<i>Atoh1-cre</i> is expressed in hair cells and causes transient limited expression of <i>Atoh1</i> in CKO ears.

<p>(<b>a</b>) This diagram shows that <i>Atoh1-cre</i> is driven by an <i>Atoh1</i> enhancer element (En) which is activated when endogenous Atoh1 protein binds. After the Cre protein is expressed, it excises the genomic <i>Atoh1</i> region flanked by loxP sites, resulting in conditional deletion of <i>Atoh1</i> after a transient expression of mRNA and protein. (<b>b–c’</b>) Immunohistochemistry of Cre protein (red) at E18.5 confirms that Cre is expressed in all hair cells in the control ear. The expression in the CKO mutant cochlea is limited to one to two rows of cells in the organ of Corti and becomes discontinuous with gaps (arrows in c’) in the base. (<b>d–k’</b>) <i>In situ</i> hybridization of <i>Atoh1</i> shows its expression in the control and CKO mutant ears. The expression initiates in vestibular sensory epithelia (d) followed by progressive expression from the base to the apex in the cochlea (f, h, j). In the CKO ears <i>Atoh1</i> expression is less profound and later is eliminated in all sensory epithelia (e, g, i, k). The loss of <i>Atoh1</i> in the CKO cochlea also progresses from base to apex. At P4, only a small number of cells at the apical tip show <i>Atoh1</i> expression (k, k’). All control and mutant ears of the same stages are from littermates processed simultaneously as left and right ears for identification. Images were electronically adjusted to the same orientation. AC, anterior crista; Co, cochlea; HC, horizontal crista; OC, organ of Corti; PC, posterior crista; S, saccule; U, utricle. Bar indicates 100 µm.