Journal
SCIENCE SIGNALING
Volume 10, Issue 502, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.aan0804
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Funding
- Swedish Cancer Society [2015/391]
- Swedish Childhood Cancer Foundation [15-0096, NC2014-0045]
- Swedish Research Council [2015-04466]
- Swedish Foundation for Strategic Research [RB13-0204]
- Goran Gustafsson Foundation [RHP2016]
- American Cancer Society [RPG-96-13504-DDC]
- NIH [1 P50 DK57301-01]
- Sven and Lily Lawski Foundation
- Carl Tryggers Foundation (CTS) [KF15:15]
- Vinnova [2015-04466] Funding Source: Vinnova
- Swedish Research Council [2015-04466] Funding Source: Swedish Research Council
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In Drosophila melanogaster, the receptor tyrosine kinase (RTK) anaplastic lymphoma kinase (Alk) and its ligand jelly belly (Jeb) are required to specify muscle founder cells in the visceral mesoderm. We identified a critical role for the scaffolding protein Cnk (connector enhancer of kinase suppressor of Ras) in this signaling pathway. Embryos that ectopically expressed the minimal Alk interaction region in the carboxyl terminus of Cnk or lacked maternal and zygotic cnk did not generate visceral founder cells or a functional gut musculature, phenotypes that resemble those of jeb and Alk mutants. Deletion of the entire Alk-interacting region in the cnk locus affected the Alk signaling pathway in the visceral mesoderm and not other RTK signaling pathways in other tissues. In addition, the Cnk-interacting protein Aveugle (Ave) was critical for Alk signaling in the developing visceral mesoderm. Alk signaling stimulates the MAPK/ERK pathway, but the scaffolding protein Ksr, which facilitates activation of this pathway, was not required to promote visceral founder cell specification. Thus, Cnk and Ave represent critical molecules downstream of Alk, and their loss genocopies the lack of visceral founder cell specification of Alk and jeb mutants, indicating their essential roles in Alk signaling.
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