![]() Both PTI and ETI trigger similar downstream responses, including the release of reactive oxygen species (ROS), activation of mitogen-activated protein kinases (MAPKs), and the production of pathogenesis-related (PR) proteins such as chitinases, glucanases, and proteases ( Dodds and Rathjen, 2010). ETI often culminates in a form of programmed cell death (PCD) known as the hypersensitive response (HR) at the site of infection, limiting the spread of the pathogen ( Morel and Dangl, 1997). Resistant plants can recognize some of these effectors through nucleotide-binding leucine-rich repeat (NB-LRR) proteins, resulting in effector-triggered immunity (ETI) ( Zipfel, 2014). Adapted pathogens use effector proteins to perturb PTI. ![]() Upon pathogen entry, pathogen-associated molecular patterns (PAMPs) such as chitin and flagellin are recognized by pattern recognition receptors (PRRs), resulting in PAMP-triggered immunity (PTI) ( Jones and Dangl, 2006). Plant proteases perform critical functions during the interaction between plants and pathogens. ![]() This cleavage serves not only to degrade proteins, thereby rendering them non-functional and facilitating protein turnover, but also to activate proteins through the removal of inhibitory or regulatory domains and changing their subcellular location ( Van der Hoorn, 2008). Proteases are present throughout the tree of life, determining the fate of proteins by irreversibly cleaving peptide bonds. ![]()
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