Plants are engaged in a continuous co-evolutionary struggle for dominance with their pathogens. The outcomes of these interactions are of particular importance to human activities, as they can have dramatic effects on agricultural systems. The recent convergence of molecular studies of plant immunity and pathogen infection strategies is revealing an integrated picture of the plant-pathogen interaction from the perspective of both organisms. Plants have an amazing capacity to recognize pathogens through strategies involving both conserved and variable pathogen elicitors, and pathogens manipulate the defence response through secretion of virulence effector molecules. These insights suggest novel biotechnological approaches to crop protection.

No abstract

SARM1 (sterile alpha and TIR motif containing 1) is responsible for depletion of nicotinamide adenine dinucleotide in its oxidized form (NAD+) during Wallerian degeneration associated with neuropathies. Plant nucleotide-binding leucine-rich repeat (NLR) immune receptors recognize pathogen effector proteins and trigger localized cell death to restrict pathogen infection. Both processes depend on closely related Toll/interleukin-1 receptor (TIR) domains in these proteins, which, as we show, feature self-association–dependent NAD+ cleavage activity associated with cell death signaling. We further show that SARM1 SAM (sterile alpha motif) domains form an octamer essential for axon degeneration that contributes to TIR domain enzymatic activity. The crystal structures of ribose and NADP+ (the oxidized form of nicotinamide adenine dinucleotide phosphate) complexes of SARM1 and plant NLR RUN1 TIR domains, respectively, reveal a conserved substrate binding site. NAD+ cleavage by TIR domains is therefore a conserved feature of animal and plant cell death signaling pathways.

Virus‐induced gene silencing was used to assess the function of random Nicotiana benthamiana cDNAs in disease resistance. Out of 4992 cDNAs tested from a normalized library, there were 79 that suppressed a hypersensitive response (HR) associated with Pto‐mediated resistance against Pseudomonas syringae. However, only six of these clones blocked the Pto‐mediated suppression of P.syringae growth. The three clones giving the strongest loss of Pto resistance had inserts corresponding to HSP90 and also caused loss of Rx‐mediated resistance against potato virus X and N‐mediated tobacco mosaic virus resistance. The role of HSP90 as a cofactor of disease resistance is associated with stabilization of Rx protein levels and could be accounted for in part by SGT1 and other cofactors of disease resistance acting as co‐chaperones. This approach illustrates the potential benefits and limitations of RNA silencing in forward screens of gene function in plants.

Plant innate immunity relies on a set of pattern recognition receptors (PRRs) that respond to ligands known as pathogen-associated molecular patterns (PAMPs). To overcome such immunity, phytopathogenic bacteria deliver virulence molecules called effector proteins into the plant cell that collectively promote pathogenesis. The vast majority of PRRs controlling PAMP-triggered immunity (PTI) and the mechanisms used by specific effectors to suppress these pathways are mostly unknown. Here, we show that the Arabidopsis LysM receptor kinase CERK1, which is critical for chitin elicitor signaling and resistance to fungal pathogens, plays an essential role in restricting bacterial growth on plants. This is supported by the fact that CERK1 is a target of the bacterial type III effector protein AvrPtoB, which blocks all defense responses through this receptor. AvrPtoB ubiquitinates the CERK1 kinase domain in vitro and targets CERK1 for degradation in vivo. We show that CERK1 is a determinant of bacterial immunity, but its contribution is overcome by bacteria expressing AvrPtoB. Our results reveal a new pathway for plant immunity against bacteria and a role for AvrPtoB E3-ligase activity in suppressing PTI.

AvrPto from the Pseudomonas cell. To examine this, avrPto deletions C⌬25, C⌬41, and C⌬74 were placed into pBI121 and tested with the Agrobacterium transient assay. Agrobacterium EHA105 containing avrPto induced an HR in 2 days, whereas EHA105 containing the avrPto deletion C⌬25 induced an HR after 4 days; the other deletions did not elicit an HR ( X. Tang and G. Martin, unpublished results). This suggests that the carboxyl terminal 25 amino acids of AvrPto are not required for secretion from the bacterial cell; this portion of AvrPto may serve as an activation domain, interact with other components in the signaling pathway, or have a role in AvrPto stability.

Plants and animals use innate immunity as a first defense against pathogens, a costly yet necessary tradeoff between growth and immunity. In Arabidopsis, the regulatory leucine-rich repeat receptor-like kinase (LRR-RLK) BAK1 combines with the LRR-RLKs FLS2 and EFR in pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and the LRR-RLK BRI1 in brassinosteroid (BR)-mediated growth. Therefore, a potential tradeoff between these pathways mediated by BAK1 is often postulated. Here, we show a unidirectional inhibition of FLS2-mediated immune signaling by BR perception. Unexpectedly, this effect occurred downstream or independently of complex formation with BAK1 and associated downstream phosphorylation. Thus, BAK1 is not rate-limiting in these pathways. BRs also inhibited signaling triggered by the BAK1-independent recognition of the fungal PAMP chitin. Our results suggest a general mechanism operative in plants in which BR-mediated growth directly antagonizes innate immune signaling.flagellin sensing 2 | brassinosteroid insensitive 1 | BRI1-associated kinase 1 | cross-talk

No abstract