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

Research output: Contribution to journalArticle (Academic Journal)peer-review

3 Citations (Scopus)
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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
Number of pages9
JournaleLife
Volume7
DOIs
Publication statusPublished - 27 Sep 2018

Keywords

  • D. melanogaster
  • damage-associated molecular pattern
  • DAMP
  • immunology
  • inflammation
  • innate immunity
  • JAK/STAT pathway
  • sterile inflammation
  • tissue injury

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