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Banana is an important tropical crop and trading commodity in the world. However, Fusarium wilt is a severe risk for the world banana industry. Caused by the soil-borne fungal pathogen, Fusarium oxysporum f. sp. cubense (Foc), the disease is spreading insidiously and has been a source of enormous losses worldwide since the 1800s. Unfortunately, effective control methods are not available yet. The current study used an RNAi strategy, referred to as host-induced gene silencing (HIGS), to confer durable resistance against Fusarium by inhibiting in planta expression of Foc essential genes that are conserved in all Foc races and crucial for fungal virulence. In order to find efficient target genes, a wide search of literature has been conducted and four conserved target regions have been chosen after bioinformatics analysis. Preliminary findings from in vitro fungal inhibition assays showed significant reductions in fungal spore count, germination rate and mycelia growth after treating fungal cultures with double-stranded RNA (dsRNA) targeting four Foc genes, suggesting silencing of these genes was effective to reduce fungal growth. Intron hairpin constructs encoding dsRNA targeting selected Foc genes are in the process of being transformed into Arabidopsis thaliana for proof-of-concept of in planta fungal resistance.

Fusarium oxysporum f. sp. cubense (Foc) is a fungal pathogen of banana and is a significant threat to global banana production. A novel strain of Foc (named tropical race 4) first emerged in Southeast Asia and has recently been detected in Africa and Jordan. Tropical race 4 of Foc is of significant concern to the banana industry as it is extremely pathogenic towards all commercial banana cultivars. Currently, very few genes involved in pathogenicity have been identified in Foc. However, many pathogenicity-associated genes have been studied in the F oxysporum species complex. This study sought to identify the orthologues of genes previously demonstrated to be involved in the pathogenicity of F oxysporum in a collection of Foc isolates. Of those genes assessed, we detected all pathogenicity-associated genes in all Foc isolates, with the exception of SIX8, which was only detected in race 4 isolates. Our results indicate that many genes are required for general pathogenicity towards plants and are widely distributed across the F oxysporum species complex. However, the host-specific pathogenicity of Foc may be attributed to fungal effectors, such as SIX8. Previous work in the tomato-infecting lineage of E oxysporum has demonstrated that the SIX gene effector family is localized on a small, dispensable chromosome which has also been associated with the host-specific pathogenicity of the tomato infecting lineages. The current work sheds light on the pathogenomics of Fusarium. The results of this study are significant for the diagnosis and management of Foc. The identification and characterization of the genes controlling pathogenicity in Foc should be an ongoing field of research. It will also be of substantial value to better understand the genomic organization of each VCG of Foc for the development a pangenome of Foc and the E oxysporum species complex. An improved understanding of the pathogenomics of Foc is critical for the ongoing improvement of disease management strategies for Fusarium wilt of banana.

Fusarium wilt of banana, caused by the fungal pathogen Fusarium oxysporum f. sp. cubense (Foc), is one of the most destructive diseases of banana. A particularly virulent strain of the pathogen, tropical race 4 (TR4), presents an emerging threat to banana producing regions throughout the world. No commercially acceptable banana cultivar is resistant to TR4 and, as with all strains of the Fusarium wilt pathogen, there is no effective chemical control. Genetic resistance to TR4 has been observed in the diploid wild banana Musa acuminata subsp. malaccensis, which has consequently received attention as a potential source of Fusarium resistance genes. The aim of this research was to determine the pattern of inheritance of the resistance trait by screening plants for resistance to Foc subtropical race 4 (SR4) and TR4. Our results showed that the F1 progeny of self-fertilized malaccensis plants challenged in pot trials against SR4 (VCGs 0120, 0129, 01211) and TR4 (VCG 01213/16) segregated for resistance according to a Mendelian ratio of 3:1 which is consistent with a single dominant gene hypothesis.

Apart from morphology and genetic characteristics, species status of Pythium zingiberis and P. myriotylum may also be confirmed based on their pathogenicity and host range. An Australian putative P. zingiberis isolate and imported type isolates of P. myriotylum and P. zingiberis were subject to both in vitro and in vivo pathogenicity tests. In vitro tests were carried out on excised carrot, ginger, potato, radish, and sweet potato tuber/root sections, and on seeds and seedlings of cucumber, cauliflower, millet, rye, sweet corn, tomato, and wheat. In all assays conducted, the Australian isolate was found to be the most pathogenic, followed by type specimen of P. zingiberis (UOP 275), and then the type specimen P. myriotylum (CBS 254.70). An in vivo experiment on ginger plants at 35°C (with 10 h day light) in quarantine conditions showed that the ginger plants inoculated with the Australian isolate and also the type specimen of P. zingiberis died at 21 days after inoculation, whereas those inoculated with P. myriotylum CBS 254.70 were still green and healthy. Along with cardinal growth rate, the Australian isolate was confirmed to be closely related to P. zingiberis. This is also the first direct comparison in pathogenicity of P. zingiberis and P. myriotylum.

Laboratory experiments were established to study the influence of silicon on improvements in the defense response of cucumber seedlings to Pythium-induced damping-off disease. Supplementing cucumber seedlings with different concentrations of silicon (0, 100, 200, 500, 1000 and 2500 ppm) for 7 days prior to inoculation with P. aphanidermatum isolates did not result in a significant reduction in seedling mortality at 20 and 25 degrees C. Extending the period of supplementation to 14 days also did not result in any improvement of defense responses. In addition, mortality levels in the presence of silicon were not reduced when cucumber seedlings were inoculated with three isolates of P. aphanidermatum differing in their aggressiveness levels (weak, moderate and very aggressive). This could be related to a rapid infection by Pythium of cucumber seedlings in relation to a slower rate of induction of defense responses by silicon.

Breeding improved commercially acceptable Musa cultivars with disease resistance has proven to be a difficult task. This is mostly because of the ploidy levels involved and subsequent sterility. Fusarium oxysporum f.sp. cubense (Foc) race 4 is a pathogen that threatens to decimate 'Cavendish' plantations around the world. No chemical control exists and the only hope lies in the development of a resistant cultivar. To assess germplasm from breeding programs for resistance, the plants are exposed to the pathogen in the field. Field screening is, however, greatly influenced by environmental factors and requires a lot of area and time. Molecular markers have increased the efficiency of breeding programs in other crops. In this paper we shall discuss how molecular markers can aid in the search for a Foc race 4 resistant cultivar.