The gene encoding myosin VIIA is responsible for the mouse shaker-1 ph
enotype, which consists of deafness and balance deficiency related to
cochlear and vestibular neuroepithelial defects. In humans, a defectiv
e myosin VIIA gene is responsible for Usher syndrome type IB, which as
sociates congenital deafness, vestibular dysfunction and retinitis pig
mentosa. In an attempt to progress in the understanding of the functio
n(s) of myosin VIIA, we studied the expression of the myosin VIIA gene
during mouse embryonic development. Embryos from day 9 (E9) to E18 we
re analyzed by in situ hybridization and immunohistofluorescence. The
myosin VIIA mRNA and protein were consistently detected in the same em
bryonic tissues throughout development. Myosin VIIA was first observed
in the otic vesicle at E9, and later in a variety of tissues. The olf
actory epithelium and the liver express it as early as E10. In the ret
inal pigment epithelium, choroid plexus, adrenal gland and tongue, exp
ression begins at E12 and in the testis and the adenohypophysis at E13
. In the small intestine, kidney and hair follicles of the vibrissae,
expression of myosin VIIA starts only at E15. Myosin VIIA expression w
as observed only in epithelial cell types, most of which possess micro
villi or cilia. Interestingly, myosin VIIA expression seems to be conc
omitant with the appearance of these structures in the epithelial cell
s, suggesting a role for this myosin in their morphogenesis. The cellu
lar location of myosin VIIA within sensory hair cells and olfactory re
ceptor neurons also argues for a role of this system vesicle trafficki
ng.