The partial recovery of spermatogenesis in DKO mice over time can be attributed to potential compensatory mechanisms triggered in response to the initial disruption caused by the loss of CDK8/19 and Cyclin C. Several factors may contribute to this partial recovery:
Compensatory gene expression: In response to the disruption of key genes involved in spermatogenesis and steroidogenesis, the cells may activate compensatory pathways to restore some level of functionality. Upregulation of certain genes or activation of alternative pathways could help in partially overcoming the initial blockage in spermatogenesis.
Cellular adaptation: The cells in the testes, including spermatogonia, Sertoli cells, and Leydig cells, may undergo adaptive changes to cope with the loss of CDK8/19 and Cyclin C. This adaptation could involve alterations in gene expression, cellular processes, and signaling pathways to maintain essential functions for spermatogenesis.
Reprogramming of cell fate: In some cases, cells may undergo reprogramming or differentiation changes to compensate for the loss of critical regulatory factors. This reprogramming could lead to the restoration of certain cell types or functions necessary for spermatogenesis.
Feedback mechanisms: The disruption caused by the loss of CDK8/19 and Cyclin C may trigger feedback mechanisms within the testicular microenvironment. These feedback loops could involve hormonal signaling, cell-cell interactions, and signaling cascades that help in restoring some level of spermatogenesis.
Overall, the partial recovery of spermatogenesis in DKO mice over time is likely a result of complex interplay between compensatory mechanisms, cellular adaptation, and feedback responses within the testicular environment.