Citation

BibTex format

@article{Brosh:2022:10.1073/pnas.2122026119,
author = {Brosh, O and Fabian, DK and Cogni, R and Tolosana, I and Day, JP and Olivieri, F and Merckx, M and Akilli, N and Szkuta, P and Jiggins, FM},
doi = {10.1073/pnas.2122026119},
journal = {Proc Natl Acad Sci U S A},
title = {A novel transposable element-mediated mechanism causes antiviral resistance in Drosophila through truncating the Veneno protein.},
url = {http://dx.doi.org/10.1073/pnas.2122026119},
volume = {119},
year = {2022}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Hosts are continually selected to evolve new defenses against an ever-changing array of pathogens. To understand this process, we examined the genetic basis of resistance to the Drosophila A virus in Drosophila melanogaster. In a natural population, we identified a polymorphic transposable element (TE) insertion that was associated with an ∼19,000-fold reduction in viral titers, allowing flies to largely escape the harmful effects of infection by this virulent pathogen. The insertion occurs in the protein-coding sequence of the gene Veneno, which encodes a Tudor domain protein. By mutating Veneno with CRISPR-Cas9 in flies and expressing it in cultured cells, we show that the ancestral allele of the gene has no effect on viral replication. Instead, the TE insertion is a gain-of-function mutation that creates a gene encoding a novel resistance factor. Viral titers remained reduced when we deleted the TE sequence from the transcript, indicating that resistance results from the TE truncating the Veneno protein. This is a novel mechanism of virus resistance and a new way by which TEs can contribute to adaptation.
AU - Brosh,O
AU - Fabian,DK
AU - Cogni,R
AU - Tolosana,I
AU - Day,JP
AU - Olivieri,F
AU - Merckx,M
AU - Akilli,N
AU - Szkuta,P
AU - Jiggins,FM
DO - 10.1073/pnas.2122026119
PY - 2022///
TI - A novel transposable element-mediated mechanism causes antiviral resistance in Drosophila through truncating the Veneno protein.
T2 - Proc Natl Acad Sci U S A
UR - http://dx.doi.org/10.1073/pnas.2122026119
UR - https://www.ncbi.nlm.nih.gov/pubmed/35858337
VL - 119
ER -