FIGURE 2.

CK and hormonal crosstalks during biotic stress responses. Pathogen attacks stimulated by PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI) correlate with a dramatic production of SA and CK. The accumulation of CK will induce the production and accumulation of phytoalexins in a SA-independent manner and also enhance the SA-dependent immunity. In response to pathogens, NPR1 monomerizes and translocates to the nucleus where it interacts with TGA3. The NPR1-TGA3 activity is further regulated through interaction with the type-B ARR2 response regulator, a component of the CK signaling pathway. The TGA3-NPR1-ARR2 complex is required to induce the SA-mediated resistance and to trigger the expression of PR1 and PR2. High CK levels, induced after pathogen attacks, can activate the CRF5-mediated branch of the CK signaling pathway and contribute to the regulation of the PR1, PR3, PR4, and PR5 expression.