AKAP9 is essential for spermatogenesis and sertoli cell maturation in mice.

Document Type

Article

Publication Date

6-1-2013

Keywords

A Kinase Anchor Proteins, Animals, Anti-Mullerian Hormone, Connexin 43, Cyclin-Dependent Kinase Inhibitor p27, Gap Junctions, Male, Meiosis, Mice, Mice, Mutant Strains, Microtubule-Associated Proteins, Organ Specificity, Protein Transport, Sertoli Cells, Spermatogenesis, Spermatozoa, Spindle Apparatus, Thyroid Hormone Receptors alpha, Tight Junctions, Zonula Occludens-1 Protein

JAX Source

Genetics 2013 Jun; 194(2):447-57.

Volume

194

Issue

2

First Page

447

Last Page

457

ISSN

1943-2631

PMID

23608191

Abstract

Mammalian male fertility relies on complex inter- and intracellular signaling during spermatogenesis. Here we describe three alleles of the widely expressed A-kinase anchoring protein 9 (Akap9) gene, all of which cause gametogenic failure and infertility in the absence of marked somatic phenotypes. Akap9 disruption does not affect spindle nucleation or progression of prophase I of meiosis but does inhibit maturation of Sertoli cells, which continue to express the immaturity markers anti-Mullerian hormone and thyroid hormone receptor alpha in adults and fail to express the maturation marker p27(Kip1). Furthermore, gap and tight junctions essential for blood-testis barrier (BTB) organization are disrupted. Connexin43 (Cx43) and zona occludens-1 are improperly localized in Akap9 mutant testes, and Cx43 fails to compartmentalize germ cells near the BTB. These results identify and support a novel reproductive tissue-specific role for Akap9 in the coordinated regulation of Sertoli cells in the testis. Genetics 2013 Jun; 194(2):447-57.

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