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Signal Transduction
In most eukaryotic organisms pathogen recognition and defence responses are linked by means of signal transduction cascades (Nürnberger and Scheel, 2001). Plant tissues acquire resistance by relying on transmissible signal molecules that, at low concentration, can activate resistance mechanisms in cells not directly invaded by the pathogen (Ross, 1961; Schenk et al. 2000). Molecules are classified as signal molecules if they are synthesised in the plant, increase systemically following pathogen attack, move throughout the plant, induce defence-related proteins and phytochemicals and if they enhance resistance in the plant against pathogens. The events following pathogen recognition are still poorly understood. Downstream pathways seem to vary for different host plants, resistance genes, elicitors and pathogens (Bent, 1996; Ebel and Mïthofer, 1998; Glazebrook, 2001). Consequently, general models are unable to explain signal transduction and resistance for every plant-pathogen interaction. Despite the complexity and diversity of plant-pathogen interactions, signalling events and resistance mechanisms for many similar plant responses have been identified. During early signal transduction events, cells in and around the recognition site experience large ion fluxes and undergo changes in lipid oxidation, protein phosphorylation, and concentration and accumulation of ROS (Dixon et al., 1994; Hammond-Kosack and Jones, 1996; Ebel and Mïthofer, 1998; Holt et al., 2000). Different kinases are involved downstream of pathogen recognition in different plantpathogen systems. These include receptor-like kinases, protein kinases, calciumdependant protein kinase (CDPK’s) and mitogen-activated protein kinases (MAPKs) (Fig. 1) (Torii, 2000; Guillaume et al., 2001; Romeis, 2001; Asai et al., 2002).
Cell wall-bound phenolics
The ester-bound phenols incorporated into the cell wall were extracted following alkaline hydrolysis (Campbell and Ellis, 1992). Dry cell wall material (AIR) was weighed (0.01 g) and resuspended in 0.5 M NaOH (1 ml for 10 mg) for 1 h at 96°C. Cell wall-esterified hydroxycinnamic acid derivatives were selectively released under these mild saponification conditions. The supernatant was acidified to pH 2 with HCl, centrifuged at 12 000 x g for 10 min and then extracted with 1 ml diethyl ether (Saarchem, Merck Laboratories). The extract was dried in a speedy vac and the precipitate was resuspended in 250 µl 50% aqueous MeOH. This solution was used to determine the cell wall-esterified phenolic acids content with Folin-Ciocalteau reagent. Statistical analysis for the phenolic assay data was conducted using the General Linear Models (GLM) procedure of STATISTICA, version 7 (STATSOFT Inc. 2004). Experiments were analysed using One-way analysis of variance (ANOVA) and the Tukey Honest Significant Difference (HSD) test. Significance was evaluated at P<0.05.
CHAPTER 1 Resistance to Fusarium wilt in banana: A Review
INTRODUCTION
FUSARIUM WILT OF BANANA (PANAMA DISEASE)
THE HOST: BANANA
RESISTANCE IN PLANTS TO PATHOGENSTerminology
COMPONENTS OF PLANT DEFENCE MECHANISMS AGAINST FUSARIUM WILT
CONCLUSION
REFERENCES
CHAPTER 2 Evaluation of the Cavendish banana GCTCV-218 for tolerance to Fusarium Oxysporum f. sp. cubense ‘subtropical’ race 4 (VCG 0120)
INTRODUCTION
MATERIALS AND METHODS RESULTS
DISCUSSION
REFERENCES
CHAPTER 3 Construction of a cDNA library with genes associated with tolerance to Fusarium oxysporum f. sp. cubense in Cavendish bananas
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
DISCUSSION
REFERENCES
CHAPTER 4 High-throughput screening of a Banana cDNA library using DNA microarray analysis
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS AND DISCUSSION
CHAPTER 5 Identification of genes associated with tolerance to Fusarium oxysporum f.sp cubense in Cavendish bananas
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
DISCUSSION
REFERENCES
SUMMARY
