Mapping of adult plant recessive resistance to anthracnose in Indian common bean landrace Baspa/KRC 8.

BACKGROUND: The common bean (Phaseolus vulgaris) has become the food of choice owing to its wealthy nutritional profile, leading to a considerable increase in its cultivation worldwide. However, anthracnose has been a major impediment to production and productivity, as elite bean cultivars are vulnerable to this disease. To overcome barriers in crop production, scientists worldwide are working towards enhancing the genetic diversity of crops. One way to achieve this is by introducing novel genes from related crops, including landraces like KRC 8. This particular landrace, found in the North Western Himalayan region, has shown adult plant resistance against anthracnose and also possesses a recessive resistance gene. METHODS AND RESULTS: In this study, a population of 179 F2:9 RIL individuals (Jawala × KRC 8) was evaluated at both phenotypic and genotypic levels using over 830 diverse molecular markers to map the resistance gene present in KRC 8. We have successfully mapped a resistance gene to chromosome Pv01 using four SSR markers, namely IAC 238, IAC 235, IAC 259, and BM 146. The marker IAC 238 is closely linked to the gene with a distance of 0.29 cM, while the other markers flank the recessive resistance gene at 10.87 cM (IAC 259), 17.80 cM (BM 146), and 25.22 cM (IAC 235). Previously, a single recessive anthracnose resistance gene (co-8) has been reported in the common bean accession AB 136. However, when we performed PCR amplification with our tightly linked marker IAC 238, we got different amplicons in AB 136 and KRC 8. Interestingly, the susceptible cultivar Jawala produced the same amplicon as AB 136. This observation indicated that the recessive gene present in KRC 8 is different from co-8. As the gene is located far away from the Co-1 locus, we suggest naming the recessive gene co-Indb/co-19. Fine mapping of co-Indb in KRC 8 may provide new insights into the cloning and characterization of this recessive gene so that it can be incorporated into future bean improvement programs. Further, the tightly linked marker IAC 238 can be utilized in marker assisted introgression in future bean breeding programs. CONCLUSION: The novel co-Indb gene present in Himalayan landrace KRC 8, showing adult plant resistance against common bean anthracnose, is independent from all the resistance genes previously located on chromosome Pv01.

Fine mapping of a new common bean anthracnose resistance gene (Co-18) to the proximal end of Pv10 in Indian landrace KRC-5.

KEY MESSAGE: Mapping and fine mapping of bean anthracnose resistance genes is a continuous process. We report fine mapping of anthracnose resistance gene Co-18 which is the first anthracnose gene mapped to Pv10. The discovery of resistance gene is a major gain in the bean anthracnose pathosystem research. Among the Indian common bean landraces, KRC-5 exhibit high levels of resistance to the bean anthracnose pathogen Colletotrichum lindemuthianum. To precisely map the anthracnose resistance gene, we used a Recombinant Inbred Line (F2:9 RIL) population (KRC-5 × Jawala). The inheritance test revealed that KRC-5 carries a dominant resistance gene temporarily designated as Co-18. We discovered two RAPD markers linked to Co-18 among 287 RAPD markers. These RAPD markers were eventually developed into SCARs (Sc-OPR15 and Sc-OPF6) and flank Co-18 on chromosome Pv10 at a distance of 5.3 and 4.2 cM, respectively. At 4.0-4.1 Mb on Pv10, we detected a SNP (single-nucleotide polymorphism) signal. We synthesized 58 SSRs and 83 InDels from a pool of 135 SSRs and 1134 InDels, respectively. Five SSRs, four InDels, and two SCARs were used to generate the high-density linkage map, which led to the identification of two SSRs (SSR24 and SSR36) that are tightly linked to Co-18. These two SSRs flank the Co-18 to 178 kb genomic region with 13 candidate genes including five NLR (nucleotide-binding and leucine-rich repeat) genes. The closely linked markers SSR24 and SSR36 will be used in cloning and pyramiding of the Co-18 gene with other R genes to develop durable resistant bean varieties.

Microbial interaction mediated programmed cell death in plants.

Food demand of growing population can only be met by finding solutions for sustaining the crop yield. The understanding of basic mechanisms employed by microorganisms for the establishment of parasitic relationship with plants is a complex phenomenon. Symbionts and biotrophs are dependent on living hosts for completing their life cycle, whereas necrotrophs utilize dead cells for their growth and establishment. Hemibiotrophs as compared to other microbes associate themselves with plants in two phase's, viz. early bio-phase and later necro-phase. Plants and microbes interact with each other using receptors present on host cell surface and elicitors (PAMPs and effectors) produced by microbes. Plant-microbe interaction either leads to compatible or incompatible reaction. In response to various biotic and abiotic stress factors, plant undergoes programmed cell death which restricts the growth of biotrophs or hemibiotrophs while necrotrophs as an opportunist starts growing on dead tissue for their own benefit. PCD regulation is an outcome of plant-microbe crosstalk which entirely depends on various biochemical events like generation of reactive oxygen species, nitric oxide, ionic efflux/influx, CLPs, biosynthesis of phytohormones, phytoalexins, polyamines and certain pathogenesis-related proteins. This phenomenon mostly occurs in resistant and non-host plants during invasion of pathogenic microbes. The compatible or incompatible host-pathogen interaction depends upon the presence or absence of host plant resistance and pathogenic race. In addition to host-pathogen interaction, the defense induction by beneficial microbes must also be explored and used to the best of its potential. This review highlights the mechanism of microbe- or symbiont-mediated PCD along with defense induction in plants towards symbionts, biotrophs, necrotrophs and hemibiotrophs. Here we have also discussed the possible use of beneficial microbes in inducing systemic resistance in plants against pathogenic microbes.

Biology and molecular interactions of Parastagonospora nodorum blotch of wheat.

MAIN CONCLUSION: Parastagonospora nodorum is one of the important necrotrophic pathogens of wheat which causes severe economical loss to crop yield. So far, a number of effectors of Parastagonospora nodorum origin and their target interacting genes on the host plant have been characterized. Since targeting effector-sensitive gene carefully can be helpful in breeding for resistance. Therefore, constant efforts are required to further characterize the effectors, their interacting genes, and underlying biochemical pathways. Furthermore, to develop effective counter-strategies against emerging diseases, continuous efforts are required to determine the qualitative resistance that demands to screen of diverse genotypes for host resistance. Stagonospora nodorum blotch also refers to as Stagonospora glume blotch and leaf is caused by Parastagonospora nodorum. The pathogen deploys necrotrophic effectors for the establishment and development on wheat plants. The necrotrophic effectors and their interaction with host receptors lead to the establishment of infection on leaves and extensive lesions formation which either results in host cell death or suppression/activation of host defence mechanisms. The wheat Stagonospora nodorum interaction involves a set of nine host gene-necrotrophic effector interactions. Out of these, Snn1-SnTox1, Tsn1-SnToxA and Snn-SnTox3 are one of the most studied interaction, due to its role in the suppression of reactive oxygen species production, regulating the cytokinin content through ethylene-dependent wayduring initial infection stage. Further, although the molecular basis is not fully unveiled, these effectors regulate the redox state and influence the ethylene biosynthesis in infected wheat plants. Here, we have discussed the biology of the wheat pathogen Parastagonospora nodorum, role of its necrotrophic effectors and their interacting sensitivity genes on the redox state, how they hijack the resistance mechanisms, hormonal regulated immunity and other signalling pathways in susceptible wheat plants. The information generated from effectors and their corresponding sensitivity genes and other biological processes could be utilized effectively for disease management strategies.