We knocked out two important genes, occludin and moesin. Here we summarized the results on moesin-null mice.
ERM (ezrin/radixin/moesin) proteins are general cross-linkers between plasmamembranes and actin filaments. Since their expression is regulated in a tissue specific manner, unique function has been supposed for each of ERM proteins. On the other hand, experiments at the cellular level has suggested the functional redundancy of ERM proteins. To assess the possible overlapping functions of ERM proteins invivo, the moesin gene located on X chromosome was disrupted by gene targeting in embryonic stem cells. Hemizygous male as well as homozygous female mice for the mutation were completely devoid of moesin but were normally developed and fertile, showing no obvious histological abnormalities in all the tissues examined. In tissues of the mutant mice, moesin completely disappeared without affecting the expression levels and subcellular distribution of ezrin and radixin. Also in platelets, fibroblasts, and mast cells isolated from moesin-deficient mice, targeted disruption of moesin gene did not affect their ERM-dependent functions, i.e.platelet aggregation, stress fiber/focal contact formation of fibroblasts, and microvillar formation of mast cells, without compensatory up-regulation of ezrin and radixin. These findings favor the notion that ERM proteins are functionally redundant at the cellular as well as the whole body levels.