Calcium-dependent protein kinase (CDPK/CPK)-mediated salicylic acid cascade: the key arsenal of plants under pathogens attack.

Upon pathogen attack, cytosolic Ca²⁺ levels increase in plant cells. The first innate immune response is activated by detecting microbe/pathogen-associated molecular patterns (MAMPs/PAMPs) and is called PAMPs-triggered immunity (PTI). The second immune response is triggered by recognizing pathogens' effector proteins named effectors-triggered immunity (ETI). Calcium-dependent protein kinases (CDPKs or CPKs) are well-known calcium sensors that have a mediator role both in PTI and ETI. Calcium can bind to the elongation factor (EF)-hand domain at the C-terminus of CDPKs, which then phosphorylates substrates at the N-terminal catalytic kinase domain to transfer calcium signals directly. Improving the stress resilience of crops is a critical strategy in attaining global food security. In plants, when a stimulus is seen, there is an increase in Ca²⁺ concentration, which activates CDPKs which are in charge of sending out the immunological signals needed for disease tolerance. During the immune response, CDPKs are subject to numerous levels of regulation, including Ca²⁺ dependency to decipher various Ca²⁺ signals. Furthermore, salicylic acid (SA) regulation by CDPKs provides a comprehensive overview of CDPKs-mediated SA signaling during immune response in plants under pathogen attack. The critical part of CDPKs in SA biosynthesis, from the regulation of SA biosynthesis to how NPR1 perceives SA upon biotic stress, is comprehensively reviewed in this paper with the latest advancements in research. However, more research about CDPKs-mediated SA signaling under pathogen attack is mandatory to further dissect their co-role in crop protection against various diseases to achieve sustainable production goals in the future.