Scientific breeding for disease resistance originated with Sir Rowland Biffen , who identified a single recessive gene for resistance to wheat yellow rust. Nearly every crop was then bred to include disease resistance R genes, many by introgression from compatible wild relatives. The term GM "genetically modified" is often used as a synonym of transgenic to refer to plants modified using recombinant DNA technologies. Transgenic plant disease resistance against microbial pathogens was first demonstrated in Expression of viral coat protein gene sequences conferred virus resistance via small RNAs.
This proved to be a widely applicable mechanism for inhibiting viral replication.
Complete genome sequence of the plant commensal Pseudomonas fluorescens Pf The genome of WCS therefore remained distributed over eight scaffolds. Bold, H. Dordrecht, Germany: Kluwer Academic Publishers. Theophrastus c. Induced resistance - orchestrating defence mechanisms through cross-talk and priming. Pseudomonas syringae — tomato interactions: an unfolding New York story.
Similar levels of resistance to this variety of viruses had not been achieved by conventional breeding. Field trials demonstrated excellent efficacy and high fruit quality. By the first transgenic virus-resistant papaya was approved for sale. Disease resistance has been durable for over 15 years.
The fruit is approved for sale in the U. Potato lines expressing viral replicase sequences that confer resistance to potato leafroll virus were sold under the trade names NewLeaf Y and NewLeaf Plus, and were widely accepted in commercial production in , until McDonald's Corp. No other crop with engineered disease resistance against microbial pathogens had reached the market by , although more than a dozen were in some state of development and testing.
Research aimed at engineered resistance follows multiple strategies.
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One is to transfer useful PRRs into species that lack them. Identification of functional PRRs and their transfer to a recipient species that lacks an orthologous receptor could provide a general pathway to additional broadened PRR repertoires. Research performed at Sainsbury Laboratory demonstrated that deployment of EFR into either Nicotiana benthamiana or Solanum lycopersicum tomato , which cannot recognize EF-Tu , conferred resistance to a wide range of bacterial pathogens.
EFR expression in tomato was especially effective against the widespread and devastating soil bacterium Ralstonia solanacearum. The second strategy attempts to deploy multiple NLR genes simultaneously, a breeding strategy known as stacking. Cultivars generated by either DNA-assisted molecular breeding or gene transfer will likely display more durable resistance, because pathogens would have to mutate multiple effector genes. The avrBs2 effector gene from Xanthomona perforans is the causal agent of bacterial spot disease of pepper and tomato. The Bs2 NLR gene from the wild pepper, Capsicum chacoense , was moved into tomato, where it inhibited pathogen growth.
Field trials demonstrated robust resistance without bactericidal chemicals. However, rare strains of Xanthomonas overcame Bs2 -mediated resistance in pepper by acquisition of avrBs2 mutations that avoid recognition but retain virulence. Stacking R genes that each recognize a different core effector could delay or prevent adaptation. More than 50 loci in wheat strains confer disease resistance against wheat stem, leaf and yellow stripe rust pathogens. The Stem rust 35 Sr35 NLR gene, cloned from a diploid relative of cultivated wheat, Triticum monococcum , provides resistance to wheat rust isolate Ug Similarly, Sr33 , from the wheat relative Aegilops tauschii , encodes a wheat ortholog to barley Mla powdery mildew—resistance genes.
Both genes are unusual in wheat and its relatives. Combined with the Sr2 gene that acts additively with at least Sr33, they could provide durable disease resistance to Ug99 and its derivatives. Xanthomonas and Ralstonia transcription activator —like TAL effectors are DNA-binding proteins that activate host gene expression to enhance pathogen virulence.
Both the rice and pepper lineages independently evolved TAL-effector binding sites that instead act as an executioner that induces hypersensitive host cell death when up-regulated.
Executor genes are expressed only in the presence of a specific TAL effector. Engineered executor genes were demonstrated by successfully redesigning the pepper Bs3 promoter to contain two additional binding sites for TAL effectors from disparate pathogen strains. Subsequently, an engineered executor gene was deployed in rice by adding five TAL effector binding sites to the Xa27 promoter. The synthetic Xa27 construct conferred resistance against Xanthomonas bacterial blight and bacterial leaf streak species.
Most plant pathogens reprogram host gene expression patterns to directly benefit the pathogen. For example, a mutation disabled an Arabidopsis gene encoding pectate lyase involved in cell wall degradation , conferring resistance to the powdery mildew pathogen Golovinomyces cichoracearum. Lr34 is a gene that provides partial resistance to leaf and yellow rusts and powdery mildew in wheat. The dominant allele that provides disease resistance was recently found in cultivated wheat not in wild strains and, like MLO provides broad-spectrum resistance in barley.
Natural alleles of host translation elongation initiation factors eif4e and eif4g are also recessive viral-resistance genes. Some have been deployed to control potyviruses in barley, rice, tomato, pepper, pea, lettuce and melon. The discovery prompted a successful mutant screen for chemically induced eif4e alleles in tomato. Natural promoter variation can lead to the evolution of recessive disease-resistance alleles.
For example, the recessive resistance gene xa13 in rice is an allele of Os-8N3.
Os-8N3 is transcriptionally activated by Xanthomonas oryzae pv. The xa13 gene has a mutated effector-binding element in its promoter that eliminates PthXo1 binding and renders these lines resistant to strains that rely on PthXo1. This finding also demonstrated that Os-8N3 is required for susceptibility. Genome-edited rice plants with altered Os11N3 binding sites remained resistant to Xanthomonas oryzae pv.
RNA silencing -based resistance is a powerful tool for engineering resistant crops. The advantage of RNAi as a novel gene therapy against fungal, viral and bacterial infection in plants lies in the fact that it regulates gene expression via messenger RNA degradation, translation repression and chromatin remodelling through small non-coding RNAs.
Among the thousands of species of plant pathogenic microorganisms, only a small minority have the capacity to infect a broad range of plant species.
Most pathogens instead exhibit a high degree of host-specificity. Non-host plant species are often said to express non-host resistance. The term host resistance is used when a pathogen species can be pathogenic on the host species but certain strains of that plant species resist certain strains of the pathogen species. The causes of host resistance and non-host resistance can overlap. Native populations are often characterized by substantial genotype diversity and dispersed populations growth in a mixture with many other plant species.
They also have undergone of plant-pathogen coevolution. These factors make modern agriculture more prone to disease epidemics. Deletions in the Repertoire of Pseudomonas syringae pv. Kvitko, B.
A Draft Genome Sequence of Pseudomonas syringae pv. Almeida, N.
Advances in experimental methods for the elucidation of Pseudomonas syringae effector function with a focus on AvrPtoB. Molecular Plant Pathology. Shan, L. A bacterial E3 ubiquitin ligase targets a host protein kinase to disrupt plant immunity. Rosebrock, T.
Xiao, F. A Pseudomonas syringae pv. Wei, C. HEJ, Vossen, J.