Resistance Breeding in Apple at Dresden-Pillnitz

Resistance breeding in apple has a long tradition at the Institute of Fruit Breeding now Julius Kuehn-institute in Dresden-Pillnitz. The breeding was aimed at the production of multiple resistance cultivars to allow a more sustainable and environmentally friendly production of apple. In the last decades a series of resistant cultivars (Re®-cultivars) bred in Dresden-Pillnitz has been released, ‘Recolor’ and ‘Rekarda’ in 2006. The main topic in the resistance breeding programme was scab resistance and the donor of scab resistance in most cultivars was Malus x floribunda 821. Due to the development of strains that are able to overcome resistance genes inherited by M. x floribunda 821 and due to the fact that single resistance genes can be broken easily, pyramiding of resistance genes is necessary. Besides scab, fire blight and powdery mildew are the main disease for which a pyramiding of genes is aspired in Pillnitz. Biotechnical approaches are necessary for the early detection of pyramided resistance genes in breeding clones. This paper will give an overview of the resistance breeding of apple in Pillnitz and the methods used

The integrated concept of disease resistance; a new view including horizontal and vertical resistance in plants

Horizontal, uniform, race-non-specific or stable resistance can be discerned according to Van der Plank, from vertical, differential, race-specific or unstable resistance by a test in which a number of host genotypes (cultivars or clones) are tested against a number of pathogen genetypes traces of isolatest. If the total non-environmental variance in levels of resistance is due to main effects only differences between cultivars and differences between isolates) the resistance and the pathogen many (in the broad sense) are horizontal in nature. Vertical resistance and pathogenicity are characterized by the interaction between host and pathogen showing up as a variance compenent in this test due to interaction between cultivars and isolates. A host and pathogen model was made in which resistance and pathogenicity are governed by live polygenic loci. Within the host the resistance genes show additivity. Two models were investigated in model I resistance and pathogenicity genes operate in an additive way as envisaged by Van der Plank in his horizontal resistance. Model II is characterized by a gene-for-gene action between the polygenes of the host and those of the pathogen. The cultivar isolate test in model I showed only main effect variance. Surprisingly, the variance in model II was also largely due to main effects. The contribution of the interaction to the variance uppeared so small, that it would be difficult to discern it from a normal error variance. So-called horizontal resistance can therefore be explained by a polygenic resistance, where the individual genes are vertical and operating on a gene-for-gene basis with virulence genes in the pathogen. The data reported so far support the idea that model II rather than model I is the realistic one. The two models also revealed that populations with a polygenic resistance based on the gene-for-gene action have an increased level of resistance compared with the addition model, while its stability as far as mutability of the pathogen is concerned, is higher compared to those with an additive gene action. Mathematical studies of Mode too support the gene-for-gene concept. The operation of all resistance and virulence genes in a natural population is therefore seen as one integrated system. All genes for true resistance in the host population, whether they are major or minor genes are considered to interact in a gene-for-gene way with virulence genes either major or minor, in the pathogen population. The models revealed other important aspects. Populations with a polygenic resistance based on a gene-for-gene action have an increased level of resistance compared to populations following the addition model. The stability, as far as mutability of the pathogen is concerned, is higher in the interaction model than in the addition model. The effect of a resistance gene on the level of resistance of the population consists of its effect on a single plant times its gene frequency in the population. Due to the adaptive forces in both the host and the pathogen population and the gene-for-gene nature of the gene action an equilibrium develops that allows all resistance genes to remain effective although their corresponding virulence genes are present. The frequencies of the resistance and virulence genes are such that the effective frequencies of resistance genes tend to be negatively related to the magnitude of the gene effect. This explains why major genes often occur at low frequencies, while minor genes appear to be frequent. It is in this way that the host and the pathogen, both as extremely variable and vigorous populations, can co-exist. Horizontal and vertical resistance as meant by Van der Plank therefore do not represent different kinds of resistances, they represent merely polygenic and oligogenic resistances resp. In both situations the individual host genes interact specifically with virulence genes in the pathogen. Van der Plank's test for horizontal resistance appears to be a simple and sound way to test for polygenic inheritance of resistance. The practical considerations have been discussed. The agro-ecosystems should be made as diverse as possible. Multilines, polygenic resistance, tolerance, gene deployment and other measures should be employed, if possible in combination

The distribution of plasmids that carry virulence and resistance genes in Staphylococcus aureus is lineage associated.

BACKGROUND: Staphylococcus aureus is major human and animal pathogen. Plasmids often carry resistance genes and virulence genes that can disseminate through S. aureus populations by horizontal gene transfer (HGT) mechanisms. Sequences of S. aureus plasmids in the public domain and data from multi-strain microarrays were analysed to investigate (i) the distribution of resistance genes and virulence genes on S. aureus plasmids, and (ii) the distribution of plasmids between S. aureus lineages. RESULTS: A total of 21 plasmid rep gene families, of which 13 were novel to this study, were characterised using a previously proposed classification system. 243 sequenced plasmids were assigned to 39 plasmid groups that each possessed a unique combination of rep genes. We show some resistance genes (including ermC and cat) and virulence genes (including entA, entG, entJ, entP) were associated with specific plasmid groups suggesting there are genetic pressures preventing recombination of these genes into novel plasmid groups. Whole genome microarray analysis revealed that plasmid rep, resistance and virulence genes were associated with S. aureus lineages, suggesting restriction-modification (RM) barriers to HGT of plasmids between strains exist. Conjugation transfer (tra) complex genes were rare. CONCLUSION: This study argues that genetic pressures are restraining the spread of resistance and virulence genes amongst S. aureus plasmids, and amongst S. aureus populations, delaying the emergence of fully virulent and resistant strains

Debate on the Exploitation of Natural Plant Diversity to Create Late Blight Resistance in Potato

This paper reports on a debate on intriguing propositions relating to the scientific, agronomic, societal and economic impact of the BIOEXPLOIT project, focusing on late blight resistance in potato. It discusses (i) whether identifying pathogen effectors will facilitate selecting durable R genes, (ii) whether breeding for durable late blight resistance requires deploying Rpi (for Resistance to P hytophthora i nfestans) genes, (iii) whether breeding strategies and cultural practices determine the durability of new resistance genes, (iv) whether marker-assisted breeding for Phytophthora infestans resistance is already in the stage of adoption, (v) to what extent genetically-modified organism technology can advance realizing late-blight resistant potato cultivars, and (vi) whether modifying R genes will result in novel broad spectrum resistanc

Conserved defense responses between maize and sorghum to Exserohilum turcicum.

BACKGROUND:Exserohilum turcicum is an important pathogen of both sorghum and maize, causing sorghum leaf blight and northern corn leaf blight. Because the same pathogen can infect and cause major losses for two of the most important grain crops, it is an ideal pathosystem to study plant-pathogen evolution and investigate shared resistance mechanisms between the two plant species. To identify sorghum genes involved in the E. turcicum response, we conducted a genome-wide association study (GWAS). RESULTS:Using the sorghum conversion panel evaluated across three environments, we identified a total of 216 significant markers. Based on physical linkage with the significant markers, we detected a total of 113 unique candidate genes, some with known roles in plant defense. Also, we compared maize genes known to play a role in resistance to E. turcicum with the association mapping results and found evidence of genes conferring resistance in both crops, providing evidence of shared resistance between maize and sorghum. CONCLUSIONS:Using a genetics approach, we identified shared genetic regions conferring resistance to E. turcicum in both maize and sorghum. We identified several promising candidate genes for resistance to leaf blight in sorghum, including genes related to R-gene mediated resistance. We present significant advancements in the understanding of host resistance to E. turcicum, which is crucial to reduce losses due to this important pathogen

Epigenetics as a mechanism driving polygenic clinical drug resistance

Aberrant methylation of CpG islands located at or near gene promoters is associated with inactivation of gene expression during tumour development. It is increasingly recognised that such epimutations may occur at a much higher frequency than gene mutation and therefore have a greater impact on selection of subpopulations of cells during tumour progression or acquisition of resistance to anticancer drugs. Although laboratory-based models of acquired resistance to anticancer agents tend to focus on specific genes or biochemical pathways, such 'one gene : one outcome' models may be an oversimplification of acquired resistance to treatment of cancer patients. Instead, clinical drug resistance may be due to changes in expression of a large number of genes that have a cumulative impact on chemosensitivity. Aberrant CpG island methylation of multiple genes occurring in a nonrandom manner during tumour development and during the acquisition of drug resistance provides a mechanism whereby expression of multiple genes could be affected simultaneously resulting in polygenic clinical drug resistance. If simultaneous epigenetic regulation of multiple genes is indeed a major driving force behind acquired resistance of patients' tumour to anticancer agents, this has important implications for biomarker studies of clinical outcome following chemotherapy and for clinical approaches designed to circumvent or modulate drug resistance

Draft Genome Sequences of Pandrug-Resistant Serratia marcescens Clinical Isolates Harboring bla NDM-1

The draft genome sequences of two clonal, pandrug-resistant Serratia marcescens clinical isolates were determined. The resistance phenotype was plasmid driven, as 14 of 17 resistance genes were present on large IncFIB(K), IncHI2, and IncA/C2 plasmids indicating a large pool of transmissible antibiotic resistance genes

SolRgene: an online database to explore disease resistance genes in tuber-bearing Solanum species

Background The cultivated potato (Solanum tuberosum L.) is an important food crop, but highly susceptible to many pathogens. The major threat to potato production is the Irish famine pathogen Phytophthora infestans, which causes the devastating late blight disease. Potato breeding makes use of germplasm from wild relatives (wild germplasm) to introduce resistances into cultivated potato. The Solanum section Petota comprises tuber-bearing species that are potential donors of new disease resistance genes. The aim of this study was to explore Solanum section Petota for resistance genes and generate a widely accessible resource that is useful for studying and implementing disease resistance in potato. Description The SolRgene database contains data on resistance to P. infestans and presence of R genes and R gene homologues in Solanum section Petota. We have explored Solanum section Petota for resistance to late blight in high throughput disease tests under various laboratory conditions and in field trials. From resistant wild germplasm, segregating populations were generated and assessed for the presence of resistance genes. All these data have been entered into the SolRgene database. To facilitate genetic and resistance gene evolution studies, phylogenetic data of the entire SolRgene collection are included, as well as a tool for generating phylogenetic trees of selected groups of germplasm. Data from resistance gene allele-mining studies are incorporated, which enables detection of R gene homologs in related germplasm. Using these resources, various resistance genes have been detected and some of these have been cloned, whereas others are in the cloning pipeline. All this information is stored in the online SolRgene database, which allows users to query resistance data, sequences, passport data of the accessions, and phylogenic classifications. Conclusion Solanum section Petota forms the basis of the SolRgene database, which contains a collection of resistance data of an unprecedented size and precision. Complemented with R gene sequence data and phylogenetic tools, SolRgene can be considered the primary resource for information on R genes from potato and wild tuber-bearing relatives

A degenerate PCR-based strategy as a means of identifying homologues of aminoglycoside and ß-lactam resistance genes in the gut microbiota

peer-reviewedBackground: The potential for the human gut microbiota to serve as a reservoir for antibiotic resistance genes has been the subject of recent discussion. However, this has yet to be investigated using a rapid PCR-based approach. In light of this, here we aim to determine if degenerate PCR primers can detect aminoglycoside and β-lactam resistance genes in the gut microbiota of healthy adults, without the need for an initial culture-based screen for resistant isolates. In doing so, we would determine if the gut microbiota of healthy adults, lacking recent antibiotic exposure, is a reservoir for resistance genes. Results: The strategy employed resulted in the identification of numerous aminoglycoside (acetylation, adenylation and phosphorylation) and β-lactam (including bla OXA, bla TEM, bla SHV and bla CTX-M) resistance gene homologues. On the basis of homology, it would appear that these genes originated from different bacterial taxa, with members of the Enterobacteriaceae being a particularly rich source. The results demonstrate that, even in the absence of recent antibiotic exposure, the human gut microbiota is a considerable reservoir for antibiotic resistance genes. Conclusions: This study has demonstrated that the gut can be a significant source of aminoglycoside and β-lactam resistance genes, even in the absence of recent antibiotic exposure. The results also demonstrate that PCR-based approaches can be successfully applied to detect antibiotic resistance genes in the human gut microbiota, without the need to isolate resistant strains. This approach could also be used to rapidly screen other complex environments for target genes.Fiona Fouhy is in receipt of an Irish Research Council EMBARK scholarship and is a Teagasc Walsh fellow. Research in the PDC laboratory is also supported by the Irish Government under the National Development Plan through the Science Foundation Ireland Investigator award 11/PI/113

Genomic evidence for genes encoding leucine-rich repeat receptors linked to resistance against the eukaryotic extra- and intracellular Brassica napus pathogens Leptosphaeria maculans and Plasmodiophora brassicae

© 2018 Stotz et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Genes coding for nucleotide-binding leucine-rich repeat (LRR) receptors (NLRs) control resistance against intracellular (cell-penetrating) pathogens. However, evidence for a role of genes coding for proteins with LRR domains in resistance against extracellular (apoplastic) fungal pathogens is limited. Here, the distribution of genes coding for proteins with eLRR domains but lacking kinase domains was determined for the Brassica napus genome. Predictions of signal peptide and transmembrane regions divided these genes into 184 coding for receptor-like proteins (RLPs) and 121 coding for secreted proteins (SPs). Together with previously annotated NLRs, a total of 720 LRR genes were found. Leptosphaeria maculans-induced expression during a compatible interaction with cultivar Topas differed between RLP, SP and NLR gene families; NLR genes were induced relatively late, during the necrotrophic phase of pathogen colonization. Seven RLP, one SP and two NLR genes were found in Rlm1 and Rlm3/Rlm4/Rlm7/Rlm9 loci for resistance against L. maculans on chromosome A07 of B. napus. One NLR gene at the Rlm9 locus was positively selected, as was the RLP gene on chromosome A10 with LepR3 and Rlm2 alleles conferring resistance against L. maculans races with corresponding effectors AvrLm1 and AvrLm2, respectively. Known loci for resistance against L. maculans (extracellular hemi-biotrophic fungus), Sclerotinia sclerotiorum (necrotrophic fungus) and Plasmodiophora brassicae (intracellular, obligate biotrophic protist) were examined for presence of RLPs, SPs and NLRs in these regions. Whereas loci for resistance against P. brassicae were enriched for NLRs, no such signature was observed for the other pathogens. These findings demonstrate involvement of (i) NLR genes in resistance against the intracellular pathogen P. brassicae and a putative NLR gene in Rlm9-mediated resistance against the extracellular pathogen L. maculans.Peer reviewe