Identification of Live Germ-Cell Desquamation as a Major Mechanism of Seasonal Testis Regression in Mammals: A Study in the Iberian Mole (Talpa occidentalis)

• Published in: Biology of reproduction 2013-04, Vol.88 (4), p.101-101
• Main Authors: DADHICH, Rajesh K, BARRIONUEVO, Francisco J, REAL, Francisca M, LUPIANEZ, Darío G, ORTEGA, Esperanza, BURGOS, Miguel, JIMENEZ, Rafael
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Cell Count; Cell Death; Down-Regulation; Fundamental and applied biological sciences. Psychology; Germ Cells - cytology; Germ Cells - metabolism; Germ Cells - physiology; Male; Moles - anatomy & histology; Moles - genetics; Moles - metabolism; Moles - physiology; Organ Size; Seasons; Sertoli Cells - cytology; Sertoli Cells - metabolism; Sertoli Cells - physiology; Testis - anatomy & histology; Testis - cytology; Testis - metabolism; Testis - ultrastructure; Transcriptome; Vertebrates: reproduction
• ISSN: 0006-3363; 1529-7268
• DOI: 10.1095/biolreprod.112.106708

In males of seasonally breeding species, testes undergo a severe involution at the end of the breeding season, with a major volume decrease due to massive germ-cell depletion associated with photoperiod-dependent reduced levels of testosterone and gonadotropins. Although it has been repeatedly suggested that apoptosis is the principal effector of testicular regression in vertebrates, recent studies do not support this hypothesis in some mammals. The purpose of our work is to discover alternative mechanisms of testis regression in these species. In this paper, we have performed a morphological, hormonal, ultrastructural, molecular, and functional study of the mechanism of testicular regression and the role that cell junctions play in the cell-content dynamics of the testis of the Iberian mole, Talpa occidentalis, throughout the seasonal breeding cycle. Desquamation of live, nonapoptotic germ cells has been identified here as a new mechanism for seasonal testis involution in mammals, indicating that testis regression is regulated by modulating the expression and distribution of the cell-adhesion molecules in the seminiferous epithelium. During this process, which is mediated by low intratesticular testosterone levels, Sertoli cells lose their nursing and supporting function, as well as the impermeability of the blood-testis barrier. Our results contradict the current paradigm that apoptosis is the major testis regression effector in vertebrates, as it is clearly not true in all mammals. The new testis regression mechanism described here for the mole could then be generalized to other mammalian species. Available data from some previously studied mammals should be reevaluated.