Premium
ROCK‐I and ROCK‐II cooperatively regulate closure of eyelid and ventral body wall in mouse embryo
Author(s) -
Thumkeo Dean,
Shimizu Yoshihiko,
Sakamoto Satoko,
Yamada Shuichi,
Narumiya Shuh
Publication year - 2005
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2005.00882.x
Subject(s) - biology , embryo , closure (psychology) , eyelid , anatomy , microbiology and biotechnology , medicine , surgery , economics , market economy
Rho‐associated kinase (ROCK) is a serine/threonine kinase working in the Rho signaling to actin cytoskeleton. We previously reported that loss of ROCK‐I results in the eyelid open at birth (EOB) and omphalocele phenotype in mice, while loss of ROCK‐II results in placental dysfunction leading to intrauterine growth retardation and fetal death. Here, we report that after backcross to the C57BL/6 N genetic background, ROCK‐II knockout (KO) neonates are born also with open eyelid and umbilical hernia, a phenotype similar to that of ROCK‐I KO mice. ROCK‐II KO embryos show impaired extension of the eyelid epithelial sheet with disorganized actin bundles in the leading edge of the sheet. These results suggest that ROCK‐I and ROCK‐II cooperatively regulates the assembly of actin bundles essential for closure of the eyelid and ventral body wall in mouse embryos. Consistently, ROCK‐I +/– ROCK‐II +/– double heterozygous mice also show the EOB and omphalocele phenotype.