ArticlePLoS pathogens2015
The epigenetic regulator G9a mediates tolerance to RNA virus infection in Drosophila.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Infections by Transovarially Transmitted DMelSV in Drosophila Have No Impact on Ovarian Transposable Element Transcripts but Increase Their Amounts in the Soma.Genome biology and evolution · 2021Pooled it
- The JAK-STAT pathway in invertebrates: An emerging battleground for host‒virus warfare.Insect science · 2026Review
- Article
- Heterochromatin-based silencing of a foreign tandem repeat inbioRxiv : the preprint server for biology · 2025Article
- Treatment with mitochondrial targeting antibiotics improves survival outcomes after Flock House virus infection in young and aged Drosophila melanogaster.Research square · 2025Article
- Article
- Prolonged exposure to heat enhances mosquito tolerance to viral infection.Communications biology · 2025Article
- Article
- Arboviruses antagonize insect Toll antiviral immune signaling to facilitate the coexistence of viruses with their vectors.PLoS pathogens · 2024Article
- Investigating the Evolution of Drosophila STING-Dependent Antiviral Innate Immunity by Multispecies Comparison of 2'3'-cGAMP Responses.Molecular biology and evolution · 2024Article
- The Role of Protein Methyltransferases in Immunity.Molecules (Basel, Switzerland) · 2024Review
- SetDB1 and Su(var)3-9 are essential for late stages of larval development of Drosophila melanogaster.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Article
- G9a and Sirtuin6 epigenetically modulate host cholesterol accumulation to facilitate mycobacterial survival.PLoS pathogens · 2023Article
- Article
- Intraspecific genetic variation in host vigour, viral load and disease tolerance during Drosophila C virus infection.Open biology · 2023Article
- Hidden variable models reveal the effects of infection from changes in host survival.PLoS computational biology · 2023Article
- Article
- Elucidating Mechanisms of Tolerance tomBio · 2022Article
- Innate immune pathways act synergistically to constrain RNA virus evolution in Drosophila melanogaster.Nature ecology & evolution · 2022Article
- Hsc70-4 aggravates PolyQ-mediated neurodegeneration by modulating NF-κB mediated immune response inFrontiers in molecular neuroscience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Little is known about the tolerance mechanisms that reduce the negative effects of microbial infection on host fitness. Here, we demonstrate that the histone H3 lysine 9 methyltransferase G9a regulates tolerance to virus infection by shaping the response of the evolutionary conserved Jak-Stat pathway in Drosophila. G9a-deficient mutants are more sensitive to RNA virus infection and succumb faster to infection than wild-type controls, which was associated with strongly increased Jak-Stat dependent responses, but not with major differences in viral load. Genetic experiments indicate that hyperactivated Jak-Stat responses are associated with early lethality in virus-infected flies. Our results identify an essential epigenetic mechanism underlying tolerance to virus infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.