Snail transcription factors induce the epithelial-mesenchymal transition (EMT), as epithelial cells acquire migratory/invasive properties of mesenchymal cells to mediate embryonic development and tumour progression. Cells undergoing EMT exhibit stem-cell-like traits, including decreased E-cadherin expression (1), raising the question of whether genes involved in EMT also function in stem cells. In several organs, including intestine, Snail proteins are also present in multipotent cells. An initial description of Snai2-deficient mice revealed males exhibit reduced seminiferous tubule size and infertility (2), implicating Snai2 in normal spermatogenesis. However, expression and function of the three mammalian Snails (1-2) are yet to be elucidated in the mammalian testis.
This study defines the cellular distribution of Snail mRNAs and proteins in mouse and human testes. In situ hybridisation of adult mouse testis revealed Snai1 and Snai2 are predominantly detected in spermatogonia and spermatocytes; Snai3 is similar, but more widespread, with signal also detected in all spermatogenic stages and in Sertoli cells. Immunohistochemistry on adult mouse testis detected Snai1 in round and elongated spermatid nuclei between Stages IX-XII, Snai2 in the cytoplasm of all germ cells, and Snai3 in the Sertoli cell cytoplasm. In the developing mouse testis, Snai1 is robustly detected in the gonocyte cytoplasm at 0 dpp, and becomes nuclear by 5 dpp; Snai3 is detected in Sertoli cell cytoplasm only after the formation of the blood-testis barrier at 15 dpp.
To regulate gene expression, Snails need to be nuclear. These data reveal a potential role for Snai1 at specific stages of spermatogenesis, including during chromatin remodelling in spermatids and in gonocyte migration and differentiation at the very start of spermatogenesis.