Change search
ReferencesLink to record
Permanent link

Direct link
Genetic Screen in Drosophila Larvae Links ird1 Function to Toll Signaling in the Fat Body and Hemocyte Motility
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). BioMediTech, University of Tampere, Tampere, Finland.
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
Show others and affiliations
2016 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 11, no 7, e0159473Article in journal (Refereed) Published
Abstract [en]

To understand how Toll signaling controls the activation of a cellular immune response in Drosophila blood cells (hemocytes), we carried out a genetic modifier screen, looking for deletions that suppress or enhance the mobilization of sessile hemocytes by the gain-of-function mutation Toll(10b) (Tl-10b). Here we describe the results from chromosome arm 3R, where five regions strongly suppressed this phenotype. We identified the specific genes immune response deficient 1 (ird1), headcase (hdc) and possibly Rab23 as suppressors, and we studied the role of ird1 in more detail. An ird1 null mutant and a mutant that truncates the N-terminal kinase domain of the encoded Ird1 protein affected the Tl-10b phenotype, unlike mutations that affect the C-terminal part of the protein. The ird1 null mutant suppressed mobilization of sessile hemocytes, but enhanced other Tl-10b hemocyte phenotypes, like the formation of melanotic nodules and the increased number of circulating hemocytes. ird1 mutants also had blood cell phenotypes on their own. They lacked crystal cells and showed aberrant formation of lamellocytes. ird1 mutant plasmatocytes had a reduced ability to spread on an artificial substrate by forming protrusions, which may explain why they did not go into circulation in response to Toll signaling. The effect of the ird1 mutation depended mainly on ird1 expression in hemocytes, but ird1-dependent effects in other tissues may contribute. Specifically, the Toll receptor was translocated from the cell membrane to intracellular vesicles in the fat body of the ird1 mutant, and Toll signaling was activated in that tissue, partially explaining the Tl-10b-like phenotype. As ird1 is otherwise known to control vesicular transport, we conclude that the vesicular transport system may be of particular importance during an immune response.

Place, publisher, year, edition, pages
2016. Vol. 11, no 7, e0159473
National Category
Cell and Molecular Biology
URN: urn:nbn:se:umu:diva-126336DOI: 10.1371/journal.pone.0159473ISI: 000381516100034PubMedID: 27467079OAI: diva2:1039783
Available from: 2016-10-25 Created: 2016-10-03 Last updated: 2016-10-25Bibliographically approved

Open Access in DiVA

fulltext(6378 kB)17 downloads
File information
File name FULLTEXT01.pdfFile size 6378 kBChecksum SHA-512
Type fulltextMimetype application/pdf

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Schmid, Martin R.Anderl, InesYang, HairuKronhamn, JesperHultmark, Dan
By organisation
Department of Molecular Biology (Faculty of Medicine)
In the same journal
Cell and Molecular Biology

Search outside of DiVA

GoogleGoogle Scholar
Total: 17 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 42 hits
ReferencesLink to record
Permanent link

Direct link