Transcriptional regulator that acts in the TORC1 signaling pathway to regulate energy homeostasis and promote survival during nutrient deprivation. Interacts with REPTOR to form a transcriptional activator complex that functions downstream of TORC1 to up-regulate the expression of most target genes induced by TORC1 inhibition. In the complex, acts as the transcriptional activator. Under normal conditions TORC1 is active, inhibiting the formation of the REPTOR/REPTOR-BP complex by phosphorylating REPTOR and mediates its cytoplasmic retention by forming a docking site for 14-3-3 proteins. Upon TORC1 inhibition resulting from nutrient stress, REPTOR is recruited into the nucleus where it interacts with REPTOR-BP and together they maintain organismal metabolism by activating the expression of target stress response genes including those involved in glycogenesis and triglyceride biosynthesis. The complex also appears to negatively regulate some aspects of TORC1-dependent larval growth. Interacts (via C-terminus) with REPTOR-BP (via C-terminus). Interacts with the TORC1 complex component raptor. Interacts (when phosphorylated) with 14-3-3zeta, this interaction may assist its cytoplasmic retention. Translocation from the cytoplasm to the nucleus is promoted by dephosphorylation and inhibited by phosphorylation. Binds to chromatin. Phosphorylation by the TORC1 kinase complex at Ser-527 and Ser-530 abolishes nuclear localization. Upon TORC1 inhibition, dephosphorylated in a mts/PP2a-dependent manner leading to nuclear localization. Sensitive to nutrient stress. Larvae display no obvious phenotype under normal feeding conditions; larval growth and development is normal, and there is no effect on triglyceride and glycogen levels. However when mutants pupate and become adults they display reduced triglyceride and glycogen stores leading to adults dying within 18 hours of starvation whereas controls survive 2.5 days without food. Larvae are also sensitive to nutrient stress displaying 50% lethality when fed a low nutrient diet. Double knockouts of REPTOR with a hypomorphic Tor, rescue the Tor-mediated increase in triglyceride levels and partially rescue the larval growth defect. Belongs to the bZIP family. CREBRF subfamily.