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230,442 result(s) for "disease resistance"
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Resistance gene cloning from a wild crop relative by sequence capture and association genetics
Disease resistance (R) genes from wild relatives could be used to engineer broad-spectrum resistance in domesticated crops. We combined association genetics with R gene enrichment sequencing (AgRenSeq) to exploit pan-genome variation in wild diploid wheat and rapidly clone four stem rust resistance genes. AgRenSeq enables R gene cloning in any crop that has a diverse germplasm panel.The treasure trove of disease resistance genes present in wild relatives of domesticated crops is rapidly discovered using association genetics and enrichment sequencing.
New reference genome sequences of hot pepper reveal the massive evolution of plant disease-resistance genes by retroduplication
Background Transposable elements are major evolutionary forces which can cause new genome structure and species diversification. The role of transposable elements in the expansion of nucleotide-binding and leucine-rich-repeat proteins (NLRs), the major disease-resistance gene families, has been unexplored in plants. Results We report two high-quality de novo genomes ( Capsicum baccatum and C. chinense ) and an improved reference genome ( C. annuum ) for peppers. Dynamic genome rearrangements involving translocations among chromosomes 3, 5, and 9 were detected in comparison between C. baccatum and the two other peppers. The amplification of athila LTR-retrotransposons, members of the gypsy superfamily, led to genome expansion in C. baccatum . In-depth genome-wide comparison of genes and repeats unveiled that the copy numbers of NLRs were greatly increased by LTR-retrotransposon-mediated retroduplication. Moreover, retroduplicated NLRs are abundant across the angiosperms and, in most cases, are lineage-specific. Conclusions Our study reveals that retroduplication has played key roles for the massive emergence of NLR genes including functional disease-resistance genes in pepper plants.
Two unequally redundant \helper\ immune receptor families mediate Arabidopsis thaliana intracellular \sensor\ immune receptor functions
Plant nucleotide-binding (NB) leucine-rich repeat (LRR) receptor (NLR) proteins function as intracellular immune receptors that perceive the presence of pathogen-derived virulence proteins (effectors) to induce immune responses. The 2 major types of plant NLRs that \"sense\" pathogen effectors differ in their N-terminal domains: these are Toll/interleukin-1 receptor resistance (TIR) domain-containing NLRs (TNLs) and coiled-coil (CC) domain-containing NLRs (CNLs). In many angiosperms, the RESISTANCE TO POWDERY MILDEW 8 (RPW8)-CC domain containing NLR (RNL) subclass of CNLs is encoded by 2 gene families, ACTIVATED DISEASE RESISTANCE 1 (ADR1) and N REQUIREMENT GENE 1 (NRG1), that act as \"helper\" NLRs during multiple sensor NLR-mediated immune responses. Despite their important role in sensor NLR-mediated immunity, knowledge of the specific, redundant, and synergistic functions of helper RNLs is limited. We demonstrate that the ADR1 and NRG1 families act in an unequally redundant manner in basal resistance, effector-triggered immunity (ETI) and regulation of defense gene expression. We define RNL redundancy in ETI conferred by some TNLs and in basal resistance against virulent pathogens. We demonstrate that, in Arabidopsis thaliana, the 2 RNL families contribute specific functions in ETI initiated by specific CNLs and TNLs. Time-resolved whole genome expression profiling revealed that RNLs and \"classical\" CNLs trigger similar transcriptome changes, suggesting that RNLs act like other CNLs to mediate ETI downstream of sensor NLR activation. Together, our genetic data confirm that RNLs contribute to basal resistance, are fully required for TNL signaling, and can also support defense activation during CNL-mediated ETI.
Receptor Kinases in Plant-Pathogen Interactions
Receptor-like kinases (RLKs) and Receptor-like proteins (RLPs) play crucial roles in plant immunity, growth, and development. Plants deploy a large number of RLKs and RLPs as pattern recognition receptors (PRRs) that detect microbe- and host-derived molecular patterns as the first layer of inducible defense. Recent advances have uncovered novel PRRs, their corresponding ligands, and mechanisms underlying PRR activation and signaling. In general, PRRs associate with other RLKs and function as part of multiprotein immune complexes at the cell surface. Innovative strategies have emerged for the rapid identification of microbial patterns and their cognate PRRs. Successful pathogens can evade or block host recognition by secreting effector proteins to “hide” microbial patterns or inhibit PRR-mediated signaling. Furthermore, newly identified pathogen effectors have been shown to manipulate RLKs controlling growth and development by mimicking peptide hormones of host plants. The ongoing studies illustrate the importance of diverse plant RLKs in plant disease
Rice phenylalanine ammonia-lyase gene OsPAL4 is associated with broad spectrum disease resistance
Most agronomically important traits, including resistance against pathogens, are governed by quantitative trait loci (QTL). QTL-mediated resistance shows promise of being effective and long-lasting against diverse pathogens. Identification of genes controlling QTL-based disease resistance contributes to breeding for cultivars that exhibit high and stable resistance. Several defense response genes have been successfully used as good predictors and contributors to QTL-based resistance against several devastating rice diseases. In this study, we identified and characterized a rice (Oryza sativa) mutant line containing a 750 bp deletion in the second exon of OsPAL4, a member of the phenylalanine ammonia-lyase gene family. OsPAL4 clusters with three additional OsPAL genes that co-localize with QTL for bacterial blight and sheath blight disease resistance on rice chromosome 2. Self-pollination of heterozygous ospal4 mutant lines produced no homozygous progeny, suggesting that homozygosity for the mutation is lethal. The heterozygous ospal4 mutant line exhibited increased susceptibility to three distinct rice diseases, bacterial blight, sheath blight, and rice blast. Mutation of OsPAL4 increased expression of the OsPAL2 gene and decreased the expression of the unlinked OsPAL6 gene. OsPAL2 function is not redundant because the changes in expression did not compensate for loss of disease resistance. OsPAL6 co-localizes with a QTL for rice blast resistance, and is down-regulated in the ospal4 mutant line; this may explain enhanced susceptibility to Magnoporthe oryzae. Overall, these results suggest that OsPAL4 and possibly OsPAL6 are key contributors to resistance governed by QTL and are potential breeding targets for improved broad-spectrum disease resistance in rice.
Understanding sheath blight resistance in rice: the road behind and the road ahead
Rice sheath blight disease, caused by the basidiomycetous necrotroph Rhizoctonia solani, became one of the major threats to the rice cultivation worldwide, especially after the adoption of high-yielding varieties. The pathogen is challenging to manage because of its extensively broad host range and high genetic variability and also due to the inability to find any satisfactory level of natural resistance from the available rice germplasm. It is high time to find remedies to combat the pathogen for reducing rice yield losses and subsequently to minimize the threat to global food security. The development of genetic resistance is one of the alternative means to avoid the use of hazardous chemical fungicides. This review mainly focuses on the effort of better understanding the host–pathogen relationship, finding the gene loci/markers imparting resistance response and modifying the host genome through transgenic development. The latest development and trend in the R. solani–rice pathosystem research with gap analysis are provided.
Genome Editing: Targeting Susceptibility Genes for Plant Disease Resistance
Plant pathogens pose a major threat to crop productivity. Typically, phytopathogens exploit plants’ susceptibility (S) genes to facilitate their proliferation. Disrupting these S genes may interfere with the compatibility between the host and the pathogens and consequently provide broad-spectrum and durable disease resistance. In the past, genetic manipulation of such S genes has been shown to confer disease resistance in various economically important crops. Recent studies have accomplished this task in a transgene-free system using new genome editing tools, including clustered regularly interspaced palindromic repeats (CRISPR). In this Opinion article, we focus on the use of genome editing to target S genes for the development of transgene-free and durable disease-resistant crop varieties. CRISPR has emerged as a revolutionary tool for plant genome editing. Although developed recently, it has been established in several important plant species, including rice, wheat, and maize, to introduce agronomically important traits such as heat/cold tolerance, disease resistance, herbicide tolerance, and yield improvement. Transgene-free methods are being introduced in CRISPR-mediated plant genome editing, such as segregating out transgenes, delivering the ribonucleoprotein complex of Cas9 and gRNA through particle bombardment or using a protoplast system, and using viral vectors for editing germline cells. Targeting susceptibility (S) genes using CRISPR methodologies offers new frontiers to break molecular plant–microbe compatibility and introducing durable pathogen resistance.
Wheat receptor-kinase-like protein Stb6 controls gene-for-gene resistance to fungal pathogen Zymoseptoria tritici
Deployment of fast-evolving disease-resistance genes is one of the most successful strategies used by plants to fend off pathogens 1 , 2 . In gene-for-gene relationships, most cloned disease-resistance genes encode intracellular nucleotide-binding leucine-rich-repeat proteins (NLRs) recognizing pathogen-secreted isolate-specific avirulence (Avr) effectors delivered to the host cytoplasm 3 , 4 . This process often triggers a localized hypersensitive response, which halts further disease development 5 . Here we report the map-based cloning of the wheat Stb6 gene and demonstrate that it encodes a conserved wall-associated receptor kinase (WAK)-like protein, which detects the presence of a matching apoplastic effector 6 – 8 and confers pathogen resistance without a hypersensitive response 9 . This report demonstrates gene-for-gene disease resistance controlled by this class of proteins in plants. Moreover, Stb6 is, to our knowledge, the first cloned gene specifying resistance to Zymoseptoria tritici , an important foliar fungal pathogen affecting wheat and causing economically damaging septoria tritici blotch (STB) disease 10 – 12 . The authors report map-based cloning of the wheat Stb6 gene, which encodes a conserved wall-associated receptor kinase (WAK)-like protein. Stb6 confers gene-for-gene disease resistance to fungal pathogen Zymoseptoria tritici by recognition of a matching pathogen effector.
Plant Disease Resistance-Related Signaling Pathways: Recent Progress and Future Prospects
Plant–pathogen interactions induce a signal transmission series that stimulates the plant’s host defense system against pathogens and this, in turn, leads to disease resistance responses. Plant innate immunity mainly includes two lines of the defense system, called pathogen-associated molecular pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). There is extensive signal exchange and recognition in the process of triggering the plant immune signaling network. Plant messenger signaling molecules, such as calcium ions, reactive oxygen species, and nitric oxide, and plant hormone signaling molecules, such as salicylic acid, jasmonic acid, and ethylene, play key roles in inducing plant defense responses. In addition, heterotrimeric G proteins, the mitogen-activated protein kinase cascade, and non-coding RNAs (ncRNAs) play important roles in regulating disease resistance and the defense signal transduction network. This paper summarizes the status and progress in plant disease resistance and disease resistance signal transduction pathway research in recent years; discusses the complexities of, and interactions among, defense signal pathways; and forecasts future research prospects to provide new ideas for the prevention and control of plant diseases.