The mammalian target of rapamycin (mTOR), is a serine/threonine protein kinase and belongs to the phosphatidylinositol 3-kinase (PI3K)-related kinase (PIKK) family. mTOR interacts with other subunits to form two distinct complexes, mTORC1 and mTORC2. mTORC1 coordinates cell growth and metabolism in response to environmental input, including growth factors, amino acid, energy and stress. mTORC2 mainly controls cell survival and migration through phosphorylating glucocorticoid-regulated kinase (SGK), protein kinase B (Akt), and protein kinase C (PKC) kinase families. The dysregulation of mTOR is involved in human diseases including cancer, cardiovascular diseases, neurodegenerative diseases, and epilepsy. Tissue damage caused by trauma, diseases or aging disrupt the tissue functions. Tissue regeneration after injuries is of significance for recovering the tissue homeostasis and functions. Mammals have very limited regenerative capacity in multiple tissues and organs, such as the heart and central nervous system (CNS). Thereby, understanding the mechanisms underlying tissue regeneration is crucial for tissue repair and regenerative medicine. mTOR is activated in multiple tissue injuries. In this review, we summarize the roles of mTOR signaling in tissue regeneration such as neurons, muscles, the liver and the intestine.

Germline stem cells (GSCs) sustain gametogenesis during the organismal life cycle. Although evidence suggests that GSCs are consistently present in the zebrafish ovary and support oogenesis, whether GSCs are involved in zebrafish ovary regeneration is poorly understood. Here, we found that nanos2, a conserved vertebrate GSC marker, is required for maintaining GSCs in zebrafish. We applied genetic ablation and tissue resection techniques to delineate the function of GSCs in zebrafish ovary regeneration. After GSC ablation, ovaries fail to regenerate and are converted to sterile testes. Amputated ovarian tissues completely regenerate as a result of the proliferation of residual GSCs, but nanos2 mutant ovaries fail to regenerate after amputation due to a lack of GSCs. The repression of Wnt signaling leads to reduced numbers of GSCs and delayed ovary regeneration. Our results provide insight into the key role of GSCs in driving ovary regeneration.