Premium
Laminin matrix assembly and the mediation of epithelial differentiation
Author(s) -
Yurchenco Peter D,
Yang DongHua,
Li Shaohua,
Chen ZuLin,
Strickland Sidney
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.21.5.a90-d
Subject(s) - laminin , epiblast , microbiology and biotechnology , basal lamina , basement membrane , endoderm , conditional gene knockout , extracellular matrix , chemistry , embryonic stem cell , biology , anatomy , embryogenesis , embryo , gastrulation , ultrastructure , biochemistry , phenotype , gene
Laminins‐111 and ‐511 are key basal lamina constituents of early embryonic and renal epithelia whose particular inductive effects depend upon the type of attached epithelia. In early development, knockout of the laminin gamma1 chain results in a failure of basal laminia assembly associated with a loss of epiblast but not of endoderm. Rescue of the defect with exogenous laminin requires both laminin self‐assembly mediated by LN domains and anchorage to cells mediated by LG domains, with the vector of epiblast polarity established by the location of the laminin polymer. Ureteric bud specific knockout of the laminin‐gamma1 chain initiated by HoxB7cre expression is also associated with a failure of basal lamina assembly. Here epithelial polarization is altered, but not prevented, and is accompanied by slowed growth of epithelia leading to absent or small kidneys. The latter may depend upon the loss of growth factor anchorage to the basal surface.