
This function is essential under normal feeding conditions to promote TORC1-dependent growth during larval development and, in adults and larvae to prevent the REPTOR-dependent expression of nutrient stress response genes ( PubMed:25920570). When TORC1 activity is high it phosphorylates REPTOR which inhibits its recruitment into the nucleus and antagonizes their function ( PubMed:25920570). REPTOR functions downstream of TORC1 to regulate the expression of stress response genes in response to TORC1 inhibition resulting from nutrient deprivation ( PubMed:25920570). As part of the TORC1 complex regulates energy homeostasis and promotes certain aspects of larval growth by negatively regulating REPTOR ( PubMed:25920570).

Thus, in addition to controlling growth of the cell in which it resides, it can also influence growth of distant cells and organs during development via a humoral mechanism ( PubMed:14505573). Hyperactivation of the signaling leads to accelerated differentiation, whereas inhibition of the signaling retards differentiation ( PubMed:15454083). Affects the timing of neuronal cell differentiation ( PubMed:15454083). Overexpression inhibits growth and reduces cell size ( PubMed:14505573). May regulate the activity of S6K ( PubMed:11069885). May also be involved, directly or indirectly, in the control of neuronal function ( PubMed:15454083). May be involved in atg1 phosphorylation ( PubMed:19225150). Regulates growth during animal development by coupling growth factor signaling to nutrient availability ( PubMed:11069888). Promotes cell and tissue growth, maintains tissue homeostatis and controls responses to environmental stress and aging ( PubMed:11069885, PubMed:11069888, PubMed:19211682, PubMed:19225150). Vienna Drosophila Resource Center (VDRC).


