published_or_final_version / Botany / Master / Master of Philosophy

No description available.

M.Sc. / As part of an investigation into differential gene expression in response to abiotic and chemical inducers of acquired resistance in tobacco, a PCR fragment of 660bp was repeatedly found in RNA preparations from treated cell suspensions by differential display analysis. The fragment (D1B) was isolated, purified, cloned and sequenced. The nucleotide sequence of the fragment was compared with sequences in the BLAST sequence database and was found to be homologous to the mitochondrial orfx genes from Arabidopsis thaliana, Beta vulgaris, Oenothera berteriana, Oryza sativa and Marchantia polymorpha. In order to obtain the full sequence of the gene specific primers were designed using the Arabidopsis sequence as template. The primers were designed to complete the 5’-end of the gene and were designed to overlap the D1B fragment previously found. A fragment (C3Y) of 460bp was isolated, purified, cloned and sequenced. The complete sequence (D1B and C3Y combined) was 851bp long and showed 96% homology with the Arabidopsis orfx gene on the nucleotide level and 87% homology on the translated amino acid level. The sequence was submitted to the Basic Local Alignment Search Tool (BLAST) database as accession gi: 24209907. In plant genomes, the orfx gene is closely linked to important structural genes such as the nad subunits of complex I (NADH: ubiquinone oxidoreductase). Orfx codes for a hypothetical protein that shows homology to the mttB (membrane targeting and translocation) gene found in E. coli. In bacteria the gene is essential because if deleted, the organism was no longer viable. Functional analysis of the bacterial gene revealed a novel pathway specific for membrane targeting and secretion of cofactor containing proteins, such as iron-sulphur (Fe-S) clusters, of which the mttB gene encodes one subunit. It is thought that a similar pathway might be responsible for the correct localisation and assembly of such Fe-S containing protein complexes in the inner mitochondrial membrane of higher plants. The differential display result may be indicative of a general up-regulation of mitochondrial gene expression in response to the triggering of plant defences or a possible specific effect on the expression of the orfx gene. A hypothesis was formulated that chemical inducers of plant defences affect the mitochondria of treated plant cells to result in increased production of reactive oxygen intermediates (ROI), similar to the oxidative microbursts proposed to be involved in systemic required resistance. Using a dichlorodihidrofluorescein (H2DCFDA) assay, it was found that salicylic acid (SA), benzo (1,2,3) thiadiazole-7-carbothioc acid S-methyl ester (BTH) and isonitrosoacetophenone (INAP) increased ROI production within cells in a dose dependant manner. The biochemical basis of this effect could possibly be related to the inhibition of the NADH:ubiquinone oxidoreductase activity of complex I of the mitochondrial electron transport chain by SA, BTH and INAP. / Prof. I.A. Dubery

M.Sc. / Polygalacturonase-inhibiting proteins (PGIPs) are cell wall-associated plant proteins that inhibit endopolygalacturonases from phytopathogenic fungi. It has been proposed that pgip encoding genes could be utilised for engineering increased resistance in transgenic crops against important fungal pathogens such as Botrytis cinerea. During this study a pgip gene from Malus domestica cv Granny Smith apple fruit was cloned by the degenerate and inverse polymerase chain reaction (PCR) techniques. An alignment of the pear and bean PGIP sequences was used to design degenerate PCR primers in highly conserved regions. Degenerate PCR allowed the amplification of a 351bp internal fragment of the pgip gene, termed ipgip. The DNA sequence of ipgip was used to design inverse PCR primers. A Southern blot of apple genomic DNA probed with the ipgip fragment was used to identify restriction enzyme sites for inverse PCR. Inverse PCR enabled cloning of the remainder of the gene, from which a composite pgip gene sequence was constructed. The composite apple pgip gene comprised an open reading frame of 990bp that is predicted to encode a 330 amino acid polypeptide. The polypeptide contains a putative 24 amino acid N-terminal leader sequence that may function as a signal peptide for secretion. The deduced apple PGIP contains nine cysteine residues and seven potential N-linked glycosylation sites. Ten loosely conserved leucine-rich repeat motifs characteristic of PG1Ps were identified in the apple PGIP sequence. The apple PGIP showed 97% and 55% amino acid identity to the pear and bean PGIPs, respectively. The full-length apple pgip gene was re-isolated from genomic DNA by PCR using primers designed to the 5' and 3' ends of the composite pgip gene. The apple pgip gene was cloned into a plant transformation vector and transformed into tobacco by Agrobacterium-mediated transformation. Phenotypically normal transgenic tobacco plants were produced. Stable transgene insertion into the transgenic tobacco genomes was verified by PCR and Southern blot analyses. Sequence analysis of the pgip construct used for transformation revealed two potential mutations in the deduced amino acid sequence. The substitutions of Asp residues with Asn and Tyr at positions 43 and 196, respectively, could interfere with the secondary structure of the expressed transgene protein. To test whether the apple PGIP was effective against Botrytis cinerea, protein extracts were prepared from apple fruit and transgenic tobacco and tested for inhibitory activity against B. cinerea polygalacturonases. Biochemical assays showed that a heat-denaturable PGIP extract prepared from apple fruit inhibited the polygalacturonases produced by a virulent isolate of Botrytis cinerea grown on pectin and apple cell walls. Protein extracts prepared from transgenic tobacco did not show any inhibitory activity towards Botrytis polygalacturonases. This suggests the absence of active PGIP in the extracts possibly due to inefficient transcription of the transgene or due to the introduced mutations.

No description available.

Ph.D. / Current models regarding plant : pathogen interactions assume that recognition of pathogen-associated molecular pattern (PAMP) molecules can occur through pattern recognition receptors (PRRs) on the surface of plant cells. Lipopolysaccharides (LPS) embedded in the cell wall of Gram-negative bacteria can trigger defence responses or prime the plant in order to respond more rapidly, following perception of bacterial pathogens. Limited data has been reported on signal transduction and the nature of the LPS receptors in plants since no receptors have been identified yet. Parallels have been shown to exist between self-incompatibility and pathogen recognition with regard to self / non-self recognition. The two processes were reviewed and conceptual and mechanistic links between microbial recognition and self-incompatibility were discussed herein. The role of S-domain receptor-like kinases (RLKs) in defence mechanisms has previously not been widely recognized or explored. It was reasoned that S-domain RLKs could be utilized to function as resistance (R) genes or as pattern recognition receptors in perception of PAMPs of a non-protein nature. It has been found that genes encoding receptors may be up-regulated in response to perception of its ligand. A putative receptor-like kinase was previously reported to be induced by LPS. This 153 bp differentially expressed transcript, HAP3-15 (GenBank accession number DR109311), might be an expressed sequence tag (EST) for a gene encoding a receptor for LPS. The experimental characterisation of this EST was reported herein. Gene-walking, reverse transcriptase polymerase chain reaction (RT-PCR), rapid amplification of cDNA ends (RACE), cloning, sequencing and bio-informatic analyses were used to identify the full gene. These results revealed that it encoded a receptor-like protein kinase with an extracellular S-domain recognition motif. The 2842 bp genomic sequence obtained, showed that the sequence had a defined promoter region and six major domains. The first five domains were encoded by the first exon. These domains included a B-lectin / agglutinin domain, an S-locus glycoprotein domain, an EGF-like repeat, a PAN domain, a transmembrane region and part of the 6th domain. The 6th domain was a kinase domain consisting of eleven sub-domains interspersed by three introns. The gene was therefore designated as the N. tabacum S-domain Receptor-like kinase (NS-RLK).

Shuk-man Chow. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (leaves 171-186). / Abstracts in English and Chinese. / Thesis committee --- p.i / Statement --- p.ii / Abstract --- p.iii / Acknowledgement --- p.viii / General abbreviations --- p.x / Abbreviations of chemicals --- p.xi / List of figures --- p.xii / List of Tables --- p.xiii / Table of contents --- p.xv / Chapter 1. --- Literature review / Chapter 1.1. --- General introduction to rice disease --- p.1 / Chapter 1.1.1. --- Pathogenesis of Bacterial Leaf Blight (BLB) --- p.1 / Chapter 1.1.2. --- Pathogenesis of rice blast --- p.2 / Chapter 1.1.3. --- Control of rice diseases --- p.3 / Chapter 1.2. --- Plant defense mechanisms --- p.4 / Chapter 1.2.1. --- Basal resistance in plants --- p.4 / Chapter 1.2.2. --- Wound induced defense response --- p.5 / Chapter 1.2.3. --- Pathogen induced host defense response --- p.6 / Chapter 1.3. --- Structure of R gene products --- p.7 / Chapter 1.4. --- Recognition between R and Avr proteins in rice --- p.8 / Chapter 1.5 --- Current knowledge on Xa resistance and AvrXa avirulence protein --- p.9 / Chapter 1.6 --- Current knowledge on Pi resistance and AvrPi avirulence protein --- p.10 / Chapter 1.7 --- Pathogen induced signal transduction cascade --- p.12 / Chapter 1.7.1. --- R gene mediated signal transduction cascade --- p.12 / Chapter 1.7.2. --- Signal events of G-protein activation --- p.12 / Chapter 1.7.3. --- Signaling events for the accumulation of Ca2+ in cytosol --- p.13 / Chapter 1.7.4. --- Signaling events for oxidative burst --- p.14 / Chapter 1.7.5. --- MAPK cascade in defense signaling --- p.15 / Chapter 1.7.6. --- Transcriptional regulation of disease resistance related genes --- p.16 / Chapter 1.7.7. --- Translational regulation of disease resistance related genes --- p.17 / Chapter 1.8. --- Defense responses and defense related genes --- p.19 / Chapter 1.8.1. --- Pathogenesis related (PR) proteins --- p.20 / Chapter 1.8.2. --- Phytoalexins --- p.21 / Chapter 1.9. --- Disease resistance related genes common between rice blast and BLB resistance --- p.22 / Chapter 1.10. --- SA induced signal transduction pathway in rice --- p.23 / Chapter 1.11. --- Important tools facilitating the identification of disease resistance related genes from BLB resistant rice lines --- p.24 / Chapter 1.12. --- Hypothesis --- p.26 / Chapter 1.13. --- Project objective --- p.26 / Chapter 2. --- Materials and Methods --- p.27 / Chapter 2.1. --- Plant Materials --- p.27 / Chapter 2.2. --- Pathogen Inoculation --- p.27 / Chapter 2.3. --- RNA extraction --- p.29 / Chapter 2.4. --- Denaturing gel electrophoresis --- p.29 / Chapter 2.5. --- Subtraction libraries construction --- p.30 / Chapter 2.5.1. --- Cloning of disease resistance related genes --- p.32 / Chapter 2.5.1.1. --- pBluescript II KS (+) T-vector preparation --- p.32 / Chapter 2.5.1.2. --- Ligation --- p.32 / Chapter 2.5.1.3. --- Transformation --- p.32 / Chapter 2.5.1.4. --- Colony picking --- p.33 / Chapter 2.5.1.5. --- PCR amplification of DNA inserts --- p.33 / Chapter 2.5.1.6. --- Purification of PCR products --- p.34 / Chapter 2.6. --- Gene chips printing --- p.34 / Chapter 2.7. --- Probes synthesis and gene chips hybridization --- p.35 / Chapter 2.8. --- Standard-RNAs synthesis --- p.35 / Chapter 2.9. --- Data collection and analysis --- p.36 / Chapter 2.10. --- Sequencing --- p.36 / Chapter 2.11. --- cDNA synthesis --- p.37 / Chapter 2.12. --- RT-PCR --- p.38 / Chapter 2.13. --- DNA gel electrophoresis --- p.39 / Chapter 3. --- Results --- p.58 / Chapter 3.1. --- Construction of BLB gene chips --- p.58 / Chapter 3.1.1. --- Preparation of cDNA clones for gene chips construction --- p.58 / Chapter 3.1.2. --- Purification of PCR products on microtiter plate --- p.59 / Chapter 3.1.3. --- Gene chips construction --- p.59 / Chapter 3.1.4. --- DNA immobilization --- p.62 / Chapter 3.1.5. --- Probe synthesis --- p.62 / Chapter 3.1.6. --- Gene chip analysis --- p.65 / Chapter 3.1.6.1. --- Scanning --- p.65 / Chapter 3.1.6.2. --- Data analysis --- p.65 / Chapter 3.2. --- "Identification of disease resistance related genes commonly regulated by Xa2, Xal2 and Xal4 BLB resistance loci" --- p.70 / Chapter 3.2.1. --- "Signal perception, transduction and regulatory elements" --- p.71 / Chapter 3.2.1.1. --- Proteins involved in reversible phosphorylation cascade --- p.71 / Chapter 3.2.1.2. --- Proteins potentiate signal transduction through specific protein-protein interaction --- p.72 / Chapter 3.2.1.3. --- Other signal transduction components --- p.73 / Chapter 3.2.2. --- Transcriptional and translational regulatory elements --- p.74 / Chapter 3.2.2.1. --- Proteins involved in transcriptional regulation --- p.74 / Chapter 3.2.2.2. --- Proteins involved in post-transcriptional regulation --- p.75 / Chapter 3.2.2.3. --- Proteins involved in translational regulation --- p.76 / Chapter 3.2.3. --- "Oxidative burst, stress, apoptotic related genes" --- p.77 / Chapter 3.2.3.1. --- Stress related proteins --- p.77 / Chapter 3.2.3.2. --- Proteins involved in induction of oxidative burst --- p.78 / Chapter 3.2.3.3. --- PR proteins --- p.79 / Chapter 3.2.3.4. --- Proteolysis related proteins --- p.79 / Chapter 3.2.4. --- Cell maintenance and metabolic genes --- p.80 / Chapter 3.2.4.1. --- Antioxidant --- p.80 / Chapter 3.2.4.2. --- Metabolic genes --- p.81 / Chapter 3.2.4.3. --- Molecular chaperone --- p.82 / Chapter 3.2.4.4. --- Cell cycle regulators --- p.82 / Chapter 3.2.4.5. --- Cell wall maintenance --- p.83 / Chapter 3.2.4.6. --- Proteins involved in protein transport --- p.83 / Chapter 3.2.5. --- Unclassified/others --- p.84 / Chapter 3.3. --- Expression analysis of disease resistance related genes --- p.88 / Chapter 4. --- Discussion --- p.141 / Chapter 4.1. --- Differential expression of disease resistance candidates --- p.141 / Chapter 4.2. --- Disease resistance signal transduction components --- p.143 / Chapter 4.2.1. --- Reversible phosphorylation cascade --- p.143 / Chapter 4.2.2. --- Signal transduction potentiated by protein-protein interaction --- p.144 / Chapter 4.3. --- Other signaling molecules --- p.145 / Chapter 4.3.1. --- PRL1-interacting factor G --- p.145 / Chapter 4.3.2. --- Vacuolar-type H+-ATPasen subunit G --- p.146 / Chapter 4.4. --- Regulation of expression of disease resistance candidates --- p.146 / Chapter 4.4.1. --- Transcriptional regulation of disease resistance related genes --- p.146 / Chapter 4.4.1.1. --- G-box binding protein --- p.147 / Chapter 4.4.1.2. --- MYB TF --- p.147 / Chapter 4.4.2. --- Post-transcriptional modification of disease resistance candidates --- p.148 / Chapter 4.4.2.1. --- RNA splicing factor --- p.148 / Chapter 4.4.2.2. --- Glycine rich RNA binding proteins --- p.149 / Chapter 4.4.3. --- Translational regulation of disease resistance related genes --- p.149 / Chapter 4.5. --- Induction of oxidative burst --- p.150 / Chapter 4.6. --- PR proteins --- p.151 / Chapter 4.7. --- Cell maintenance --- p.152 / Chapter 4.7.1. --- Protein folding --- p.152 / Chapter 4.7.2. --- Protein degradation --- p.153 / Chapter 4.7.3. --- ROS scavenging --- p.154 / Chapter 4.7.4. --- Regulation of cell cycle --- p.154 / Chapter 4.8. --- "Confirmation and profiling of disease resistance related candidates commonly regulated in Xa2, Xal2 and Xal4 BLB resistance NILs at different time points" --- p.155 / Chapter 4.8.1. --- Basal resistance related genes --- p.156 / Chapter 4.8.2. --- General disease resistance related genes --- p.161 / Chapter 4.8.3. --- Pathogen responsive genes --- p.164 / Chapter 4.8.4. --- Prediction of novel genes functions --- p.168 / Chapter 4.9. --- Future prospect --- p.169 / Chapter 4.10. --- Conclusion --- p.169 / References --- p.171 / Appendix --- p.187

Au Yeung, Wan Kin. / "August 2011." / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 89-103). / Abstracts in English and Chinese. / Thesis committee --- p.i / Statement --- p.ii / Abstract --- p.iii / Acknowledgements --- p.v / General abbreviations --- p.vi / Abbreviations of chemicals --- p.vii / List of figures --- p.ix / List of figures in Appendix VI --- p.xii / List of tables --- p.xiv / Table of Contents --- p.xv / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- The significance of studying rice disease resistance --- p.1 / Chapter 1.1.1 --- Economic importance of rice --- p.1 / Chapter 1.1.2 --- Diseases caused by pathogens virulent to rice --- p.1 / Chapter 1.1.2.1 --- Bacterial leaf blight diseases --- p.1 / Chapter 1.1.2.2 --- Fungal blast diseases --- p.2 / Chapter 1.1.3 --- Approach to enhance resistance of crops towards pathogens --- p.2 / Chapter 1.2 --- Literature review on plant immunity system --- p.3 / Chapter 1.2.1 --- Pathogen associated molecular patterns (PAMP) and PAMP -triggered immunity (PTI) --- p.4 / Chapter 1.2.2 --- Pathogen effectors and effector-triggered immunity (ETI) --- p.5 / Chapter 1.2.3 --- Roles of phytohormones in plant defense responses --- p.6 / Chapter 1.2.4 --- G protein signaling and plant defense responses --- p.9 / Chapter 1.3 --- Literature review on FK506 binding proteins (FKBPs) --- p.10 / Chapter 1.4 --- Background information of this study - origin of the clone chosen for study in this project --- p.11 / Chapter 1.5 --- Hypothesis and Objectives --- p.12 / Chapter Chapter 2 --- Materials and Methods --- p.13 / Chapter 2.1 --- Materials --- p.13 / Chapter 2.1.1 --- "Plants, bacterial strains and vectors" --- p.13 / Chapter 2.1.2 --- Chemicals and Regents --- p.18 / Chapter 2.1.3 --- Commercial kits --- p.18 / Chapter 2.1.4 --- Primers and Adaptors --- p.19 / Chapter 2.1.5 --- Equipments and facilities used --- p.23 / Chapter 2.1.6 --- "Buffer, solution, gel and medium" --- p.23 / Chapter 2.2 --- Methods --- p.24 / Chapter 2.2.1. --- Bacterial and yeast cultures --- p.24 / Chapter 2.2.2 --- Plant growth conditions and treatments --- p.25 / Chapter 2.2.2.1 --- Surface sterilization of J. thaliana seeds --- p.25 / Chapter 2.2.2.2 --- Environmental conditions of A. thaliana for germination of seeds and growing of seedlings --- p.26 / Chapter 2.2.2.3 --- Environmental conditions of A. thaliana for growing of plants --- p.26 / Chapter 2.2.2.4 --- Pathogen inoculation test of A. thaliana with Pst DC3000 --- p.27 / Chapter 2.2.3 --- Cloning and subcloning of OsFKBP 12 and OsUCCl --- p.27 / Chapter 2.2.3.1 --- Sub-cloning of OsFKBP12 to pGEX-4T-l and pMAL-c2 --- p.27 / Chapter 2.2.3.2 --- Cloning of OsUCCl to pGEX-4T-l --- p.29 / Chapter 2.2.4 --- "DNA, RNA and protein extractions" --- p.29 / Chapter 2.2.4.1 --- Plasmid extraction from bacterial cells --- p.29 / Chapter 2.2.4.2 --- Genomic DNA extraction from plant through CTAB method --- p.29 / Chapter 2.2.4.3 --- RNA extraction from plant tissues --- p.30 / Chapter 2.2.4.4 --- Protein extraction from plant tissues --- p.31 / Chapter 2.2.4.5 --- Fusion protein extraction from E. coli --- p.31 / Chapter 2.2.5 --- Western blot analyses --- p.32 / Chapter 2.2.5.1 --- Western blot analysis of GST tag and MBP tag fusion proteins --- p.32 / Chapter 2.2.5.2 --- Western blot analysis native OsYchFl proteins --- p.33 / Chapter 2.2.6 --- Real-time PCR study --- p.33 / Chapter 2.2.6.1 --- cDNA synthesis --- p.33 / Chapter 2.2.6.2 --- Real-time PCR --- p.34 / Chapter 2.2.7 --- Yeast two hybrid --- p.35 / Chapter 2.2.7.1 --- Screening of OsFKBP 12 interaction protein partners by yeast mating --- p.35 / Chapter 2.2.7.2 --- Identification of positive interacting protein partners by extracting DNA plasmid from yeast --- p.35 / Chapter 2.2.7.3 --- Re-transformation of pGBKTl-OsFKBP 12 with their interacting partner clones into yeast (AH 109) by co-transformation --- p.36 / Chapter 2.2.8 --- In vitro pull down assay of OsFKBP 12 with their putative protein interacting partner --- p.36 / Chapter 2.2.8.1 --- In vitro pull down of native OsYchFl by MBP-His-OsFKBP12 --- p.36 / Chapter 2.2.8.2 --- In vitro pull down of GST-AtYchF 1 by MBP-His-OsFKBP12 --- p.37 / Chapter 2.2.8.3 --- In vitro pull down of MBP-His-OsFKBP12 by GST-OsUCCl --- p.37 / Chapter 2.2.8.4 --- In vitro pull down of MBP-His-OsFKBP12 by GST-OsYchFl G domain --- p.38 / Chapter 2.2.9 --- GTPase assay ofOsYchF with OsFKBP12 --- p.38 / Chapter 2.3.0 --- Phylogenetic analysis and sequence alignment --- p.39 / Chapter Chapter 3 --- Results --- p.40 / Chapter 3.1 --- Identification of OsFKBP 12 encoding a FKBP (FK506 binding protein)-domain containing protein in Oryza sativa (rice) --- p.40 / Chapter 3.2 --- OsFKBP12 was down-regulated in the pathogen-inoculated Xal4 rice line CBB14 --- p.47 / Chapter 3.3 --- Ecotpic expression of OsFKBP 12 repressed the expression of defense marker genes in transgenic A. thaliana --- p.50 / Chapter 3.4 --- Expressing OsFKBP 12 in transgenic A. thaliana enhanced the susceptibility to the bacterial pathogen Pst DC3000 --- p.54 / Chapter 3.5 --- OsFKBP 12 protein interacted with a putative defense-related G-protein and a copper binding protein --- p.57 / Chapter 3.6 --- "OsFKBP 12 protein interacted with the G domain of defense-related G protein, OsYchFl" --- p.69 / Chapter 3.7 --- OsFKBP 12 protein enhanced the in vitro phosphate release of OsYchFl --- p.72 / Chapter Chapter 4 --- Discussion --- p.74 / Chapter 4.1 --- The identification and characterization of OsFKBP 12 --- p.74 / Chapter 4.2 --- Expression pattern of OsFKBP 12 upon biotic stress in bacterial blight resistant near isogenic line (NIL) --- p.75 / Chapter 4.3 --- OsFKBP 12 repressed the expression of SA-regulated defense marker genes when ectopically expressed in A. thaliana --- p.75 / Chapter 4.4 --- Ectopic expression of OsFKBP 12 enhanced susceptibility towards Pst DC3000 in transgenic A. thaliana --- p.76 / Chapter 4.5 --- The interacting partners of OsFKBP 12 in relation to plant defense response --- p.78 / Chapter 4.6 --- The specific biochemical interaction of OsFKBP 12 with OsYchFl --- p.80 / Chapter 4.7 --- Future perspectives --- p.85 / Chapter Chapter 5 --- Conclusion --- p.87 / References --- p.89 / Appendix --- p.104

Graduation date: 1994

Resistance (R) genes, a key factor in determining the resistance of plants, have been shown often to be highly allelic entities existing in duplicated regions of the genome. This characteristic suggests that R-gene acquisition may have arisen through frequent genetic rearrangements as a result of transient, reduced genome stability. Tabacco plants transgenic for a recombination construct exhibited reduced genome stability upon infection with a virulent pathogen (tobacco mosaic virus). The reduced genome stability manifested as an increase in recombination events in the transgene. Such increases were observed following a virulent pathogen attack. This increase in recombination was shown to be systemic and was observed prior to systemic viral movement suggesting the presence of a systemic recombination signal. Further molecular analyses revealed that specific R-gene loci experience a large frequency of rearrangements following a virulent pathogen encounter. The possible targeting of instability to R-gene regions may be controlled through epigenetic processes, in particular, DNA methylation. / xiii, 119 leaves ; 29 cm.