title: RNAi gene silencing affects cell and developmental plasticity in hydra.
abstract: The recent establishment of gene silencing through RNA interference upon feeding opens avenues to decipher the genetic control of regeneration in hydra. Following that approach, we identified three main stages for head regeneration. Immediately post-amputation, the serine protease inhibitor Kazal1 gene produced by the gland cells prevents from an excessive autophagy in regenerating tips. This cytoprotective function, or self-preservation, is similar to that played by Kazal-type proteins in the mammalian exocrine pancreas, in homeostatic or post-injury conditions, likely reflecting an evolutionarily conserved mechanism linking cell survival to tissue repair. Indeed, in wild-type hydra, within the first hours following mid-gastric section, an extensive cellular remodelling is taking place, including phenotypic cellular transitions and cell proliferation. The activation of the MAPK pathway, which leads to the RSK-dependent CREB phosphorylation, is required for these early cellular events. Later, at the early-late stage, the expression of the Gsx/cnox-2 ParaHox gene in proliferating apical neuronal progenitors is required for the de novo neurogenesis that precedes the emergence of the tentacle rudiments. Hence, head regeneration in wild-type hydra relies on spatially restricted and timely orchestrated cellular modifications, which display similarities with those reported during vertebrate epimorphic regeneration. These results suggest some conservation across evolution of the mechanisms driving the post-amputation reactivation of developmental programs.
authors.affiliation: Department of Zoology and Animal Biology, University of Geneva, 30, quai Ernest-Ansermet, CH-1211 Geneva 4, Switzerland. brigitte.galliot@zoo.unige.ch
authors.forename: Brigitte
authors.initials: B
authors.lastname: Galliot
authors.forename: Marijana
authors.initials: M
authors.lastname: Miljkovic-Licina
authors.forename: Luiza
authors.initials: L
authors.lastname: Ghila
authors.forename: Simona
authors.initials: S
authors.lastname: Chera
mesh_terms: D000818:Animals; D005075:Biological Evolution; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D006829:Hydra / Q000166:cytology* / Q000254:growth & development*; D009420:Nervous System / Q000166:cytology / Q000254:growth & development; D009473:Neuronal Plasticity / Q000502:physiology; D010641:Phenotype; D010766:Phosphorylation; D011494:Protein Kinases / Q000378:metabolism; D034622:RNA Interference / Q000502:physiology*; D012038:Regeneration / Q000235:genetics* / Q000502:physiology*; D019893:Ribosomal Protein S6 Kinases; D015842:Serine Proteinase Inhibitors / Q000494:pharmacology
chemical_list: D017362:Cyclic AMP Response Element-Binding Protein; D015842:Serine Proteinase Inhibitors; D011494:Protein Kinases; D019893:Ribosomal Protein S6 Kinases; D038362:Glycogen Synthase Kinase 3