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J. Biol. Chem., Vol. 281, Issue 31, 22352-22359, August 4, 2006

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Interaction between Fidgetin and Protein Kinase A-anchoring Protein AKAP95 Is Critical for Palatogenesis in the Mouse^*

From the Jackson Laboratory, Bar Harbor, Maine 04609

The gene defective in fidget mice encodes fidgetin, a member of the AAA (ATPases associated with diverse cellular activities) family of ATPases. Using a yeast two-hybrid screen, we identified cAMP-dependent protein kinase A anchoring protein 95 kDa (AKAP95) as a potential fidgetin-binding protein. Epitope-tagged fidgetin co-localized with endogenous AKAP95 in the nuclear matrix, and the physical interaction between fidgetin and AKAP95 was further confirmed by reciprocal immunoprecipitation. To evaluate the biological significance of the fidgetin-AKAP95 binding, we created AKAP95 mutant mice through a gene trap strategy. Akap95 mutant mice are surprisingly viable with no overt phenotype. However, a significant number of mice carrying both Akap95 and fidget mutations die soon after birth due to cleft palate, consistent with the overlapping expression of AKAP95 and fidgetin in the branchial arches during mouse embryogenesis. These results expand the spectrum of the pleiotropic phenotypes of fidget mice and provide new leads on the in vivo function of AKAP95.

Received for publication, April 14, 2006 , and in revised form, May 11, 2006.

^* This work was supported in part by Grant DC03611 from the National Institutes of Health (to W. N. F.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Supported by a postdoctoral fellowship from the Jackson Laboratory.

² To whom correspondence should be addressed: The Jackson Laboratory, 600 Main St., Bar Harbor, ME 04609. Tel.: 207-288-6354; Fax: 207-288-6077; E-mail: wayne.frankel{at}jax.org.

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