Normal development of mice and unimpaired cell adhesion cell motility actin-based cytoskeleton without compensatory up-regulation of ezrin or radixinin moesin gene knockout

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.