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Targeted connexin26 ablation arrests postnatal development of the organ of Corti.

Abstract：

:Mutations in the gene coding for connexin26 (Cx26) is the most common cause of human nonsyndromic hereditary deafness. To investigate deafness mechanisms underlying Cx26 null mutations, we generated three independent lines of conditional Cx26 null mice. Cell differentiation and gross cochlear morphology at birth seemed normal. However, postnatal development of the organ of Corti was stalled as the tunnel of Corti and the Nuel's space were never opened. Cell degeneration was first observed in the Claudius cells around P8. Outer hair cell loss was initially observed around P13 at middle turn when inner hair cells were still intact. Massive cell death occurred in the middle turn thereafter and gradually spread to the basal turn, resulting in secondary degeneration of spiral ganglion neurons in the corresponding cochlear locations. These results demonstrated that Cx26 plays essential roles in postnatal maturation and homoeostasis of the organ of Corti before the onset of hearing.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Wang Y,Chang Q,Tang W,Sun Y,Zhou B,Li H,Lin X

doi

10.1016/j.bbrc.2009.05.023

subject

Has Abstract

pub_date

2009-07-17 00:00:00

pages

33-7

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(09)00911-5

journal_volume

385

pub_type

杂志文章

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