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Title

Protein kinase VRK-1 regulates cell invasion and EGL-17/FGF signaling in Caenorhabditis elegans

AuthorsKlerkx, Elke P. F. CSIC; Alarcón, Pilar CSIC; Waters, Katherine; Reinke, Valerie; Sternberg, Paul W.; Askjaer, Peter CSIC ORCID
KeywordsAnchor cell
Caenorhabditis elegans
Cell invasion
Cell polarity
Cell signaling
FGF
Uterus
Vaccinia-related kinase
vrk-1
Vulva
Issue Date11-Aug-2009
PublisherElsevier
CitationDevelopmental Biology 335(1): 12-21 (2009)
AbstractThe 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-1::GFP 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.
Description11 pages, 6 figures.-- PMID: 19679119 [PubMed].-- Printed version published Nov 1, 2009.
Supporting information available at: http://dx.doi.org/10.1016/j.ydbio.2009.08.007
Publisher version (URL)http://dx.doi.org/10.1016/j.ydbio.2009.08.007
URIhttp://hdl.handle.net/10261/17712
DOI10.1016/j.ydbio.2009.08.007
ISSN0012-1606
Appears in Collections:(CABD) Artículos

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