Figure 8.

Model for TCH3- and CPK5-dependent activation of CBP60g. Plants deploy PRRs to sense the invasion of pathogens. Perception of PAMPs triggers activation of calcium channels and a cytosolic increase of Ca²⁺, leading to activation of calcium sensors, such as CDPKs. Perception of PAMPs also induces the expression of the gene encoding the calcium sensor TCH3. TCH3 directly binds to CBP60g and enhances its activity. TCH3 targets the autoinhibitory region of CPK5 and enhances CPK5-mediated phosphorylation of CBP60g. Alternatively, binding of TCH3 to CBP60g may also contribute to CBP60g phosphorylation by CPKs. Phosphorylation of CBP60g enhances its transcription factor activity and regulates the expression of defense-related genes and thereby triggers defense against V. dahliae. In addition to post-translational phosphorylation-mediated activation, CBP60g is transcriptionally induced by PAMP perception or pathogen infection.