title: Protein kinase VRK-1 regulates cell invasion and EGL-17/FGF signaling in Caenorhabditis elegans.
abstract: The vaccinia-related kinases (VRKs) are highly conserved throughout the animal kingdom and phosphorylate several chromatin proteins and transcription factors. In early Caenorhabditis elegans embryos, VRK-1 is required for proper nuclear envelope formation. In this work, we present the first investigation of the developmental role of VRKs by means of a novel C. elegans vrk-1 mutant allele. We found that VRK-1 is essential in hermaphrodites for formation of the vulva, uterus, and utse and for development and maintenance of the somatic gonad and thus the germ line. VRK-1 regulates anchor cell polarity and the timing of anchor cell invasion through the basement membranes separating vulval and somatic gonadal cells during the L3 larval stage. VRK-1 is also required for proper specification and proliferation of uterine cells and sex myoblasts. Expression of the fibroblast growth factor-like protein EGL-17 and its receptor EGL-15 is reduced in vrk-1 mutants, suggesting that VRK-1 might act at least partially through activation of FGF signaling. Expression of a translational VRK-1Colon, two colonsGFP fusion protein in the ventral nerve cord and vulva precursor cells restores vulva and uterus formation, suggesting both cell autonomous and non-autonomous roles of VRK-1.
authors.affiliation: Centro Andaluz de Biología del Desarrollo (CABD), Consejo Superior de Investigaciones Científicas, Universidad Pablo de Olavide, Seville 41013, Spain.
authors.forename: Elke P F
authors.initials: EP
authors.lastname: Klerkx
authors.forename: Pilar
authors.initials: P
authors.lastname: Alarcón
authors.forename: Katherine
authors.initials: K
authors.lastname: Waters
authors.forename: Valerie
authors.initials: V
authors.lastname: Reinke
authors.forename: Paul W
authors.initials: PW
authors.lastname: Sternberg
authors.forename: Peter
authors.initials: P
authors.lastname: Askjaer
mesh_terms: D000818:Animals; D017173:Caenorhabditis elegans / Q000033:anatomy & histology / Q000196:embryology / Q000502:physiology; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism*; D005346:Fibroblast Growth Factors / Q000235:genetics / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference; D017468:Receptors, Fibroblast Growth Factor / Q000235:genetics / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D019076:Transgenes
chemical_list: D029742:Caenorhabditis elegans Proteins; C112493:EGL-15 protein, C elegans; C105157:Egl-17 protein, C elegans; D036341:Intercellular Signaling Peptides and Proteins; D017468:Receptors, Fibroblast Growth Factor; D011993:Recombinant Fusion Proteins; D005346:Fibroblast Growth Factors; D017346:Protein Serine-Threonine Kinases; C517796:VRK-1 protein, C elegans
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