Plant immunity: towards an integrated view of plant–pathogen interactions

Abstract

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.

Identification of Plasmodiophora brassicae effectors — A challenging goal

“…In order to manipulate plant defenses and enable parasitic colonization, many eukaryotic biotrophic plant pathogens have evolved advanced strategies to deliver effector proteins into the host cell during infection [31]. Successful infection relies primarily on the success of the release of the effectors, which in many cases are responsible for the suppression of plant immunity [32].…”

“…Successful infection relies primarily on the success of the release of the effectors, which in many cases are responsible for the suppression of plant immunity [32]. The initial recognition of conserved microbial features, known as pathogen – associated molecular patterns (PAMPs), leads to PAMP-triggered immunity (PTI) in the host [31]. PAMP-triggered immunity is a first level of immune response that can be overcome by effector proteins produced by adapted pathogens.…”

“…Sequence identity between plant pathogen effectors and other protein sequences is often low such that the assessment of functions based on putative orthology alone has been limited [31,50]. In many cases, the three-dimensional structure of the protein, the disulfide bond pattern, and the cysteine spacing have been used to identify protease and/or protease inhibitors as putative effectors in obligate biotrophic soil-born plant pathogens [34,51,52].…”

The Co-4 locus on chromosome Pv08 contains a unique cluster of 18 COK-4 genes and is regulated by immune response in common bean

“…Understanding common bean resistance against anthracnose is one of the main goals in breeding 67 programs as genetic resistance is the most-efficient and environmentally friendly control of crop diseases 68 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 (Dodds and Rathjen 2010). Until now, 14 anthracnose resistance loci were discovered (Co-1 to in 69 common bean genome (Ferreira et al 2013).…”

Not to be suppressed? Rethinking the host response at a root-parasite interface

“…Our current understanding of host defense responses at the molecular level is primarily based on the interaction between plant leaves and pathogenic microorganisms, which are considered to follow a zig-zag model where the final unmatched pathogen-or host-derived activity determines the outcome of susceptibility or immunity [6]. Under the zig-zag model, there are two paths to immunity that differ according to their activating stimuli: the first is triggered by molecular patterns from the pathogen or damaged host cells in the apoplast, whereas the second is triggered by specific recognition of effectors introduced into the host cell by the pathogen [6,7]. Successful pathogens are able to prevent immunity either by avoiding/suppressing recognition of the molecular patterns or by introducing effectors that effectively block the relevant defense signaling pathways once activated.…”