JAK/STAT signaling in Drosophila muscles controls the cellular immune response against parasitoid infection

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

The role of JAK/STAT signaling in the cellular immune response of Drosophila is not well understood. Here, we show that parasitoid wasp infection activates JAK/STAT signaling in somatic muscles of the Drosophila larva, triggered by secretion of the cytokines Upd2 and Upd3 from circulating hemocytes. Deletion of upd2 or upd3, but not the related os ( upd1) gene, reduced the cellular immune response, and suppression of the JAK/STAT pathway in muscle cells reduced the encapsulation of wasp eggs and the number of circulating lamellocyte effector cells. These results suggest that JAK/STAT signaling in muscles participates in a systemic immune defense against wasp infection.

Related collections

Most cited references 55

Record: found
Abstract: found
Article: not found

Cytokine/Jak/Stat signaling mediates regeneration and homeostasis in the Drosophila midgut.

Huaqi Jiang, Parthive Patel, Alexander Kohlmaier … (2009)

Cells in intestinal epithelia turn over rapidly due to damage from digestion and toxins produced by the enteric microbiota. Gut homeostasis is maintained by intestinal stem cells (ISCs) that divide to replenish the intestinal epithelium, but little is known about how ISC division and differentiation are coordinated with epithelial cell loss. We show here that when enterocytes (ECs) in the Drosophila midgut are subjected to apoptosis, enteric infection, or JNK-mediated stress signaling, they produce cytokines (Upd, Upd2, and Upd3) that activate Jak/Stat signaling in ISCs, promoting their rapid division. Upd/Jak/Stat activity also promotes progenitor cell differentiation, in part by stimulating Delta/Notch signaling, and is required for differentiation in both normal and regenerating midguts. Hence, cytokine-mediated feedback enables stem cells to replace spent progeny as they are lost, thereby establishing gut homeostasis.

0 comments Cited 404 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

The dorsoventral regulatory gene cassette spätzle/Toll/cactus controls the potent antifungal response in Drosophila adults.

B. Lemaitre, E. Nicolás, L Michaut … (1996)

The cytokine-induced activation cascade of NF-kappaB in mammals and the activation of the morphogen dorsal in Drosophila embryos show striking structural and functional similarities (Toll/IL-1, Cactus/I-kappaB, and dorsal/NF-kappaB). Here we demonstrate that these parallels extend to the immune response of Drosophila. In particular, the intracellular components of the dorsoventral signaling pathway (except for dorsal) and the extracellular Toll ligand, spätzle, control expression of the antifungal peptide gene drosomycin in adults. We also show that mutations in the Toll signaling pathway dramatically reduce survival after fungal infection. Antibacterial genes are induced either by a distinct pathway involving the immune deficiency gene (imd) or by combined activation of both imd and dorsoventral pathways.

0 comments Cited 370 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

GFP reporters detect the activation of the Drosophila JAK/STAT pathway in vivo.

Erika A Bach, Laura A Ekas, Aidee Ayala-Camargo … (2007)

JAK/STAT signaling is essential for a wide range of developmental processes in Drosophila melanogaster. The mechanism by which the JAK/STAT pathway contributes to these processes has been the subject of recent investigation. However, a reporter that reflects activity of the JAK/STAT pathway in all Drosophila tissues has not yet been developed. By placing a fragment of the Stat92E target gene Socs36E, which contains at least two putative Stat92E binding sites, upstream of GFP, we generated three constructs that can be used to monitor JAK/STAT pathway activity in vivo. These constructs differ by the number of Stat92E binding sites and the stability of GFP. The 2XSTAT92E-GFP and 10XSTAT92E-GFP constructs contain 2 and 10 Stat92E binding sites, respectively, driving expression of enhanced GFP, while 10XSTAT92E-DGFP drives expression of destabilized GFP. We show that these reporters are expressed in the embryo in an overlapping pattern with Stat92E protein and in tissues where JAK/STAT signaling is required. In addition, these reporters accurately reflect JAK/STAT pathway activity at larval stages, as their expression pattern overlaps that of the activating ligand unpaired in imaginal discs. Moreover, the STAT92E-GFP reporters are activated by ectopic JAK/STAT signaling. STAT92E-GFP fluorescence is increased in response to ectopic upd in the larval eye disc and mis-expression of the JAK kinase hopscotch in the adult fat body. Lastly, these reporters are specifically activated by Stat92E, as STAT92E-GFP reporter expression is lost cell-autonomously in stat92E homozygous mutant tissue. In sum, we have generated in vivo GFP reporters that accurately reflect JAK/STAT pathway activation in a variety of tissues. These reporters are valuable tools to further investigate and understand the role of JAK/STAT signaling in Drosophila.

0 comments Cited 156 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): EMBO Rep

Journal ID (iso-abbrev): EMBO Rep

Journal ID (publisher-id): embr

Title: EMBO Reports

Publisher: Blackwell Publishing Ltd (Oxford, UK )

ISSN (Print): 1469-221X

ISSN (Electronic): 1469-3178

Publication date (Print): December 2015

Publication date (Electronic): 27 September 2015

Volume: 16

Issue: 12

Pages: 1664-1672

Affiliations

[1 ]Department of Molecular Biology, Umeå University Umeå, Sweden

[2 ]Institute of Biomedical Technology, BMT, Tampere University Tampere, Finland

Author notes

*Corresponding author. Tel: +46 90 785 67 78; E-mail: dan.hultmark@ 123456ucmp.umu.se

[†]

Present address: Department of Comparative Physiology, Evolutionary Biology Center, Uppsala University, Uppsala, Sweden

Subject Categories Immunology; Microbiology, Virology & Host Pathogen Interaction

Article

DOI: 10.15252/embr.201540277

PMC ID: 4687419

PubMed ID: 26412855

SO-VID: 1f19bc91-8755-48a7-acdb-d598bbabda45

License:

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

History

Date received : 24 February 2015

Date revision received : 27 August 2015

Date accepted : 28 August 2015

Comments

Comment on this article

scite_

Smart Citations

Citing PublicationsSupportingMentioningContrasting

View Citations

See how this article has been cited at scite.ai

scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.