Eye‐open at birth phenotype with reduced keratinocyte motility in LGR4 null mice
Copyright policy )Eye‐open at birth phenotype with reduced keratinocyte motility in LGR4 null mice
We observed a consistent eye‐open at birth (EOB) phenotype in mouse pups homozygous for a leucine‐rich repeat containing G‐protein coupled receptor 4 (Lgr4) allele deleting the whole transmembrane domain coding region. An in vitro wound‐healing scratch assay showed notably reduced keratinocyte motility in the null mice. Phalloidin staining of F‐actin in the eyelid epidermis was also reduced. We also generated keratinocyte‐specific Lgr4 deficient mice, circumventing the embryonic/neonatal lethality and kidney abnormalities. Most of the conditional Lgr4 knockout mice showed the EOB phenotype. Thus, Lgr4 might be a novel gene class regulating cell motility.
- MRC Laboratory of Molecular Biology United Kingdom
- Tohoku University Japan
- Medical Research Council United Kingdom
Keratinocytes, Mice, Knockout, Cell Survival, Gene Expression Regulation, Developmental, Embryonic Structures, EOB, Gene deletion mice, Eye, Receptors, G-Protein-Coupled, Mice, GPCR, Phenotype, LGR4, Animals, Newborn, GPR48, Animals, Eye Abnormalities, Keratinocyte, Cells, Cultured
Keratinocytes, Mice, Knockout, Cell Survival, Gene Expression Regulation, Developmental, Embryonic Structures, EOB, Gene deletion mice, Eye, Receptors, G-Protein-Coupled, Mice, GPCR, Phenotype, LGR4, Animals, Newborn, GPR48, Animals, Eye Abnormalities, Keratinocyte, Cells, Cultured
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