@article{4190c2aa0e5e473aa1354e925ee4f1f1,
title = "α-actinin accounts for the bioactivity of actin preparations in inducing STAT target genes in Drosophila melanogaster",
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.",
author = "Oliver Gordon and Henry, {Conor M.} and Naren Srinivasan and Susan Ahrens and Anna Franz and Safia Deddouche and Probir Chakravarty and David Phillips and Roger George and Svend Kjaer and David Frith and Snijders, {Ambrosius P.} and Valente, {Rita S.} and {Simoes da Silva}, {Carolina J.} and Luis Teixeira and Barry Thompson and Dionne, {Marc S.} and Will Wood and {E Sousa}, {Caetano Reis}",
note = "Funding Information: We thank Nic Tapon, Paul Martin, Maxine Holder, Georgina Fletcher, Ieva Gailite and members of the Immunobiology Laboratory for helpful discussions and suggestions. We are grateful to Kristina Djinovic-Carugo for the a-actinin plasmid. We thank the Francis Crick Institute Genomics Equipment Park, Proteomics, Structural Biology, and the Fly facility for assistance. We also thank the Vienna Drosophila Resource Center for Drosophila lines and Flybase for online resources. This work was supported by The Francis Crick Institute, which receives core funding from Cancer Research UK (FC001136), the UK Medical Research Council (FC001136), and the Wellcome Trust (FC001136), and by Investigator Award WT106973MA from the Wellcome Trust to CRS. LT is funded by the Fundac¸ {\~a}o para a Ci{\^e}ncia e Tecnologia (www.fct.pt) grant PTDC/BEX-GMG/3128/2014. CMH was supported by a long-term fellowship from the Federation of European Biochemical Societies (FEBS). Publisher Copyright: {\textcopyright} Gordon et al.",
year = "2018",
month = sep,
doi = "10.7554/eLife.38636",
language = "English",
volume = "7",
journal = "eLife",
issn = "2050-084X",
publisher = "eLife Sciences Publications Ltd",
}