMammalsMiceOocystsPlasmodium bergheiBreast cancer susceptibility protein 2DNA repair protein Rad51 homolog 1Homologous recombinationMeiosisPlasmodium

Identifiers

PMID35804459
PMCPMC9270840

What Socratic holds

Textmetadata
LicenceCC BY
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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.