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.
Kato
Shigeki
S
Laboratory of Molecular Biology, Graduate School of Agricultural Science, Tohoku University, 1-1 Tsutsumidori-Amamiyamachi, Aoba-ku, Sendai 981-8555, Japan.
Mohri
Yasuaki
Y
Matsuo
Tsuyoshi
T
Ogawa
Eisaku
E
Umezawa
Akihiro
A
Okuyama
Ryuhei
R
Nishimori
Katsuhiko
K
D000818:Animals; D000831:Animals, Newborn; D002470:Cell Survival; D002478:Cells, Cultured; D004628:Embryonic Structures / Q000196:embryology / Q000378:metabolism; D005123:Eye / Q000196:embryology / Q000378:metabolism / Q000503:physiopathology*; D005124:Eye Abnormalities / Q000235:genetics* / Q000503:physiopathology*; D018507:Gene Expression Regulation, Developmental; D015603:Keratinocytes / Q000166:cytology* / Q000378:metabolism*; D051379:Mice; D018345:Mice, Knockout; D010641:Phenotype; D043562:Receptors, G-Protein-Coupled / Q000172:deficiency* / Q000235:genetics / Q000378:metabolism*
C496200:LGR4 protein, mouse; D043562:Receptors, G-Protein-Coupled