Universität zu Köln

Feitosa, Natalia Martins, Zhang, Jinli, Carney, Thomas J., Metzger, Manuel, Korzh, Vladimir, Bloch, Wilhelm and Hammerschmidt, Matthias (2012). Hemicentin 2 and Fibulin 1 are required for epidermal-dermal junction formation and fin mesenchymal cell migration during zebrafish development. Dev. Biol., 369 (2). S. 235 - 249. SAN DIEGO: ACADEMIC PRESS INC ELSEVIER SCIENCE. ISSN 0012-1606

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Abstract

Hemicentin 1 (Hmcn1) and Hemicentin 2 (Hmcn2) belong to the fibulin family of extracellular matrix (ECM) proteins that play pivotal roles during development and homeostasis of a variety of vertebrate tissues. Recently, we have shown that mutations in zebrafish Hmcn1, also called Fibulin 6, lead to massive fin blistering, similar to the defects caused by the Fraser syndrome gene Fras1. In contrast, the role of Hmcn2 during vertebrate development has thus far been uncharacterized. In zebrafish, hmcn2. like fibulin 1 (fbln1), another member of the fibulin family, is predominantly expressed in fin mesenchymal cells and developing somites, contrasting the strict epithelial expression of hmcn1. While antisense morpholino oligonucleotide (MO)-based knockdown of hmcn2 did not yield any discernable defects, hmcn2/fbln1 double knockdown fish displayed blistering in the trunk, pointing to an essential contribution of these proteins from mesodermal sources for proper epidermal-dermal junction formation. In contrast, and unlike hmcn1 mutants, epidermal-dermal junctions in the fin folds of hmcn2/fbln1 double knockdown fish were only moderately affected. Instead, they displayed impaired migration of fin mesenchymal cells into the fin folds, pointing to a crucial role of Hmcn2 and Fbln1 to remodel the ECM of the fin fold interepidermal space, which is a prerequisite for fibroblast ingrowth. TEM analyses suggest that this ECM remodeling occurs at the level of actinotrichia, the collageneous migration substrate of mesenchymal cells, and at the level of cross fibers, which resemble mammalian microfibers. This work provides first insights into the role of Hmcn2 during vertebrate development, identifying it as an evolutionary conserved protein that acts in functional redundancy with FbIn1C and/or Fbln1D isoforms to regulate tissue adhesion and cell migration, while extending the current knowledge of the functions of vertebrate Fbln1. (C) 2012 Elsevier Inc. All rights reserved.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Feitosa, Natalia Martins UNSPECIFIED UNSPECIFIED UNSPECIFIED Zhang, Jinli UNSPECIFIED UNSPECIFIED UNSPECIFIED Carney, Thomas J. UNSPECIFIED UNSPECIFIED UNSPECIFIED Metzger, Manuel UNSPECIFIED UNSPECIFIED UNSPECIFIED Korzh, Vladimir UNSPECIFIED UNSPECIFIED UNSPECIFIED Bloch, Wilhelm UNSPECIFIED UNSPECIFIED UNSPECIFIED Hammerschmidt, Matthias UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-482971
DOI:	10.1016/j.ydbio.2012.06.023
Journal or Publication Title:	Dev. Biol.
Volume:	369
Number:	2
Page Range:	S. 235 - 249
Date:	2012
Publisher:	ACADEMIC PRESS INC ELSEVIER SCIENCE
Place of Publication:	SAN DIEGO
ISSN:	0012-1606
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language EXTRACELLULAR-MATRIX PROTEIN; C-ELEGANS; BLEBBED PHENOTYPE; FRASER-SYNDROME; MOUSE; DOMAIN; MORPHOGENESIS; FIBRONECTIN; BINDING; GENE Multiple languages Developmental Biology Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/48297