![]() ![]() To uncover novel genes associated with the Sugarcane mosaic virus (SCMV) response, we used RNA-Seq data to analyze differentially expressed genes (DEGs) and transcript expression pattern clusters between a tolerant/resistant (CI-RL1) and a susceptible (B73) line, in addition to the F1 progeny (CI-RL1xB73). Understanding PAMP structures and stimulatory mechanisms across multi-cellular life will provide insights into the evolutionary origins of innate immunity and may lead to the discovery of new PAMP variations of scientific and therapeutic interest. We discuss why LPS may have evolved to be immuno-stimulatory in some eukaryotes but not others and propose two hypotheses about the evolution of PAMP structure based on the ecology and environmental context of the organism in question. In this review, we examine the history of LPS as a PAMP in mammals, recent data on LPS structure and its ability to activate mammalian innate immune receptors, and how these activities compare across commonly studied eukaryotes. Mammals have evolved multiple proteins that operate as receptors for the PAMP lipopolysaccharide (LPS) from Gram-negative bacteria, but LPS is not immuno-stimulatory in all eukaryotes. Most studies in this area have been conducted in model organisms, which leaves many open questions about the universality of PAMP biology across living systems. Since the publication of the Janeway's Pattern Recognition hypothesis in 1989, study of pathogen-associated molecular patterns (PAMPs) and their immuno-stimulatory activities has accelerated. We propose to extend this zig-zag model to plant-virus interactions (Figure. The final outcome of the plant-pathogen interaction depends on the sum total of ( + ETI). This evolutionary arms race between the host and the pathogen occurs in multiple rounds of ETS followed by ETI. To counteract the action of specific pathogen effectors plants have evolved ETI, a largely NB-LRR-based recognition of the ‘modified-self’ by-products of ETS. Successful pathogens have evolved effector/virulence factors that promote pathogen growth by suppressing PTI, which results in effector-triggered susceptibility (ETS). In the zig-zag model, originally proposed by Jones and Dangl, PAMP (and DAMP) perception initiates the primary, PTI-based defense responses that limit (but do not fully stop) pathogen growth. The outcome of any plant-pathogen interaction depends on a relative contribution of susceptibility and resistance factors. ![]() These conserved components of immune system might also be targeted by viral effectors. Interestingly, SGT1 and HSP90 are essential for the mammalian inflammasome activity, linking the innate immune responses of these distant organisms. Mutations of the genes encoding the chaperone components strongly affect stability of R proteins. This complex might facilitate a conformational change of R proteins inducing the immune signaling after recognition of pathogen effectors or modified host proteins targeted by pathogen effectors. R proteins functioning depends on the chaperon complex that includes SGT1 (Suppressor of G2 allele of skp1), HSP90 (Heat-shock protein 90) and RAR1 (Required for Mla12 resistance). A new plant NB-LRR allele is then evolved and selected that can recognize the newly acquired effector, resulting again in ETI. In phase 4, pathogen isolates are selected that have lost or modified the specifically recognized effector/suppressor, and perhaps gained a new effector that can help the pathogen to suppress ETI. In phase 3, one effector or suppressor is recognized directly or indirectly by an NB-LRR protein, activating effector-triggered immunity (ETI), an amplified version of PTI that often passes a threshold for induction of hypersensitive response (HR) and programmed cell death (PCD). In phase 2, successful viral and non-viral pathogens deliver effectors/suppressors that interfere with both PTI and silencing, resulting in effector-triggered susceptibility (ETS). In phase 1, plants detect pathogen-associated molecular patterns (PAMPs) and host danger-associated molecular patterns (DAMPs) via pattern-recognition receptors (PRRs) to induce pattern-triggered immunity (PTI) and, in the case of viral pathogens, plants additionally detect viral double-stranded RNA (dsRNA) to trigger RNA silencing. The ultimate amplitude of disease resistance or susceptibility is proportional to. Zig-zag model for evolution of innate immunity- and silencing-based plant defense against viral and non-viral pathogens (adopted and extended from Jones and Dangl 2006 ). ![]()
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