Fig. 10.

Model for regulation of the transcriptional response to glucose by TORC1 and PKA. Based on the literature and our data, we depict how PKA and TORC1 regulate the glucose response. a In the absence of glucose, the PKA and TORC1 pathways are inactive. Bcy1 binds to Tpk1-3 and keeps the protein kinase A inactive. This results in activation of transcriptional repressors Dot6 and Stb3, the protein kinase Rim15 and stress-responsive transcription factors Msn2/Msn4. Sfp1, transcription factor for ribosome biogenesis and protein synthesis genes, is kept inactive. In the absence of TORC1 activity, the PP2A-like protein phosphatase Sit4/Rrd1/2 module dissociates from Tap42 and dephosphorylates unidentified proteins to inhibit the transcriptional response to glucose. b In the presence of glucose, the PKA and TORC1 pathways are activated. Ras2 and Gpa2 activate the adenylate cyclase Cyr1 to produce cAMP which binds to Bcy1 and releases Tpk1-3 from Bcy1’s inhibitory effect. PKA inactivates Dot6, Stb3, Rim15, and Msn2/Msn4 and activates Sfp1. TORC1 is activated by glucose through Gtr1/Gtr2-dependent and Gtr1/Gtr2-independent mechanisms. In the presence of active TORC1, Tap42 binds to Sit4/Rrd1/2 module and keeps it inactive thereby preventing its inhibitory effect on the transcriptional response to glucose. Activation of the transcriptional response to glucose is essential for spore germination