Explore the vast range of titles available.

Plants growing in their natural habitats are often challenged simultaneously by multiple stress factors, both abiotic and biotic. Research has so far been limited to responses to individual stresses, and understanding of adaptation to combinatorial stress is limited, but indicative of non-additive interactions. Omics data analysis and functional characterization of individual genes has revealed a convergence of signaling pathways for abiotic and biotic stress adaptation. Taking into account that most data originate from imposition of individual stress factors, this review summarizes these findings in a physiological context, following the pathogenesis timeline and highlighting potential differential interactions occurring between abiotic and biotic stress signaling across the different cellular compartments and at the whole plant level. Potential effects of abiotic stress on resistance components such as extracellular receptor proteins, R-genes and systemic acquired resistance will be elaborated, as well as crosstalk at the levels of hormone, reactive oxygen species, and redox signaling. Breeding targets and strategies are proposed focusing on either manipulation and deployment of individual common regulators such as transcription factors or pyramiding of non- (negatively) interacting components such as R-genes with abiotic stress resistance genes. We propose that dissection of broad spectrum stress tolerance conferred by priming chemicals may provide an insight on stress cross regulation and additional candidate genes for improving crop performance under combined stress. Validation of the proposed strategies in lab and field experiments is a first step toward the goal of achieving tolerance to combinatorial stress in crops.

To establish a successful infection plant viruses have to overcome a defense system composed of several layers. This review will overview the various strategies plants employ to combat viral infections with main emphasis on the current status of single dominant resistance (R) genes identified against plant viruses and the corresponding avirulence (Avr) genes identified so far. The most common models to explain the mode of action of dominant R genes will be presented. Finally, in brief the hypersensitive response (HR) and extreme resistance (ER), and the functional and structural similarity of R genes to sensors of innate immunity in mammalian cell systems will be described.

The gene-for-gene relationship of host–pathogen interaction explained by H. H. Flor in mid of the 20th century set a milestone in understanding the biochemical and genetic basis of plant diseases and several components involved in plant–pathogen interactions. It highlighted the importance of accomplishing differential sets and understanding the pathogen population structure, it further led to the identification and cloning of several resistance (R) genes in plants. These R genes have been deployed and altered for fighting against diseases in a large number of crops using various conventional approaches and biotechnological tools. Identification of R genes and their corresponding Avr genes in many cases played a significant role in understanding of R-Avr gene interactions. Rapid cloning of R genes and editing of susceptible R genes are the other avenues that have broadened the horizon of utilizing R genes in crop improvement programmes. Further, combining R genes with quantitative disease resistance genes has paved the way to develop durable resistance in cultivars. The recent advances in genetics, genomics, bioinformatics and other OMICS tools are now providing greater prospects for deeper understanding of host–pathogen interaction.

Next-generation sequencing allows the identification of mutations responsible for mutant phenotypes by whole-genome resequencing and alignment to a reference genome. However, when the resequenced cultivar/line displays significant structural variation from the reference genome, mutations in the genome regions missing from the reference (gaps) cannot be identified by simple alignment. Here we report on a method called ‘MutMap-Gap’, which involves delineating a candidate region harboring a mutation of interest using the recently reported MutMap method, followed by de novo assembly, alignment, and identification of the mutation within genome gaps. We applied MutMap-Gap to isolate the blast resistant gene Pii from the rice cv Hitomebore using mutant lines that have lost Pii function. MutMap-Gap should prove useful for cloning genes that exhibit significant structural variations such as disease resistance genes of the nucleotide-binding site-leucine rich repeat (NBSLRR) class.

Transcription activator-like (TAL) effectors are bacterial type III secretion proteins that function as transcription factors in plants during Xanthomonas/plant interactions, conditioning either host susceptibility and/or host resistance. Three types of TAL effector associated resistance (R) genes have been characterized-recessive, dominant non-transcriptional, and dominant TAL effector-dependent transcriptional based resistance. Here, we discuss the last type of R genes, whose functions are dependent on direct TAL effector binding to discrete effector binding elements in the promoters. Only five of the so-called executor R genes have been cloned, and commonalities are not clear. We have placed the protein products in two groups for conceptual purposes. Group 1 consists solely of the protein from pepper, BS3, which is predicted to have catalytic function on the basis of homology to a large conserved protein family. Group 2 consists of BS4C-R, XA27, XA10, and XA23, all of which are relatively short proteins from pepper or rice with multiple potential transmembrane domains. Group 2 members have low sequence similarity to proteins of unknown function in closely related species. Firm predictions await further experimentation on these interesting new members to the R gene repertoire, which have potential broad application in new strategies for disease resistance.

The major resistance gene BvCR4 recently bred into sugar beet hybrids provides a high level of resistance to Cercospora leaf spot caused by the fungal pathogen Cercospora beticola. The occurrence of pathogen strains that overcome BvCR4 was studied using field trials in Switzerland conducted under natural disease pressure. Virulence of a subset of these strains was evaluated in a field trial conducted under elevated artificial disease pressure. We created a new C. beticola reference genome and mapped whole genome sequences of 256 isolates collected in Switzerland and Germany. These were combined with virulence phenotypes to conduct three separate genome‐wide association studies (GWAS) to identify candidate avirulence genes. We identified a locus associated with avirulence containing a putative avirulence effector gene named AvrCR4. All virulent isolates either lacked AvrCR4 or had nonsynonymous mutations within the gene. AvrCR4 was present in all 74 isolates from non‐BvCR4 hybrids, whereas 33 of 89 isolates from BvCR4 hybrids carried a deletion. We also mapped genomic data from 190 publicly available US isolates to our new reference genome. The AvrCR4 deletion was found in only one of 95 unique isolates from non‐BvCR4 hybrids in the United States. AvrCR4 presents a unique example of an avirulence effector in which virulent alleles have only recently emerged. Most likely these were selected out of standing genetic variation after deployment of BvCR4. Identification of AvrCR4 will enable real‐time screening of C. beticola populations for the emergence and spread of virulent isolates. We found a candidate avirulence effector gene in the pathogen that causes Cercospora leaf spot on sugar beet; gene presence/absence is related to avirulence/virulence on resistant sugar beet hybrids.

Background Gene copy number divergence between species is a form of genetic polymorphism that contributes significantly to both genome size and phenotypic variation. In plants, copy number expansions of single genes were implicated in cultivar- or species-specific tolerance of high levels of soil boron, aluminium or calamine-type heavy metals, respectively. Arabidopsis halleri is a zinc- and cadmium-hyperaccumulating extremophile species capable of growing on heavy-metal contaminated, toxic soils. In contrast, its non-accumulating sister species A. lyrata and the closely related reference model species A. thaliana exhibit merely basal metal tolerance. Results For a genome-wide assessment of the role of copy number divergence (CND) in lineage-specific environmental adaptation, we conducted cross-species array comparative genome hybridizations of three plant species and developed a global signal scaling procedure to adjust for sequence divergence. In A. halleri , transition metal homeostasis functions are enriched twofold among the genes detected as copy number expanded. Moreover, biotic stress functions including mostly disease Resistance ( R ) gene-related genes are enriched twofold among genes detected as copy number reduced, when compared to the abundance of these functions among all genes. Conclusions Our results provide genome-wide support for a link between evolutionary adaptation and CND in A. halleri as shown previously for Heavy metal ATPase4 . Moreover our results support the hypothesis that elemental defences, which result from the hyperaccumulation of toxic metals, allow the reduction of classical defences against biotic stress as a trade-off.

It has frequently been hypothesized that quantitative resistance increases the durability of qualitative (R-gene mediated) resistance but supporting experimental evidence is rare. To test this hypothesis, near-isogenic lines with/without the R-gene Rlm6 introduced into two Brassica napus cultivars differing in quantitative resistance to Leptosphaeria maculans were used in a 5-yr field experiment. Recurrent selection of natural fungal populations was done annually on each of the four plant genotypes, using crop residues from each genotype to inoculate separately the four series of field trials for five consecutive cropping seasons. Severity of phoma stem canker was measured on each genotype and frequencies of avirulence alleles in L. maculans populations were estimated. Recurrent selection of virulent isolates by Rlm6 in a susceptible background rendered the resistance ineffective by the third cropping season. By contrast, the resistance was still effective after 5 yr of selection by the genotype combining this gene with quantitative resistance. No significant variation in the performance of quantitative resistance alone was noted over the course of the experiment. We conclude that quantitative resistance can increase the durability of Rlm6. We recommend combining quantitative resistance with R-gene mediated resistance to enhance disease control and crop production.

How can we best vary the application of pesticides and antibiotics to delay resistance evolution? Previous theoretical comparisons of deployment strategies have focused on qualitative resistance traits and have mostly assumed that resistance alleles are already present in a population. But many real resistance traits are quantitative, and the evolution of resistant genotypes in the field may depend on de novo mutation and recombination. Here, I use an individual‐based, forward‐time, quantitative‐genetic simulation model to investigate the evolution of quantitative resistance. I evaluate the performance of four application strategies for delaying resistance evolution, to wit, the (1) sequential, (2) mosaic, (3) periodic, and (4) combined strategies. I find that which strategy is best depends on initial efficacy. When at the onset, xenobiotics completely prevent reproduction in treated demes, a combined strategy is best. On the other hand, when populations are partially resistant, the combined strategy is inferior to mosaic and periodic strategies, especially when resistance alleles are antagonistically pleiotropic. Thus, the optimal application strategy for managing against the rise of quantitative resistance depends on pleiotropy and whether or not partial resistance is already present in a population. This result appears robust to variation in pest reproductive mode and migration rate, direct fitness costs for resistant phenotypes, and the extent of refugial habitats.

Background: Resistance (R) genes are crucial for defending Perilla against pathogens like anthracnose, downy mildew, and phytophthora blight. Nucleotide-binding site leucine-rich repeat (NBS-LRR) genes, the largest R-gene family, play a central role in immunity. This study aimed to identify and characterize NBS-LRR genes in P. citriodora ‘Jeju17’. Methods: Previously conducted genome-wide data for ‘Jeju17’ were analyzed in silico to identify NBS-LRR genes. Results: A total of 535 NBS-LRR genes were identified, with clusters on chromosomes 2, 4, and 10. A unique RPW8-type R-gene was located on chromosome 7. Conclusions: This study provides insights into the NBS-LRR gene family in ‘Je-ju17’, highlighting its role in disease resistance and evolutionary dynamics. By identifying can-didate R-genes, this research supports breeding programs to develop disease-resistant cultivars and improves our understanding of plant immunity.