Evidence map›Paper›PMID 28586288›Full record

ArticleFly2017

Genomic signatures of local adaptation in the Drosophila immune response.

Angela M Early, Andrew G Clark

Abstract read
In one paragraph

Article in Fly, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. 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

2 authors.

Angela M Earlya Department of Molecular Biology and Genetics , Cornell University , Ithaca , NY.
Andrew G Clarka Department of Molecular Biology and Genetics , Cornell University , Ithaca , NY.

Funding

Functional /Comparative Genomic of Drosophila immunityR01AI064950 · NIAID · CORNELL UNIVERSITY ITHACA · PI CLARK, ANDREW G, LAZZARO, BRIAN · 2005 to 2016
$3.7M
NIAID NIH HHS R01 AI064950
6 · The paper itself

Abstract

As environments and pathogen landscapes shift, host defenses must evolve to remain effective. Due to this selection pressure, among-species comparisons of genetic sequence data often find immune genes to be among the fastest evolving genes across the genome. The full extent and nature of these immune adaptations, however, remain largely unexplored. In a recent study, we analyzed patterns of selection within distinct components of the Drosophila melanogaster immune pathway. While we found evidence of positive selection within some immune processes, immune genes were not universally characterized by signatures of strong selection. On the contrary, we even found that some immune functions show greater than expected constraint. Overall these results highlight 2 major factors that appear to play an outsize role in determining a gene's evolutionary rate: the type of pathogen the gene targets and the gene's position within the immune network. These results join a growing body of literature that highlight the complexity of immune adaptation. Rather than there being uniformly strong selection across all immune genes, a combination of pathogen-specificity and host genetic constraints appear to play key roles in determining each immune gene's individual evolutionary trajectory.

Indexed as

Host-Pathogen InteractionsImmunity, InnateAdaptation, PhysiologicalAnimalsDrosophila melanogasterEnvironmentEvolution, MolecularGenomicsSelection, GeneticSignal Transductionevolutionhost-pathogen interactionsinnate immunitylocal adaptationpopulation genetics

Identifiers

PMID28586288
PMCPMC5721942

What OpenQuestion holds

Textmetadata
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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.