Virus Recognition by Toll-7 Activates Antiviral Autophagy in Drosophila

Margaret Nakamoto, Ryan H. Moy, Jie Xu, Shelly Bambina, Ari Yasunaga, Spencer S. Shelly, Beth Gold, Sara Cherry

Research output: Contribution to journalArticlepeer-review

157 Scopus citations

Abstract

Innate immunity is highly conserved and relies on pattern recognition receptors (PRRs) such as Toll-like receptors (identified through their homology to Drosophila Toll) for pathogen recognition. Although Drosophila Toll is vital for immune recognition and defense, roles for the other eight Drosophila Tolls in immunity have remained elusive. Here we have shown that Toll-7 is a PRR both in vitro and in adult flies; loss of Toll-7 led to increased vesicular stomatitis virus (VSV) replication and mortality. Toll-7, along with additional uncharacterized Drosophila Tolls, was transcriptionally induced by VSV infection. Furthermore, Toll-7 interacted with VSV at the plasma membrane and induced antiviral autophagy independently of the canonical Toll signaling pathway. These data uncover an evolutionarily conserved role for a second Drosophila Toll receptor that links viral recognition to autophagy and defense and suggest that other Drosophila Tolls may restrict specific as yet untested pathogens, perhaps via noncanonical signaling pathways.

Original languageEnglish (US)
Pages (from-to)658-667
Number of pages10
JournalImmunity
Volume36
Issue number4
DOIs
StatePublished - Apr 20 2012

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Fingerprint Dive into the research topics of 'Virus Recognition by Toll-7 Activates Antiviral Autophagy in Drosophila'. Together they form a unique fingerprint.

Cite this