Evidence map›Paper›PMID 42226097›Full record

ArticleBMC ecology and evolution2026

Non-additive transcriptional regulation underpins an additive survival trait in populations of Drosophila selected for increased post infection survival.

Tsering Choton, Nidhi Krishna Shrivastava, Harisankar Durga, Aindrila Das, Nagaraj Guru Prasad

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Article in BMC ecology and evolution, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Tsering ChotonDepartment of Biological Sciences, Indian Institute of Science Education and Research (IISER) Mohali, Sector 81, SAS Nagar, Mohali, Punjab, 140306, India.
Nidhi Krishna ShrivastavaDepartment of Biological Sciences, Indian Institute of Science Education and Research (IISER) Mohali, Sector 81, SAS Nagar, Mohali, Punjab, 140306, India.
Harisankar DurgaDepartment of Biological Sciences, Indian Institute of Science Education and Research (IISER) Mohali, Sector 81, SAS Nagar, Mohali, Punjab, 140306, India.
Aindrila DasDepartment of Biological Sciences, Indian Institute of Science Education and Research (IISER) Mohali, Sector 81, SAS Nagar, Mohali, Punjab, 140306, India.
Nagaraj Guru PrasadDepartment of Biological Sciences, Indian Institute of Science Education and Research (IISER) Mohali, Sector 81, SAS Nagar, Mohali, Punjab, 140306, India. prasad@iisermohali.ac.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUnderstanding how immunity evolves requires integrating organismal resistance with the underlying genetic and regulatory mechanisms. However, evolutionary gains in survival may arise from distinct genetic architectures and sex-specific regulatory strategies. Bridging this gap requires integrating phenotypic measures of resistance with mechanistic insights into gene regulation and immune deployment, allowing evolutionary responses to be interpreted in terms of their underlying biological processes. Using Drosophila melanogaster populations experimentally selected for increased survival post infection with Enterococcus faecalis, we dissected the quantitative genetic basis of post-infection survival and the transcriptional architecture associated with it.

resultsF1 hybrid analyses revealed an additive genetic basis for survivorship in both sexes, consistent with a polygenic response to selection. In contrast, gene expression showed extensive sex-specific regulation and hybrid misexpression. Males strongly upregulated antimicrobial peptides yet suffered greater mortality, suggesting a costly or inefficient immune strategy. Females relied on distinct effector pathways and exhibited superior survivorship. Notably, transcriptional induction of the melanization precursor PPO1 did not correspond to increased phenoloxidase enzyme activity, revealing a post-transcriptional constraint on immune deployment.

conclusionTogether, these results show that while the genetic basis of survivorship is additive, the evolved immune phenotype is shaped by sex-specific regulatory divergence, hybrid incompatibilities, and functional bottlenecks. This emphasizes the need to integrate quantitative genetic, transcriptomic, and functional assays to understand the evolution of immune defense.

Indexed as

Drosophila melanogasterGene Expression RegulationAnimalsAntimicrobial PeptidesEnterococcus faecalisFemaleMaleSelection, GeneticAntimicrobial PeptidesDrosophila melanogasterExperimental evolutionHybrid mis-regulationImmune responsePolygenic adaptationSex-specific regulation

Identifiers

PMID42226097
PMCPMC13449500

What Socratic holds

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LicenceCC BY-NC-ND
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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.