Host-pathogen coevolution promotes the evolution of general, broad-spectrum resistance and reduces foreign pathogen spillover risk.

Breeding crops with the quality of broad-spectrum disease resistance using genetic resources is one of the principal goals of crop improvement. However, the molecular mechanism of broad-spectrum resistance remains largely unknown. Here, we show that GH3-2, encoding an indole-3-acetic acid (IAA)-amido synthetase, mediates a broad-spectrum resistance to bacterial Xanthomonas oryzae pv oryzae and Xanthomonas oryzae pv oryzicola and fungal Magnaporthe grisea in rice (Oryza sativa). IAA, the major form of auxin in rice, results in rice more vulnerable to the invasion of different types of pathogens, which is at least partly due to IAA-induced loosening of the cell wall, the natural protective barrier of plant cells to invaders. X. oryzae pv oryzae, X. oryzae pv oryzicola, and M. grisea secrete IAA, which, in turn, may induce rice to synthesize its own IAA at the infection site. IAA induces the production of expansins, the cell wall-loosening proteins, and makes rice vulnerable to pathogens. GH3-2 is likely contributing to a minor quantitative trait locus for broad-spectrum resistance. Activation of GH3-2 inactivates IAA by catalyzing the formation of an IAA-amino acid conjugate, which results in the suppression of expansin genes. Thus, GH3-2 mediates basal resistance by suppressing pathogen-induced IAA accumulation. It is expected that, regulated by a pathogen-induced strong promoter, GH3-2 alone may be used for breeding rice with a broad-spectrum disease resistance.

The identification and utilization of broad-spectrum resistance genes have been proven the most effective and economical approach to control rice blast disease. To understand the molecular mechanism of broad-spectrum resistance to rice blast, we conducted genetic and fine mapping analysis of the blast resistance gene in a Chinese rice variety: Gumei 4 (GM4) identified with broad-spectrum resistance and used in rice breeding for blast resistance for more than 20 years. Genetic and mapping analysis indicated that blast resistance to nine isolates of different Chinese races in GM4 was controlled by the same dominant locus designated as Pigm(t) that was finely mapped to an approximately 70-kb interval between markers C5483 and C0428 on chromosome 6, which contains five candidate NBS--LRR disease resistance genes. The allelism test showed that Pigm(t) was either tightly linked or allelic to Pi2 and Pi9, two known blast resistance genes. Mapping information also indicated that another blast resistance gene Pi26(t) might also be located at the same region. Candidate genes were identified by sequence analysis of the Nipponbare and Pi9 locus and the corresponding region in GM4. Sequence divergence of candidate genes was observed between GM4 and model varieties Nipponbare and 9311, and Pi9. Our current study provides essential information and new genetic resource for the cloning of functional resistance gene(s) and for marker-assisted selection in rice breeding for broad-spectrum blast resistance.

SummaryStudies conducted on natural host‐pathogen metapopulations have revealed considerable diversity of host resistance phenotypes within populations. The resistance structure of non‐infected populations has, however, been largely ignored and the role of among‐population variation in resistance profiles in the dynamics of natural pathogen populations is poorly understood.ThePlantago lanceolata–Podosphaera plantaginispathosystem in the Åland Islands in south‐west Finland is characterized by the highly fragmented distribution of the host. Only a small fraction of the host populations is infected at one point in time and pathogen turnover rate is high. I studied a sample of these populations to find out whether adjacent host populations are differentiated in their resistance structure and whether variable levels of disease resistance among host populations could be linked to disease incidence patterns.Results show striking differences in the resistance structure both within and among host populations. Sixteen resistance phenotypes were identified in a sample of 64 host individuals. Populations varied from one in which all sampled individuals represented a different resistance phenotype, to one in which half showed identical resistance responses.There was no association between local resistance composition and the geographical distance between populations, suggesting that within‐population processes, such as founder effects and genetic drift, largely determine local resistance structure.Non‐infected populations showed significantly higher mean levels of resistance than infected populations, suggesting that differences in the mean level of resistance among host populations may retard the spread of the fungus and thereby decrease the probability of regional epidemics.

As the cultivated potatoes are not resistant to late blight caused by Phytophthora infestans, wild Solanum species are considered to be great resources for achieving durable resistance. This study reports newly identified resistance loci derived from Solanum venturii. Two mapping populations from the same accession, but different genotypes were used. Three specific loci segregated in the first population based on the isolates used for the resistance assay. One has already been mapped on the same region of chromosome 9, whereas the other two were localized below the first locus. In the second population, two specific resistance loci segregated and their genetic positions were also expected to be on the south from other genes clustered on chromosome 9. The resistance loci identified in this study could be different and isolate-specific. These results, together with markers developed using sequences of previously cloned resistance genes and integrated genetic maps of different late blight resistance loci, indicate that there are two resistance gene clusters on the long arm of chromosome 9.

Eight cultivars or lines of common wheat (Triticum aestivum L.) that were thought to have adult plant or field resistance to stem rust (Puccinia graminis Pers. f. sp. tritici Eriks. and E. Henn.) were selected—‘Hope’, ‘Hopps’, ‘Marquillo’, ‘Thatcher’, ‘Bonza’, ‘Chris’, Minnesota 11‐50‐ 17 and MRFY. The eight were crossed to produce four double crosses with the objective of combining genes for field resistance. A breeding procedure was used that resulted in the elimination of specific seedling resistance to race 15B‐1 of stem rust, and the selection of lines having field resistance to 15B‐1. During several years of testing, the selected, resistant lines proved to have resistance to mixtures of the prevalent and most virulent races of stem rust in North America. Twenty lines were tested in the 1976 International Spring Wheat Rust Nursery. All 20 were resistant at every North American location, and three had some resistance at all locations. Thus, 17 of the 20 lines appeared to have some type of specific resistance, while three had resistance against a broader range of races.The inheritance of rust resistance was studied in crosses between 61 of the selected lines and a susceptible parent. The results showed that in most crosses resistance was recessive and involved several genes that have small, probably cumulative effects, and act only in adult plants. In one line there was an indication that one major gene was involved. The resistance is clearly different than that controlled by the named Sr genes for specific resistance. However, there is no reason to think that it is general resistance, although its genetic complexity may make it more durable than resistance based on major genes for specific resistance.

Towards consensus on how to measure neutral genetic diversity?

To gain insight into genetic variation for resistance to parasites, this study assayed clonal variation in cyclically parthenogenetic Daphnia magna with respect to parasitic infection. Samples were collected from natural populations, and the allozyme phenotypes of infected hosts were compared to those of uninfected hosts. Differences between the clonal composition of the infected and uninfected class were evident in only two of 16 populations examined. This result stands in contrast to a study of species in the D. pulex and D. longispina species complexes, where clonal variation for infection was found in 12 of 25 populations (Little & Ebert, 1999). Considering all populations from both studies, associations between host genotype and infection were typically evident only in populations that showed low genotypic diversity and evidence of genetic disequilibria, with D. magna showing the least amount of disequilibria. This pattern is compatible with at least two possibly overlapping hypotheses. First, it may be that those populations lacking clonal variation for infection experienced weaker parasite-mediated selection. We can not rule out variation in selection pressure as an explanation, but found no evidence that the prevalence or intensity of parasitism differed either among species, or between those populations which showed clonal variation for infection and those that did not. Second, it could be that some populations, especially those of D. magna, have more frequent sexual recruitment than others. Sexual recombination breaks up gene combinations which are in linkage disequilibrium, and our method to detect clonal variation for resistance relies on linkage between genetic markers (allozymes) and resistance loci. Past work on Daphnia has shown that the level of sexual recruitment (which is in turn mediated by habitat permanency) is indeed commonly linked to the occurrence of genetic disequilibria. Our results may thus underestimate the prevalence of clonal variation for infection (especially for D. magna), because most of the populations analysed appeared to have high levels of sexual recruitment and therefore lacked the linkage disequilibrium that underlies associations between allozymes and susceptibility.

Research into the effects of host genetics on HIV disease susceptibility and progression, and on the efficacy and toxicity of drug treatment, occupies a particular position in the landscape of HIV research...

Fusarium head blight (FHB), caused by Fusarium graminearum Schwabe [teleomorph Gibberella zeae (Schwein.)], or scab, causes severe reductions in yield and quality of wheat (Triticum aestivum L.) and barley (Hordeum vulgare L.). Evaluation of FHB resistance is laborious and subject to environmental influence; therefore, molecular markers for FHB resistance genes will greatly enhance selection for FHB resistance. This review seeks to summarize information on molecular markers associated with quantitative trait loci (QTL) for resistance to FHB in wheat and barley and the use of those markers for marker assisted selection. Our goal is to summarize the current state of knowledge on the genetics of FHB resistance, the map locations of QTL for FHB resistance, and the future directions and potential applications of this research. In wheat, five types of resistance have been described, and Type II resistance (expressed in Chinese wheat cultivar Sumai 3) is the easiest type to assess. Several research groups are developing molecular markers associated with genes for FHB resistance from Sumai 3, a widely used source of Type II resistance in wheat breeding programs worldwide. In four different populations, each having Sumai 3 or a derivative as one parent, one to four QTL have been identified that explain up to 63% of the variation in resistance. QTL were identified on chromosomes 3BS and 6BL in three or more populations. Recently, in barley, restriction fragment length polymorphism (RFLP) markers associated with genes for FHB resistance, deoxynivalenol (DON) accumulation, and kernel discoloration were identified on all seven chromosomes. Three regions, located on chromosomes 2, 3, and 5 were identified in several mapping populations. Comparing the QTL locations between wheat and barley shows that the barley chromosome 3 QTL is located in a syntenous region in wheat. The following areas of research on molecular markers associated with FHB resistance should be emphasized: (i) identifying and mapping better resistance sources in wheat and barley; (ii) validating QTL in additional populations; and (iii) developing markers that can be easily used in breeding programs and across populations.

Natural forests are increasingly invaded by nonnative pests and pathogens that threaten host species with population extirpation and cascading ecological impacts. The regeneration for resilience (R4R) framework provides a decision structure to prioritize limited resources and utilize artificial and natural regeneration management to offer the best likelihood of success in positioning stands and landscapes to support multi-generational self-sustaining host populations in the presence of the nonnative invader by (1) increasing host population size to offset invader-caused mortality, (2) increasing the frequency of genetic resistance traits in host populations in habitats that enable their expression and durability to retard future mortality and facilitate population sustainability and recovery, and (3) maintain host genetic diversity, adaptive capacity, and population connectivity. This application is designed for conditions where the nonnative invader is expected to be a persistent threat, the host species naturally has some genetic resistance to the invasive species, and the forest host populations are integral to support valued ecosystem processes and services. The R4R framework has been developed for application in high elevation five-needle pine ecosystems of North America impacted and threatened by the nonnative pathogen Cronartium ribicola that causes the lethal disease white pine blister rust (WPBR). Several examples using the R4R framework to integrate information on current forest condition, WPBR risk or hazard, genetic resistance to WPBR, and host population dynamics and silvics to prioritize areas and design interventions are discussed. Effective management of forest regeneration dynamics can increase forest resilience and adaptive capacity to mitigate impacts of invasive species.

Genetic variation for parasite resistance occurs in most host populations. Costs of resistance, manifested as reduced fitness of resistant genotypes in the absence of parasitism, can be an important factor contributing to the maintenance of this variation. One powerful tool for detecting costs of resistance is the study of correlated responses to artificial selection. Provided that experimental lines are recently derived from large outbreeding populations, and that inbreeding is minimized during the experiment, correlated responses to selection are expected to be strong indicators of pleiotropy. We artificially selected for elevated behavioral resistance against an ectoparasitic mite (Macrocheles subbadius) in replicate populations of the fly Drosophila nigrospiracula. Resistance was modeled as a threshold trait, and the realized heritability of resistance was estimated to be 12.3% (1.4% SE) across three replicate lines recently derived from nature. We contrasted the longevity and fecundity of resistant and control (unselected) flies under a variable thermal environment. We report that reduced fecundity is a correlated response to artificial selection for increased resistance, and that the strength of this effect increases from 25 degrees to 29 degrees C. In contrast, longevity differences were not detected between resistant and control lines at either temperature. These findings are robust as they were confirmed with an independent set of experimental lines. Thus, our results identify a negative genetic correlation between ectoparasite resistance and an important life-history trait. That a correlated response was only detected for fecundity, and not longevity, suggests that the genetic correlation is attributable to pleiotropic effects with narrower effects than reallocation of a general resource pool within the organism, although other interpretations are discussed. Combined with fluctuating parasite-mediated selection and temperature, the presence of this trade-off may contribute to the maintenance of genetic variation for resistance in natural populations.

Improving Rice Blast Resistance by Mining Broad-Spectrum Resistance Genes at Pik Locus

Crops carrying broad-spectrum resistance loci provide an effective strategy for controlling infectious disease because these loci typically confer resistance to diverse races of a pathogen or even multiple species of pathogens. Despite their importance, only a few crop broad-spectrum resistance loci have been reported. Here, we report the identification and characterization of the rice bsr-k1 (broad-spectrum resistance Kitaake-1) mutant, which confers broad-spectrum resistance against Magnaporthe oryzae and Xanthomonas oryzae pv oryzae with no major penalty on key agronomic traits. Map-based cloning reveals that Bsr-k1 encodes a tetratricopeptide repeats (TPRs)-containing protein, which binds to mRNAs of multiple OsPAL (OsPAL1-7) genes and promotes their turnover. Loss of function of the Bsr-k1 gene leads to accumulation of OsPAL1-7 mRNAs in the bsr-k1 mutant. Furthermore, overexpression of OsPAL1 in wild-type rice TP309 confers resistance to M. oryzae, supporting the role of OsPAL1 Our discovery of the bsr-k1 allele constitutes a significant conceptual advancement and provides a valuable tool for breeding broad-spectrum resistant rice.

An indica rice accession HR4 was found to exhibit good resistance to rice blast in previous research. Inoculation with 116 different M. oryzae isolates revealed that HR4 has the broadest resistance spectrum of the six rice cultivars used in this study, which included two well characterized broad-spectrum resistance sources. To uncover the genetic mechanism of the broad-spectrum resistance in HR4, genetic analysis was carried out with three stable isolates. The results showed that a single dominant gene controlled its resistance to isolates GD93286 and GD00193, whereas two independent dominant genes were responsible for its resistance to isolate GD08T4. The resistance (R) gene in HR4 corresponding to isolate GD93286, named Pi-h1(t), was found to reside in a region of ~235.9 kb on the long arm of chromosome 11, while the other two R genes identified with isolate GD08T4, named Pi-h2(t) and Pi-h3(t), were linked to markers on chromosomes 1 and 12, respectively. The results indicated that the broad-spectrum resistance to rice blast in HR4 could be ascribed to multiple R genes. Identification of such multiple R genes will allow us to use markers more effectively for resistance improvement in rice breeding programs.

Bacterial leaf blight caused by Xanthomonas oryzae pv oryzae (Xoo) and blast caused by Magnaporthe oryzae are major diseases responsible for significant yield loss in rice production across all rice growing regions. Host plant resistance has been advocated as a sustainable means of guarding against the diseases. This experiment was conducted with the aim to introgress multiple resistance genes against bacterial leaf blight and blast diseases through marker-assisted backcross breeding. Two dominant (Xa4 and Xa21) and two recessive (xa5 and xa13) Xoo resistance genes were introgressed into a high yielding Malaysian rice variety Putra-1 with genetic background of three blast resistance (Piz, Pi2 and Pi9) genes. Eight polymorphic tightly linked functional and SSR markers were used for foreground selection of target genes. Seventy nine polymorphic SSR markers were used in background selection. The plants were challenged at initial stage of breeding and challenged again at BC2F2 with the most virulent Malaysian pathotypes of Xoo (P7.7) and Magnaporthe oryzae (P7.2) to test their resistance. Results obtained from foreground marker segregation analysis at BC1F1 and BC2F1 showed that the marker polymorphism both fitted into the Mendel’s single gene segregation ratio of 1:1 for both Xoo and blast resistance. At BC2F2, results indicated that foreground marker polymorphism fitted into the expected Mendelian ratio of 1:2:1 for blast resistance only. Marker-assisted background selection revealed high percentage of recurrent parent genome recovery (95.9%). It was concluded that the inheritance of blast resistance in the introgressed lines was mainly due to single gene action while the inheritance of Xoo resistance was substantially due to single nuclear gene action. The incorporation of four bacterial leaf blight and three blast resistance genes (Xa4 + xa5 + xa13 + Xa21; Pi9 + Pi2 + Piz) in the newly developed lines would provide for broad spectrum and durable resistance against the two major diseases studied.