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Wnt5a is a cell-extrinsic factor that supports self-renewal of mouse spermatogonial stem cells.
A possible driver of neoplastic transformation of maturation-arrested gonocytes is the failure of these cells to downregulate expression of OCT3/4, an antiapoptotic oncofetal protein, a process that normally occurs when gonocytes relocate from the center of the seminiferous tubule to the spermatogonial niche.
However, the mechanisms involved in the regulation of spermatogonial stem cells, spermatocytes, and spermatid proliferation and differentiation have not been elucidated.
In rodents, the spermatogonial population is divided into two main categories.
Spermatogenesis is a complex and tightly-regulated process of cell proliferation and differentiation leading to production of mature spermatozoa from Spermatogonial Stem Cells (SSCs) The coordination of SSCs self-renewal and differentiation is regulated by growth factors produced by somatic cells surrounding SSCs, particularly Sertoli cells (1).
Group 1 acted as the control in which spermatogonial stem cells were co-cultured with Sertoli cells alone.
As spermatogoniais thought as spermatogonial stem cells (SSC) while Apr and Aal cells show virtually very few differentiation characteristics.
During the initial maturation, the amounts of spermatogonial cysts and spermatocytes are high, with considerable increase of the latter.
Moreover, during spermatogonial mitosis, cytokinesis is incomplete, leaving the spermatogonial clonal cells interconnected by cytoplasmic bridges (Schulz et al.
niloticus showed organized branching lobules of the unrestricted spermatogonial type (Figure 5b).
Paternal age effect mutations and selfish spermatogonial selection: causes and consequences for human disease.