Normal development of mice and unimpaired cell adhesion cell motility actin-based cytoskeleton without compensatory up-regulation of ezrin or radixinin moesin gene knockout
Y. Doi et al., Normal development of mice and unimpaired cell adhesion cell motility actin-based cytoskeleton without compensatory up-regulation of ezrin or radixinin moesin gene knockout, J BIOL CHEM, 274(4), 1999, pp. 2315-2321
Ezrin/radixin/moesin (ERM) proteins are general cross-linkers between the p
lasma membrane and actin filaments. Because their expression is regulated i
n a tissue-specific manner, each ERM protein has been proposed to have uniq
ue functions. On the other hand, experiments at the cellular level and in v
itro have suggested their functional redundancy. To assess the possible uni
que functions of ERM proteins in vivo, the moesin gene located on the X chr
omosome was disrupted by gene targeting in embryonic stem cells. Male mice
hemizygous for the mutation as well as homozygous females were completely d
evoid of moesin but developed normally and were fertile, with no obvious hi
stological abnormalities in any of the tissues examined. In the tissues of
the mutant mice, moesin completely disappeared without affecting the expres
sion levels or subcellular distribution of ezrin and radixin, Also, in plat
elets, fibroblasts, and mast cells isolated from moesin-deficient mice, tar
geted disruption of the moesin gene did not affect their ERM-dependent func
tions, i.e. platelet aggregation, stress fiber/focal contact formation of f
ibroblasts, and microvillar formation of mast cells, without compensatory u
p-regulation of ezrin or radixin, These findings favor the notion that ERM
proteins are functionally redundant at the cellular as well as the whole bo
dy level.