<scp>JAK</scp>/<scp>STAT</scp>signaling in<i><scp>D</scp>rosophila</i>muscles controls the cellular immune response against parasitoid infection

Yang, Hairu; Kronhamn, Jesper; Ekström, Jens‐Ola; Korkut, Gül Gizem; Hultmark, Dan

doi:10.15252/embr.201540277

“…They play a key role in host defense through melanization and they participate in wound healing. Lamellocytes are large (15 to 40 m in diameter), flat adherent cells which encapsulate and neutralize objects too large to be phagocytosed by plasmatocytes (30)(31)(32). Of note, the question of the involvement of hemocytes in antiviral immunity has not been a focus of interest so far for Drosophila.…”

Section: Importancementioning

confidence: 99%

Analysis of the Contribution of Hemocytes and Autophagy to Drosophila Antiviral Immunity

Lamiable

¹

,

Arnold

²

,

Faria

³

et al. 2016

J Virol

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Antiviral immunity in the model organism Drosophila melanogaster involves the broadly active intrinsic mechanism of RNA interference (RNAi) and virus-specific inducible responses. Here, using a panel of six viruses, we investigated the role of hemocytes and autophagy in the control of viral infections. Injection of latex beads to saturate phagocytosis, or genetic depletion of hemocytes, resulted in decreased survival and increased viral titers following infection with Cricket paralysis virus (CrPV), Flock House virus (FHV), and vesicular stomatitis virus (VSV) but had no impact on Drosophila C virus (DCV), Sindbis virus (SINV), and Invertebrate iridescent virus 6 (IIV6) infection. In the cases of CrPV and FHV, apoptosis was induced in infected cells, which were phagocytosed by hemocytes. In contrast, VSV did not trigger any significant apoptosis but we confirmed that the autophagy gene Atg7 was required for full virus resistance, suggesting that hemocytes use autophagy to recognize the virus. However, this recognition does not depend on the Toll-7 receptor. Autophagy had no impact on DCV, CrPV, SINV, or IIV6 infection and was required for replication of the sixth virus, FHV. Even in the case of VSV, the increases in titers were modest in Atg7 mutant flies, suggesting that autophagy does not play a major role in antiviral immunity in Drosophila. Altogether, our results indicate that, while autophagy plays a minor role, phagocytosis contributes to virus-specific immune responses in insects. IMPORTANCEPhagocytosis and autophagy are two cellular processes that involve lysosomal degradation and participate in Drosophila immunity. Using a panel of RNA and DNA viruses, we have addressed the contribution of phagocytosis and autophagy in the control of viral infections in this model organism. We show that, while autophagy plays a minor role, phagocytosis contributes to virusspecific immune responses in Drosophila. This work brings to the front a novel facet of antiviral host defense in insects, which may have relevance in the control of virus transmission by vector insects or in the resistance of beneficial insects to viral pathogens.

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“…For careful observation, we removed, from epidermal filets, underlying muscle fibers that exhibited JAK/STAT signaling activation (see below; Yang et al, 2015). JNK activation was prominent at 4 h after injury ( Fig.…”

Section: S3j-q)mentioning

confidence: 99%

Spatiotemporal regulation of cell fusion by JNK and JAK/STAT signaling during Drosophila wound healing

Lee

¹

,

Lee

²

,

Park

³

et al. 2017

Journal of Cell Science

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Cell-cell fusion is widely observed during development and disease, and imposes a dramatic change on participating cells. Cell fusion should be tightly controlled, but the underlying mechanism is poorly understood. Here, we found that the JAK/STAT pathway suppressed cell fusion during wound healing in the Drosophila larval epidermis, restricting cell fusion to the vicinity of the wound. In the absence of JAK/STAT signaling, a large syncytium containing a 3-fold higher number of nuclei than observed in wild-type tissue formed in wounded epidermis. The JAK/STAT ligand-encoding genes upd2 and upd3 were transcriptionally induced by wounding, and were required for suppressing excess cell fusion. JNK (also known as Basket in flies) was activated in the wound vicinity and activity peaked at ∼8 h after injury, whereas JAK/STAT signaling was activated in an adjoining concentric ring and activity peaked at a later stage. Cell fusion occurred primarily in the wound vicinity, where JAK/STAT activation was suppressed by fusion-inducing JNK signaling. JAK/ STAT signaling was both necessary and sufficient for the induction of βPS integrin (also known as Myospheroid) expression, suggesting that the suppression of cell fusion was mediated at least in part by integrin protein.

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“…Parasitoid wasp infection activates JAK/ STAT signaling in larval somatic muscles, which is crucial for an efficient cellular immune response (Yang et al, 2015). Wounding or tumor formation in imaginal discs induces secretion of Upd ligands and activates the systemic activation loop of JAK/STAT signaling in hemocytes and fat bodies, which results in hemocyte proliferation and suppression of tumor growth (Pastor-Pareja et al, 2008).…”

Section: Jnk Suppresses Jak/stat Activation In the Wound Vicinitymentioning

confidence: 99%

Spatiotemporal regulation of cell fusion by JNK and JAK/STAT signaling during Drosophila wound healing

Lee¹,

Lee²,

Park³

et al. 2017

View full text Add to dashboard Cite

Cell-cell fusion is widely observed during development and disease, and imposes a dramatic change on participating cells. Cell fusion should be tightly controlled, but the underlying mechanism is poorly understood. Here, we found that the JAK/STAT pathway suppressed cell fusion during wound healing in the Drosophila larval epidermis, restricting cell fusion to the vicinity of the wound. In the absence of JAK/STAT signaling, a large syncytium containing a 3-fold higher number of nuclei than observed in wild-type tissue formed in wounded epidermis. The JAK/STAT ligand-encoding genes upd2 and upd3 were transcriptionally induced by wounding, and were required for suppressing excess cell fusion. JNK (also known as Basket in flies) was activated in the wound vicinity and activity peaked at ∼8 h after injury, whereas JAK/STAT signaling was activated in an adjoining concentric ring and activity peaked at a later stage. Cell fusion occurred primarily in the wound vicinity, where JAK/STAT activation was suppressed by fusion-inducing JNK signaling. JAK/ STAT signaling was both necessary and sufficient for the induction of βPS integrin (also known as Myospheroid) expression, suggesting that the suppression of cell fusion was mediated at least in part by integrin protein.

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JAK/STATsignaling inDrosophilamuscles controls the cellular immune response against parasitoid infection

Cited by 115 publications

References 56 publications

Analysis of the Contribution of Hemocytes and Autophagy to Drosophila Antiviral Immunity

Analysis of the Contribution of Hemocytes and Autophagy to Drosophila Antiviral Immunity

Spatiotemporal regulation of cell fusion by JNK and JAK/STAT signaling during Drosophila wound healing

Spatiotemporal regulation of cell fusion by JNK and JAK/STAT signaling during Drosophila wound healing

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