FGFR-ERK signaling is an essential component of tissue separation |
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Authors: | Christian Hasse Oliver Holz Ellen Lange Lisa Pisowodzki Nicole Rebscher Marie Christin Eder Bert Hobmayer Monika Hassel |
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Affiliation: | 1. Philipps-Universität Marburg, Faculty of Biology, Morphology and Evolution of Invertebrates, D-35039 Marburg, Germany;2. C719, Institut für Zoologie, Technikerstraße 25, Victor Franz Hess Haus, A-6020 Innsbruck, Austria |
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Abstract: | Formation of a constriction and tissue separation between parent and young polyp is a hallmark of the Hydra budding process and controlled by fibroblast growth factor receptor (FGFR) signaling. Appearance of a cluster of cells positive for double phosphorylated ERK (dpERK) at the late separation site indicated that the RAS/MEK/ERK pathway might be a downstream target of the Hydra Kringelchen FGFR. In fact, inhibition of ERK phosphorylation by the MEK inhibitor U0126 reversibly delayed bud detachment and prevented formation of the dpERK-positive cell cluster indicating de novo-phosphorylation of ERK at the late bud base. In functional studies, a dominant-negative Kringelchen FGFR prevented bud detachment as well as appearance of the dpERK-positive cell cluster. Ectopic expression of full length Kringelchen, on the other hand, induced a localized rearrangement of the actin cytoskeleton at sites of constriction, localized ERK-phosphorylation and autotomy of the body column. Our data suggest a model in which (i) the Hydra FGFR targets, via an unknown pathway, the actin cytoskeleton to induce a constriction and (ii) FGFR activates MEK/ERK signaling at the late separation site to allow tissue separation. |
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Keywords: | Receptor tyrosine kinase Autotomy Actin cytoskeleton Dominant-negative FGFR |
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