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Crim1 is involved in adhesion and migration events during development
Author(s) -
Pennisi David John,
Wilkinson Lorine,
Gilbert Thierry,
Kinna Genevieve,
Little Melissa
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb5-b
Subject(s) - laminin , microbiology and biotechnology , integrin , chordin , cell migration , podocyte , glomerular basement membrane , transfection , cell adhesion , adhesion , basement membrane , ctgf , phenotype , biology , extracellular matrix , cell culture , chemistry , cell , embryo , embryogenesis , gene , kidney , growth factor , endocrinology , genetics , glomerulonephritis , organic chemistry , gastrulation , receptor , proteinuria
We investigated the role Crim1, a type‐I transmembrane protein containing Chordin‐like cysteine‐rich repeat domains, plays in development. To this end, we utilised a gene‐trap line, KST264, hypomorphic for Crim1. KST264/KST264 mice die perinatally and display phenotypes indicative of adhesion and migration defects. These include skin “blebbing” from 12.5dpc, where the Crim1‐expressing epidermis separates from the underlying dermis. From 15.5dpc, KST264/KST264 mice display renal defects, including enlarged, simplified glomerular capillaries and effacement of the Crim1‐expressing podocytes, reminiscent of alpha 3 integrin “knock‐out” mice and suggestive of defects in adhesion to the glomerular basement membrane. Furthermore, migration assays on primary cultures of epicardia from the hearts of KST264/KST264 embryos indicate that cells hypomorphic for Crim1 demonstrate increased migration. Conversely, stable transfected CHO cells over‐expressing Crim1 showed a decreased propensity to migrate in different assays. Moreover, Crim1 over‐expressing cell lines displayed increased adhesion to of collagen and laminin. We conclude that Crim1 mediates cell adhesion and/or migration in development and that this may reflect a direct interaction with ECM components. This research was supported by the National Health and Medical Research Council of Australia (grant # 455972).

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