Evidence map›Paper›PMID 41066235›Full record

ArticleCell reports2025

Histone acetylation modulation by a small molecule inhibitor recapitulates symbiont-induced cytoplasmic incompatibility.

Rupinder Kaur, Mahip Kalra, Madangchanok Imchen, Bailey L Crowley, Angelina McGarry, Leah Carpenter, Seth R Bordenstein

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. International journal of molecular sciences · 2026
    Article
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

7 authors.

Rupinder KaurPennsylvania State University, Departments of Biology and Entomology, University Park, PA, USA; Pennsylvania State University, One Health Microbiome Center, Huck Institutes of the Life Sciences, University Park, PA, USA; Vanderbilt University, Department of Biological Sciences, Nashville, TN, USA. Electronic address: r.kaur@psu.edu.
Mahip KalraVanderbilt University, Department of Biological Sciences, Nashville, TN, USA.
Madangchanok ImchenPennsylvania State University, Departments of Biology and Entomology, University Park, PA, USA; Pennsylvania State University, One Health Microbiome Center, Huck Institutes of the Life Sciences, University Park, PA, USA.
Bailey L CrowleyPennsylvania State University, Departments of Biology and Entomology, University Park, PA, USA; Pennsylvania State University, One Health Microbiome Center, Huck Institutes of the Life Sciences, University Park, PA, USA.
Angelina McGarryPennsylvania State University, Departments of Biology and Entomology, University Park, PA, USA; Pennsylvania State University, One Health Microbiome Center, Huck Institutes of the Life Sciences, University Park, PA, USA.
Leah CarpenterPennsylvania State University, Departments of Biology and Entomology, University Park, PA, USA; Pennsylvania State University, One Health Microbiome Center, Huck Institutes of the Life Sciences, University Park, PA, USA.
Seth R BordensteinPennsylvania State University, Departments of Biology and Entomology, University Park, PA, USA; Pennsylvania State University, One Health Microbiome Center, Huck Institutes of the Life Sciences, University Park, PA, USA; Vanderbilt University, Department of Biological Sciences, Nashville, TN, USA. Electronic address: s.bordenstein@psu.edu.

Funding

The Mechanism of Cytoplasmic IncompatibilityR01AI143725 · NIAID · VANDERBILT UNIVERSITY · PI BORDENSTEIN, SETH R · 2020 to 2024
$2.0M
The Epigenetics of Cytoplasmic IncompatibilityR01AI179743 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI SETH R BORDENSTEIN, Rupinder Kaur · 2024 to 2026
$1.9M
NIAID NIH HHS R01 AI143725NIAID NIH HHS R01 AI179743
6 · The paper itself

Abstract

Symbiotic relationships between arthropod hosts and microorganisms have garnered global attention for their influence on host ecology, evolution, and vector control. A major gap in the field is to mechanistically define and reconstitute symbiotic traits in the absence of microbes. Here, we address this omission by identifying an evolutionarily conserved host mechanism that recapitulates Wolbachia-induced cytoplasmic incompatibility (CI)-a paternal-effect embryonic lethality trait. We first show that Wolbachia alter histone acetylation during sperm development in Drosophila melanogaster. By chemically inhibiting histone acetyltransferase (HAT) activity in aposymbiotic males, we reprogram the chromatin landscape of developing sperm to induce a rescuable CI phenotype. This phenotype is further modulated through transgenic knockdown of HAT and histone deacetylase enzymes, providing tunable control over natural CI intensity. Our findings uncover histone acetylation as a key host-intrinsic pathway, capable of inducing symbiont-independent CI for new avenues of basic and applied studies.

Indexed as

Anacardic AcidsDrosophila melanogasterHistonesSpermatogenesisSymbiont Induced Cytoplasmic IncompatibilityWolbachiaAcetylationAnimalsDrosophila ProteinsHistone AcetyltransferasesHistone Deacetylase 1MaleSymbiosisanacardic acidAnacardic AcidsDrosophila ProteinsHDAC1 protein, DrosophilaHistone Acetyltransferaseshistone acetyltransferase type B complexHistone Deacetylase 1Histonesanacardic acidCP: Developmental biologyCP: Molecular biologycytoplasmic incompatibilityDrosophila spermatogenesishistone acetylationspermiogenesisWolbachia symbiosis

Identifiers

PMID41066235
PMCPMC12742318

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Registered trials

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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 OpenQuestion graph.