Maturation arrest in early postnatal sensory receptors by deletion of the miR-183/96/182 cluster in mouse.

ABSTRACT: The polycistronic miR-183/96/182 cluster is preferentially and abundantly expressed in terminally differentiating sensory epithelia. To clarify its roles in the terminal differentiation of sensory receptors in vivo, we deleted the entire gene cluster in mouse germline through homologous recombination. The miR-183/96/182 null mice display impairment of the visual, auditory, vestibular, and olfactory systems, attributable to profound defects in sensory receptor terminal differentiation. Maturation of sensory receptor precursors is delayed, and they never attain a fully differentiated state. In the retina, delay in up-regulation of key photoreceptor genes underlies delayed outer segment elongation and possibly mispositioning of cone nuclei in the retina. Incomplete maturation of photoreceptor

SUBMITTER: Fan J 

PROVIDER: S-EPMC5448201 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature