Evidence map›Paper›PMID 28190728›Full record

ArticleCurrent biology : CB2017

Juvenile Hormone Suppresses Resistance to Infection in Mated Female Drosophila melanogaster.

Robin A Schwenke, Brian P Lazzaro

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
19.4field-weighted citation impact, top 1% 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

59 citing papers in PubMed, 161 citations in OpenAlex.

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  16. Decoupled evolution of theProceedings of the National Academy of Sciences of the United States of America · 2024
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  17. Decoupled evolution of thebioRxiv : the preprint server for biology · 2023
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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

2 authors at 1 institution in 1 country.

Robin A SchwenkeField of Genetics, Genomics, and Development, Cornell University, Ithaca, NY 14853, USA; Department of Entomology, Cornell University, Ithaca, NY 14853, USA; Cornell Institute of Host-Microbe Interactions and Disease, Cornell University, Ithaca, NY 14853, USA. Electronic address: ras599@cornell.edu.
Brian P LazzaroField of Genetics, Genomics, and Development, Cornell University, Ithaca, NY 14853, USA; Department of Entomology, Cornell University, Ithaca, NY 14853, USA; Cornell Institute of Host-Microbe Interactions and Disease, Cornell University, Ithaca, NY 14853, USA. Electronic address: bplazzaro@cornell.edu.
Cornell University · US

Funding

Genetic Network Linking Immunity to Energetic Stress, Metabolism and ReproductionR01AI083932 · NIAID · CORNELL UNIVERSITY · PI LAZZARO, BRIAN · 2009 to 2015
$2.6M
NIAID NIH HHS R01 AI083932
6 · The paper itself

Abstract

Hormonal signaling provides metazoans with the ability to regulate development, growth, metabolism, immune defense, and reproduction in response to internal and external stimuli. The use of hormones as central regulators of physiology makes them prime candidates for mediating allocation of resources to competing biological functions (i.e., hormonal pleiotropy) [1]. In animals, reproductive effort often results in weaker immune responses (e.g., [2-4]), and this reduction is sometimes linked to hormone signaling (see [5-7]). In the fruit fly, Drosophila melanogaster, mating and the receipt of male seminal fluid proteins results in reduced resistance to a systemic bacterial infection [8, 9]. Here, we evaluate whether the immunosuppressive effect of reproduction in female D. melanogaster is attributable to the endocrine signal juvenile hormone (JH), which promotes the development of oocytes and the synthesis and deposition of yolk protein [10, 11]. Previous work has implicated JH as immunosuppressive [12, 13], and the male seminal fluid protein Sex Peptide (SP) activates JH biosynthesis in female D. melanogaster after mating [14]. We find that transfer of SP activates synthesis of JH in the mated female, which in turn suppresses resistance to infection through the receptor germ cell expressed (gce). We find that mated females are more likely to die from infection, suffer higher pathogen burdens, and are less able to induce their immune responses. All of these deficiencies are rescued when JH signaling is blocked. We argue that hormonal signaling is important for regulating immune system activity and, more generally, for governing trade-offs between physiological processes.

Indexed as

Sexual Behavior, AnimalAnimalsDrosophila melanogasterDrosophila ProteinsFemaleImmune ToleranceIntercellular Signaling Peptides and ProteinsJuvenile HormonesPeptidesReproductionDrosophila ProteinsIntercellular Signaling Peptides and ProteinsJuvenile HormonesPeptidesSP protein, Drosophilaendocrineevolutionhormoneimmune defenseinsect immunitymatingprovidenciareproductiontrade-offtradeoff

Identifiers

PMID28190728
PMCPMC5319889
OpenAlexW2587406614

What OpenQuestion holds

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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 OpenQuestion graph.