Plants cannot move to escape environmental challenges. Biotic stresses result from a battery of potential pathogens: fungi, bacteria, nematodes and insects intercept the photosynthate produced by plants, and viruses use replication machinery at the host's expense. Plants, in turn, have evolved sophisticated mechanisms to perceive such attacks, and to translate that perception into an adaptive response. Here, we review the current knowledge of recognition-dependent disease resistance in plants. We include a few crucial concepts to compare and contrast plant innate immunity with that more commonly associated with animals. There are appreciable differences, but also surprising parallels.

Plant pathogens and integrated defence responses to infection.

MYB transcription factors in Arabidopsis

Microbe-associated molecular patterns (MAMPs) are molecular signatures typical of whole classes of microbes, and their recognition plays a key role in innate immunity. Endogenous elicitors are similarly recognized as damage-associated molecular patterns (DAMPs). This review focuses on the diversity of MAMPs/DAMPs and on progress to identify the corresponding pattern recognition receptors (PRRs) in plants. The two best-characterized MAMP/PRR pairs, flagellin/FLS2 and EF-Tu/EFR, are discussed in detail and put into a phylogenetic perspective. Both FLS2 and EFR are leucine-rich repeat receptor kinases (LRR-RKs). Upon treatment with flagellin, FLS2 forms a heteromeric complex with BAK1, an LRR-RK that also acts as coreceptor for the brassinolide receptor BRI1. The importance of MAMP/PRR signaling for plant immunity is highlighted by the finding that plant pathogens use effectors to inhibit PRR complexes or downstream signaling events. Current evidence indicates that MAMPs, DAMPs, and effectors are all perceived as danger signals and induce a stereotypic defense response.

A Renaissance of Elicitors: Perception of Microbe-Associated Molecular Patterns and Danger Signals by Pattern-Recognition Receptors

Plants are constantly being challenged by aspiring pathogens, but disease is rare. Why? Broadly, there are three reasons for pathogen failure. Either (1) the plant is unable to support the niche requirements of a potential pathogen and is thus a non? host; or (2) the plant possesses preformed structural barriers or toxic compounds that confine successful infections to specialized pathogen species; or (3) upon recognition of the attacking pathogen, defense mechanisms are elaborated and the invasion remains localized. All three types of interaction are said to be incompatible, but only the latter resistance mech? anism depends on induced responses. Successful pathogen invasion and disease (compatibility) ensue if the preformed plant defenses are inappropriate, the plant does not detect the pathogen, or the activated defense responses are ineffective. In this review, we examine the essential prerequisites for patho? gen recognition and the induction of localized defense responses. Preformed defenses are considered elsewhere in this issue (see Osbourn, 1996, in this issue). Race-specific pathogen recognition is hypothesized to re? sult from the direct or indirect interaction of the product of a dominant or semidominant plant resistance (R) gene with a product derived from the corresponding dominant pathogen avirulence (Avr) gene (Keen, 1992; Staskawicz et al., 1995). Subsequent signal transduction events are assumed to coordinate the activation of an array of defense responses. This "simple" model appears to explain much but begs many questions. For example, R gene products are likely to provide key components for recognition, but how do the distinct classes of R proteins characterized to date (see Bent, 1996, in this is? sue) activate the defense response? Do different R gene classes activate distinct responses? The regulation of some components of defense mechanisms has been studied in plant cell cultures in response to non-race-specific elicitors, but to what extent do such studies provide a model for R gene func? tion? Plant resistance is often correlated with the activation of specific defense responses, but which (if any) are required to abolish or retard pathogen growth, and how? Which are pri? mary responses and which are secondary? Does the first response involve transcriptional regulation, the activation of preformed enzymes, and/or the opening of ion channels, or

Resistance gene-dependent plant defense responses.

BAK1, an Arabidopsis LRR Receptor-like Protein Kinase, Interacts with BRI1 and Modulates Brassinosteroid Signaling

Plants respond to pathogen attack by the induction of a battery of defenses, suggesting that different protective mechanisms may have complementary roles in the overall expression of disease resistance. We have investigated possible functional interactions between two different hydrolytic enzymes, chitinase and glucanase, by constitutive co-expression in transgenic tobacco of genes encoding the rice RCH10 basic chitinase and the alfalfa AGLU1 acidic glucanase. Hybrid plants were generated by crossing transgenic parental lines exhibiting strong constitutive expression of cauliflower mosaic virus (CaMV) 35S enhancer / RCH10 and CaMV 35S double promoter / AGLU1 gene fusions, respectively. Evaluation of disease development in these hybrids, heterozygous for each transgene, and in homozygous selfed progeny, showed that combination of the two transgenes gave substantially greater protection against the fungal pathogen Cercospora nicotianae, causal agent of frogeye, than either transgene alone. Productive interactions between chitinase and glucanase transgenes in vivo point to combinatorial expression of antimicrobial genes as an effective approach to engineering enhanced crop protection against fungal disease.

https://www.philadelphia.edu.jo/academics/smasoud/uploads/P5.pdf

Enhanced Protection Against Fungal Attack by Constitutive Co–expression of Chitinase and Glucanase Genes in Transgenic Tobacco

An assay was developed to study plant receptor kinase activation and signaling mechanisms The extracellular leucine-rich repeat (LRR) and transmembrane domains of the Arabidopsis receptor kinase BRI1, which is implicated in brassinosteroid signaling, were fused to the serine/threonine kinase domain of XA21, the rice disease resistance receptor The chimeric receptor initiates plant defense responses in rice cells upon treatment with brassinosteroids These results, which indicate that the extracellular domain of BRI1 perceives brassinosteroids, suggest a general signaling mechanism for the LRR receptor kinases of plants This system should allow the discovery of ligands for the LRR kinases, the largest group of plant receptor kinases

/pdf/perception-of-brassinosteroids-by-the-extracellular-domain-2lgbaez44q.pdf

Perception of Brassinosteroids by the Extracellular Domain of the Receptor Kinase BRI1

Novel chitinase gene, and its associated regulatory region, from a monocotyledon plant is described.

Rice chitinase promoter

Rice tungro bacilliform virus (RTBV) replicates only in phloem cells in infected rice plants and its promoter drives strong phloem-specific reporter gene expression in transgenic rice plants. We isolated a cDNA encoding a basic leucine zipper (bZIP) protein, RF2a, which binds to the Box II cis element that is important for expression from the promoter. RF2a, which stimulates Box II-dependent transcription in a homologous in vitro transcription system, accumulates in nuclei of phloem and certain other cell types in shoots, but is found at only very low levels in roots. Transgenic antisense plants in which RF2a accumulation was suppressed had normal roots but stunted, twisted leaves with small, disorganized vascular bundles, an enlarged sclerenchyma and large air spaces. We propose that the RTBV promoter exploits a host transcription factor that is critical for leaf tissue differentiation and vascular development for its expression.

/pdf/rf2a-a-bzip-transcriptional-activator-of-the-phloem-specific-1p6egnb05w.pdf

RF2a, a bZIP transcriptional activator of the phloem‐specific rice tungro bacilliform virus promoter, functions in vascular development

Chitinase, which catalyzes the hydrolysis of the beta-1,4-N-acetyl-D-glucosamine linkages of the fungal cell wall polymer chitin, is involved in inducible defenses of plants. A basic chitinase genomic sequence was isolated from a rice (Oryza sativa L.) genomic library using a bean chitinase gene fragment as a probe. The complete nucleotide sequence of the rice chitinase RCH10 gene was determined, and shown to contain an open reading frame with no introns, encoding a polypeptide of 336 amino acids. This polypeptide consists of a 21 amino acid signal peptide, a hevein domain, and a chitinase catalytic domain. The RCH10 gene has 63% identity at the nucleotide level and 75% identity at the amino acid level with chitinase genes from dicotyledonous plants such as bean, potato, and tobacco. A gene fusion of trpE and the coding region of RCH10 expressed in Escherichia coli gave a product that reacted with antiserum to bean chitinase, confirming the identity of RCH10 as a rice chitinase gene. Primer extension analysis identified two transcription start sites 53 bp and 55 bp upstream from the translation initiation codon. The 5' flanking region contains TATA and CAAT boxes, and the 3' region contains an AATAA polyadenylation signal. Southern blot hybridization indicated that there is a family of chitinase genes in the rice genome. Northern blot analysis showed that the RCH10 chitinase gene is induced in suspension cultured cells by a fungal cell wall elicitor. Rice chitinase transcripts accumulate to a high level in roots, but only low levels are found in stem and leaf tissue.

Qun Zhu

Papers

Enhanced Protection Against Fungal Attack by Constitutive Co–expression of Chitinase and Glucanase Genes in Transgenic Tobacco

Perception of Brassinosteroids by the Extracellular Domain of the Receptor Kinase BRI1

Rice chitinase promoter

RF2a, a bZIP transcriptional activator of the phloem‐specific rice tungro bacilliform virus promoter, functions in vascular development

Isolation and characterization of a rice gene encoding a basic chitinase.