Eye-open at birth phenotype with reduced keratinocyte motility in LGR4 null mice
Eye-open at birth phenotype with reduced keratinocyte motility in LGR4 null mice
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DOI：
10.1016/j.febslet.2007.08.064
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发表时间：
2007-10-02
期刊：
影响因子：
3.5
通讯作者：
Nishimori, Katsuhiko
中科院分区：
文献类型：
--
作者：
Kato, Shigeki;Mohri, Yasuaki;Nishimori, Katsuhiko
我们在含有删除整个跨膜域编码区的 G 蛋白偶联受体 4 (Lgr4) 等位基因的富含亮氨酸重复序列的纯合子小鼠中观察到一致的出生时睁眼 (EOB) 表型。体外伤口愈合划痕试验显示，无效小鼠的角质形成细胞运动显着降低。眼睑表皮中 F-肌动蛋白的鬼笔环肽染色也减少。我们还培育了角质形成细胞特异性 Lgr4 缺陷小鼠，避免了胚胎/新生儿致死率和肾脏异常。大多数条件性Lgr4基因敲除小鼠表现出EOB表型。因此，Lgr4 可能是调节细胞运动的新基因类。 (c) 2007 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
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. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.