Answers are grounded in this paper and cite their sources.
Recently, we found that the Pseudomonas aeruginosa type II secreted protease IV functions as a unique Arabidopsis innate immunity elicitor. The protease IV-activated pathway involves G protein signaling and raises the question of how protease elicitation leads to the activation of G protein-mediated signaling, because plants do not appear to have metazoan-like G protein-coupled receptors. Importantly, our data suggest that Arabidopsis has evolved a mechanism to detect the proteolytic activity of a pathogen-encoded protease, supporting the host-pathogen arms race model. In the case of opportunistic multi-host pathogens like P. aeruginosa, however, it is not plausible that P. aeruginosa is simultaneously co-evolving in a gene-for-gene manner with all of its potential hosts, which include plants, nematodes, insects, and mammals. This prompts us to ask what is the driving force for co-evolution of defense response in Arabidopsis and pathogenesis of P. aeruginosa, which might not have been subject to iterative cycles of evolutionary selections.
No takes yet. Share an insight, caveat, or question.
Zhenyu Cheng (2016) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: