Evidence map›Paper›PMID 18989366›Full record

ArticlePloS one2008

Anopheles gambiae APL1 is a family of variable LRR proteins required for Rel1-mediated protection from the malaria parasite, Plasmodium berghei.

Michelle M Riehle, Jiannong Xu, Brian P Lazzaro, Susan M Rottschaefer, Boubacar Coulibaly, Madjou Sacko, Oumou Niare, Isabelle Morlais, Sekou F Traore, Kenneth D Vernick

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

50 citing papers in PubMed, 75 citations in OpenAlex.

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  12. Transcriptional Profile ofInternational journal of molecular sciences · 2019
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  13. TheeLife · 2017
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  17. Review
  18. Antiviral immunity of Anopheles gambiae is highly compartmentalized, with distinct roles for RNA interference and gut microbiota.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  19. 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

10 authors at 4 institutions in 4 countries.

Michelle M RiehleDepartment of Microbiology, University of Minnesota, Saint Paul, Minnesota, USA.
Jiannong Xu
Brian P Lazzaro
Susan M Rottschaefer
Boubacar Coulibaly
Madjou Sacko
Oumou Niare
Isabelle Morlais
Sekou F Traore
Kenneth D Vernick
University of Bamako · MLUniversity of Minnesota · USCornell University · USOrganisation de Coordination pour la lutte contre les Endémies en Afrique Centrale · CM

Funding

Genomics of Mosquito Resistance to PlasmodiumR01AI042361 · NIAID · UNIVERSITY OF MINNESOTA TWIN CITIES · PI VERNICK, KENNETH D · 1998 to 2012
$4.8M
Genetic Association Mapping of Malaria Resistance in Anopheles gambiaeR01AI073685 · NIAID · UNIVERSITY OF MINNESOTA · PI VERNICK, KENNETH D · 2007 to 2011
$2.8M
Evolutionary Genomics of Anti-Malaria Genes in MosquitoR01AI062995 · NIAID · CORNELL UNIVERSITY · PI LAZZARO, BRIAN · 2006 to 2010
$1.8M
NIAID NIH HHS AI042361NIAID NIH HHS AI073685NIAID NIH HHS R01 AI042361NIAID NIH HHS R01 AI062995NIAID NIH HHS R01 AI073685
6 · The paper itself

Abstract

backgroundWe previously identified by genetic mapping an Anopheles gambiae chromosome region with strong influence over the outcome of malaria parasite infection in nature. Candidate gene studies in the genetic interval, including functional tests using the rodent malaria parasite Plasmodium berghei, identified a novel leucine-rich repeat gene, APL1, with functional activity against P. berghei. PRINCIPAL

findingsManual reannotation now reveals APL1 to be a family of at least 3 independently transcribed genes, APL1A, APL1B, and APL1C. Functional dissection indicates that among the three known APL1 family members, APL1C alone is responsible for host defense against P. berghei. APL1C functions within the Rel1-Cactus immune signaling pathway, which regulates APL1C transcript and protein abundance. Gene silencing of APL1C completely abolishes Rel1-mediated host protection against P. berghei, and thus the presence of APL1C is required for this protection. Further highlighting the influence of this chromosome region, allelic haplotypes at the APL1 locus are genetically associated with and have high explanatory power for the success or failure of P. berghei parasite infection.

conclusionsAPL1C functions as a required transducer of Rel1-dependent immune signal(s) to efficiently protect mosquitoes from P. berghei infection, and allelic genetic haplotypes of the APL1 locus display distinct levels of susceptibility and resistance to P. berghei.

Indexed as

AnimalsAnophelesBase SequenceGenes, InsectHaplotypesInsect ProteinsMolecular Sequence DataPlasmodium bergheiTranscription FactorsInsect ProteinsTranscription Factors

Identifiers

PMID18989366
PMCPMC2577063
OpenAlexW2025863286

What OpenQuestion 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 OpenQuestion graph.