Evidence map›Paper›PMID 8858179›Full record

ArticleThe Journal of cell biology1996

A developmental defect in Plasmodium falciparum male gametogenesis.

F Guinet, J A Dvorak, H Fujioka, D B Keister, O Muratova, D C Kaslow, M Aikawa, A B Vaidya, T E Wellems

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1996. 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
4.1field-weighted citation impact, top 6% of its field
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, 57 citations in OpenAlex.

  1. Article
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  4. Antimalarial Natural Products.Progress in the chemistry of organic natural products · 2022
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  6. CRISPR/Cas9 knockouts reveal genetic interaction between strain-transcendent erythrocyte determinants ofProceedings of the National Academy of Sciences of the United States of America · 2017
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  15. Review
  16. Lack of molecular correlates of Plasmodium vivax ookinete development.The American journal of tropical medicine and hygiene · 2011
    Article
  17. Article
  18. Article
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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

9 authors at 1 institution in 1 country.

F GuinetLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0425, USA.
J A Dvorak
H Fujioka
D B Keister
O Muratova
D C Kaslow
M Aikawa
A B Vaidya
T E Wellems
National Institute of Allergy and Infectious Diseases · US

Funding

ORGANELLE GENOMES OF MALARIAL PARASITESR01AI028398 · NIAID · MCP HAHNEMANN UNIVERSITY · PI AKHIL B VAIDYA · 1989 to 2026
$10.1M
THALASSEMIA AND HOST RESISTANCE TO MALARIAU01AI035827 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BRITTENHAM, GARY M · 1994 to 1999
–
NIAID NIH HHS AI-35827NIAID NIH HHS R01 AI028398
6 · The paper itself

Abstract

Asexually replicating populations of Plasmodium parasites, including those from cloned lines, generate both male and female gametes to complete the malaria life cycle through the mosquito. The generation of these sexual forms begins with the induction of gametocytes from haploid asexual stage parasites in the blood of the vertebrate host. The molecular processes that govern the differentiation and development of the sexual forms are largely unknown. Here we describe a defect that affects the development of competent male gametocytes from a mutant clone of P. falciparum (Dd2). Comparison of the Dd2 clone to the predecessor clone from which it was derived (W2'82) shows that the defect is a mutation that arose during the long-term cultivation of asexual stages in vitro. Light and electron microscopic images, and indirect immunofluorescence assays with male-specific anti-alpha-tubulin II antibodies, indicate a global disruption of male development at the gametocyte level with at least a 70-90% reduction in the proportion of mature male gametocytes by the Dd2 clone relative to W2'82. A high prevalence of abnormal gametocyte forms, frequently containing multiple and unusually large vacuoles, is associated with the defect. The reduced production of mature male gametocytes may reflect a problem in processes that commit a gametocyte to male development or a progressive attrition of viable male gametocytes during maturation. The defect is genetically linked to an almost complete absence of male gamete production and of infectivity to mosquitoes. This is the first sex-specific developmental mutation identified and characterized in Plasmodium.

Indexed as

AnimalsAnophelesAntimalarialsDNA FingerprintingFemaleGametogenesisMaleMefloquineMutationPlasmodium falciparumPolymorphism, Restriction Fragment LengthTubulinVacuolesAntimalarialsMefloquineTubulin

Identifiers

PMID8858179
PMCPMC2121010
OpenAlexW2121826111

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.