α-actinin accounts for the bioactivity of actin preparations in inducing STAT target genes in Drosophila melanogaster

  • Oliver Gordon
  • , Conor M. Henry
  • , Naren Srinivasan
  • , Susan Ahrens
  • , Anna Franz
  • , Safia Deddouche
  • , Probir Chakravarty
  • , David Phillips
  • , Roger George
  • , Svend Kjaer
  • , David Frith
  • , Ambrosius P. Snijders
  • , Rita S. Valente
  • , Carolina J. Simoes da Silva
  • , Luis Teixeira
  • , Barry Thompson
  • , Marc S. Dionne
  • , Will Wood
  • , Caetano Reis E Sousa*
  • *Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)

Abstract

Damage-associated molecular patterns (DAMPs) are molecules exposed or released by dead cells that trigger or modulate immunity and tissue repair. In vertebrates, the cytoskeletal component F-actin is a DAMP specifically recognised by DNGR-1, an innate immune receptor. Previously we suggested that actin is also a DAMP in Drosophila melanogaster by inducing STAT-dependent genes (Srinivasan et al., 2016). Here, we revise that conclusion and report that α-actinin is far more potent than actin at inducing the same STAT response and can be found in trace amounts in actin preparations. Recombinant expression of actin or α-actinin in bacteria demonstrated that only α-actinin could drive the expression of STAT target genes in Drosophila. The response to injected α-actinin required the same signalling cascade that we had identified in our previous work using actin preparations. Taken together, these data indicate that α-actinin rather than actin drives STAT activation when injected into Drosophila.

Original languageEnglish
Article numbere38636
JournaleLife
Volume7
DOIs
Publication statusPublished - Sept 2018
Externally publishedYes

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