Gordon, O; Henry, CM; Srinivasan, N; Ahrens, S; Franz, A; Deddouche, S; Chakravarty, P; ... Reis E Sousa, C; + view all Gordon, O; Henry, CM; Srinivasan, N; Ahrens, S; Franz, A; Deddouche, S; Chakravarty, P; Phillips, D; George, R; Kjaer, S; Frith, D; Snijders, AP; Valente, RS; Simoes da Silva, CJ; Teixeira, L; Thompson, B; Dionne, MS; Wood, W; Reis E Sousa, C; - view fewer (2018) α-actinin accounts for the bioactivity of actin preparations in inducing STAT target genes in Drosophila melanogaster. eLife , 7 , Article e38636. 10.7554/eLife.38636.

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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.

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