PR genes, a small part belong to the large defensesignaling network confer resistance to many pathogens. I will briefly introduce the mechnism of R gene mediated responses in the following paragraphs.
R gene mediated responses.
Each R gene confers resistance to a specific pathogen. Hypersensitive response (HR) is always the first phenotype appears in the plant defence system when respond to R gene mediated resistance. Programmed cell death (PCD) is induced by HR then, occurs at the site of infection and reveals lesions that protects virus or infections from spreading to healthy cells nearby immediately. Systemic acquired resistance (SAR) occurs in the distant tissues following the railar response, hypersensitive response, is treated as the second phenotype of this resistance. It is evolutionarily conserved that inhance the immunity of those tissues to the infection or the similar ones. Once actived by the accumulation of endogenous salicylic acid (SA) (essential condition), it can last for weeks. This response is related to the induction of several genes called PR (pathogenesis-related genes).
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SA and jasmonic acid (JA) are believed to play an important role in the complex signaling networks that mediate plant denfence response to invasion.
In response to pathogen infection, SA is synthesized via the isochorismate pathway (Wildermuth et al., 2001§). Signaling proceeds via the central regulator NPR1, which oligomerizes in the cytoplasm, facilitated by Snitrosylation (Tada et al., 2008§). Thioredoxin catalyzes the SA induced release of NPR1 monomers, which translocate to the nucleus where they interact with TGA transcription factors and induce expression of specific defense genes (Dong, 2004§; Pieterse and Van Loon, 2004§; Tada et al., 2008§). Additional components, such as the transcription factor WRKY70, are required for full expression of SAresponsive defense genes
R protein structure.
Strikingly, they all belong to the NBARCLRR superfamily of plant R genes. The nucleotide-binding site contains three motifs that are required for nucleotide binding in other ATP/GTPbinding proteins. The nucleotidebinding (NB) site domain and adjacent sequences of R genes are similar to the equivalent regions of the metazoan celldeath genes Apaf1 and CED4 (Ref. 3) and are therefore referred to as the NBARC domains. ATPase activity has been shown for two R proteins but the role of ATP hydrolysis in R protein function is unclear. Leucine-rich repeats (LRRs) are imperfect repeats that are involved in protein-protein interactions and protein-ligand interactions. The LRRs of mammalian Tolllike receptors (TLRs) interact with pathogenderived molecules to initiate defence responses. In addition, plant R proteins of this superfamily bear striking resemblance to mammalian NODS (nucleotidebinding oligomerization domain), which are intracellular NBARCLRR proteins involved in defence.
Although these R proteins are similar, they confer resistance to highly divergent viruses. For example, Arabidopsis thaliana RCY1 (resistance to C strain Y1) and HRT (HR to turnip crinkle virus) are allelic and encode proteins that share 91% similarity but confer resistance to unrelated viruses: cucumber mosaic virus (CMV, a cucumovirus) and turnip crinkle virus (TCV, a carmovirus), respectively. Any model developed to describe Rprotein recognition of a pathogen must take into account the striking molecular similarity but functional divergence of R proteins.
R protein domain function.
Extensive structure-function analyses of R protein domains have been carried out. Mutations in all three domains of the Nicotiana glutinosa N protein compromise resistance to tobacco mosaic virus (TMV), indicating that each domain might have important roles in pathogen recognition and/or signalling.
There have also been attempts to identify the domains that confer recognition specificity on R proteins. Domain swaps between different alleles of the flax L gene, which confers resistance to a fungal pathogen, indicated that both the LRR and the TIR domains have roles in the recognition of R proteins. Several residues in these proteins might be undergoing positive selection, and most of them are found within the LRR domain (J.L.M.S. and S.P.D.K., unpublished).
Intramolecular rearrangements within R proteins have also been shown to be involved in recognition. Coexpression of CCNBARC and LRR domains or CC and NBARCLRR domains of S. tuberosum Rx1 results in a HR in the presence of the PVX coatprotein Avr (avirulence) determinant, mimicking the function of the intact Rx1 protein. The CCNBARC and LRR or the CC and NBARCLRR coimmunoprecipitate, but this interaction is abrogated in the presence of the coat protein. These results indicate that there are specific interactions between the domains of S. tuberosum Rx1 and that the coat protein disturbs the native conformation of Rx1. It is probable that molecular interactions within S. tuberosum Rx1 hold the protein in a conformation that is poised for signalling but is inhibited from doing so. Addition of the Avr determinant releases the inhibition and allows defence signalling. Evidence for intramolecular interactions has also been obtained for the tomato Mi1 R protein, which confers resistance to a nematode.
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Recognition of Avr determinants.
Any protein component of a virus can function as the specific Avr determinant to elicit resistance mediated by a given R gene (Table 1). Despite the availability of several cloned R genes and their cognate Avr determinants (Table 1), progress in understanding how pathogen Avr proteins are recognized has been slow. Initially, receptor-ligand models were proposed to describe the interactions between R and Avr proteins (Fig. 2a). However, this simple model does not apply to any viral R-Avr pair examined to date, although it has been shown to apply in two cases of bacterial and one case of fungal resistance2. A more sophisticated model of R-Avr interactions invokes the involvement of Rproteincontaining complexes. The 'guard hypothesis', originally proposed by Van der Biezen and Jones19, postulates that R proteins (guards) are constitutively associated with host cellular proteins (guardees) that are required by pathogens for infection (Fig. 2b). On infection, the pathogen causes modifications to the guardee that are detected by the guard (Fig. 2c). Any protein modification that can alter the quaternary structure of the guardee could result in detection of the pathogen. This activates the guard to initiate a signalling cascade that culminates in the resistance response.
Genetic engineering enables new ways of managing fungal infections.
1. Some components of fungal cell walls, in terms of chitin or glucan can easily be broken down by enzymes chitinase or glucanase respectively. Hence, inducing genes encoding these enzymes to target plants can be a solution to fungal infections.
2. Introducing plant genes to enhance innate plant defense mechanisms (e.g. activing phytoalexins, proteinase inhibitors, or toxic proteins).
Invoking the hypersensitive reaction: Plants varieties that are naturally resistant to specific types of fungal diseases are often programmed to have individual cells quickly die at the site of fungal infection. This response, known as the hypersensitive reaction, effectively stops an infection in its tracks. Genetic engineering can help plant cells 'know' when a fungus is attacking
Four different lines were chosed to perform this experiment. Foliar resistance, tuber resistance and yield performancce were evaluated respectively. All of the RB transgenic lines exhibited an increase in resistance to P. infestans when compared with their non-transgenic counterparts. The increase in foliar resistance did not significantly de-crease tuber yield, the most important aspect of potato production value, in the absence of late blight. We also were unable to detect any significant effect on yield after the incorporation of the RB gene into various potato cultivars.
RB-transgenic tuber resistance assays
Assay of foliar resistance to P. i n -festans
To achieve durable resistance against the late blight, there are eight basic principles:
1. Bacterial vectors are used to transform target genes into plants to contain the same phenotypes as the origin. The resulting resistant potato varieties contain potato genes only without any bacterial genes and no new varieties are created. The start and end products are potato varieties made up of potato genes only.
It is better to use natural R genes from the wild potato species because it was assumed that this approach was ethically more acceptable to the public than the use of alien genes from not crossable species.
3. Due to the possibility of a single R gene being rapidly broken down, it is better to insert several resistence genes, normally two, four at most, from different species to improve the duration of resistence. In addition, Phytophthora infestans have the abbility to bypass the R genes. Hence, it is not wise to stack R genes at the same site. Instead, decorating those different varieties in different locations at different time.
4. DuRPh does not use selection markers such as herbicide tolerance or antibiotic resistance to select for insertion of the desired gene(s) in the variety. The achieved late blight resistanc e is the main marker so the variety is marker free. To assure that the R gene is (or the R genes are) present the genotypes that appear resistant to all known pathotypes of Phytopht hora infestans are tested using PCR techniques.
7. DuRPh dedicates a considerable proportion of its efforts to communication with all stakeholders concerned. By being transparent regarding philosophy, approaches, techniques, and results it is up to individuals and groups to make their own decision about appreciation of the techniques used.
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The exploitation of the R genes with proven efficacy and known not to be homologous to previously discovered ones is by protecting the intellectual proper ty and making them available (not exclusively) to private potato breeding companie s; once these genes are exploited in new varieties the prvate companies reimburse the owners through breeding right agreements. For developing countries where food security is an issue human itarianaid through R genes is an option.
PR genes are categorized into more than fifteen families (Van Loon et al., 2006§), PR1 family, most commonly used disease resistance markers, included. The PR1 family of genes are some of the most ubiquitous, showing a strong conservation across species, and as such, appear to be represented across all plant species, with homologs present in fungi, insects and vertebrates (Van Loon et al., 2006§). However only a single member of the PR1 family is actived by pathogen infection, insect feeding, or chemical treatment, while ten PR1 type genes are constitutively expressed in roots and eight in pollen (Van Loon et al., 2006§). In contrast to the PR1 family, several additional PR groups have also been widely studied, including members of the PR12 family, also known as defensins, which have members exhibiting antifungal activity.
Resistance is termed durable if it continues to be effective over multiple years of widespread use, but it somtimes appears limited value baceuse invaders may evolve quickly to overcome this resistance. However, it isvery time-consuming (only the analysis step may take several months) use recent maping based technology to discovery new R genes. Hence, it is importance to find a new method to cut the time of identifying advenced R genes
Ross, H. (1986) Potato breedin g. Problems and perspectives. Adv. Plant. Breed . Sup pl.13, 82-86.