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However, the <jats:italic>Smad5<\/jats:italic> knockout of single allele (\u00b1) could survive. We used <jats:italic>Smad5<\/jats:italic> heterozygous knockout (\u00b1) to determine the role of <jats:italic>Smad5<\/jats:italic> in the development of inner ear morphology and function. <jats:italic>In situ<\/jats:italic> hybridization showed that Smad5 was expressed predominantly in hair cells, spiral ganglion, and supporting cells. Measurements of hearing thresholds using auditory brainstem response showed that <jats:italic>Smad5<\/jats:italic> defect resulted in progressive hearing loss between 4 and 24 weeks after birth. Morphological examination revealed apoptosis in the inner ear, with significant loss of outer hair cells in adult <jats:italic>Smad5<\/jats:italic> mutant mice. Our results indicated that deficiency in the Smad5\u2010mediated signaling resulted in apoptosis of hair cells, suggesting <jats:italic>Smad5<\/jats:italic> is a gene that may be related with presbycusis. \u00a9 2008 Wiley Periodicals, Inc. 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