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MBC in Press, published online ahead of print February 21, 2007
Mol. Biol. Cell 10.1091/mbc.E06-10-0902

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Submitted on October 10, 2006
Revised on January 29, 2007
Accepted on February 2, 2007

Impaired Fertility and Spermiogenetic Disorders with Loss of Cell Adhesion in Male Mice Expressing an Interfering Rap1 Mutant

Evanthia Aivatiadou,* Elisabetta Mattei,{dagger} Michela Ceriani,{ddagger} Leila Tilia,{dagger} and Giovanna Berruti*

*Department of Biology, Laboratory of Cellular and Molecular Biology of Reproduction, University of Milano, 20133 Milano, Italy; {dagger}Institute of Neurobiology and Molecular Medicine-Consiglio Nazionale delle Ricerche, 00143 Roma, Italy; {ddagger}Department of Biotechnology and Biosciences, University of Milano-Bicocca, 20126 Milano, Italy

Monitoring Editor: Asma Nusrat

The GTPase Rap1 serves as a critical point in signal transduction, somatic cell proliferation and differentiation, and cell-cell adhesion acting through distinct mechanisms. During mouse spermiogenesis, Rap1 is activated and forms a signaling complex with its effector, the serine-threonine kinase B-Raf. To investigate about the functional role of Rap1 in male germ cell differentiation, we generated transgenic mice expressing an inactive Rap1 mutant selectively in differentiating spermatids. This expression resulted in a derailment of spermiogenesis due to an anomalous release of immature round spermatids from the seminiferous epithelium within the tubule lumen and in low sperm counts. These spermiogenetic disorders correlated with impaired fertility, being the transgenic males severely subfertile. Because mutant testis exhibited perturbations in ectoplasmic specializations (ES), a Sertoli/germ cell-specific adherens junction, we searched for expression of VE-cadherin, an adhesion molecule regulated by Rap1, in spermatogenic cells of wild-type and mutant mice. We thus found that germ cells express VE-cadherin with a timing strictly related to apical ES formation and function; immature, VE-cadherin positive, spermatids were however prematurely released in the transgenic testis. In conclusion, interfering with Rap1 function during spermiogenesis leads to reduced fertility by impairment of germ-Sertoli cell contacts; our transgenic mouse provides an in vivo model to study the regulation of ES dynamic.

Address correspondence to: Giovanna Berruti (giovanna.berruti{at}unimi.it)




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