Browsing by Author "Ssali, Reuben Tendo"

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    The identification and characterization of resistance musa to Fusarium Oxysporum F.SP cubense race 1
    (Stellenbosch : Stellenbosch University, 2016-03) Ssali, Reuben Tendo; Viljoen, Altus; Kiggundu, A.; Stellenbosch University. Faculty of AgriSciences. Dept. of Plant Pathology.
    ENGLISH ABSTRACT: Fusarium oxysporum f. sp. cubense (Foc), a soil-borne fungus affecting bananas (Musa spp.), is considered one of the most devastating pathogens in agricultural history. The fungus infects banana roots, colonises the rhizome and pseudo stem, and causes a lethal wilting disease called Fusarium wilt. Fusarium wilt can cause losses of up to 100% in banana fields planted with susceptible genotypes, without any known cure. Host plant resistance to Foc, which has been identified in the Musa gene pool, is widely considered the only feasible method to control the disease. However, conventional breeding to improve susceptible banana varieties is hampered by male and female sterility and the long generation period of the crop. The inheritance of resistance in Musa to Foc race 1 in the ‘SN8075F2’ population, derived from the cross of cultivar ‘Sukali Ndiizi’ and the diploid banana ‘TMB2X8075-7’, was investigated in this study. One hundred and sixty three F2 progenies were evaluated for their response to Fusarium wilt in a screen house experiment. The test plants were inoculated by mixing loam soil with millet grains, colonized by Foc race 1, in polythene pots. One hundred and fifteen genotypes were categorized as susceptible and 48 as resistant based on rhizome discolouration. Mendelian segregation analysis for susceptible vs. resistant fitted the segregation ratio of 3:1 (X2 =1.72, P=0.81), suggesting that resistance to Fusarium wilt in the diploid line ‘TMB2X8075-7’ is provided by a single recessive gene. The name pd1 (Panama disease 1) has been proposed for the recessive gene responsible for resistance to Fusarium wilt in the diploid line ‘TMB2X8075-7’. DArT markers were identified in a segregating population following a cross between the susceptible banana cultivar ‘Sukali Ndiizi’ and a resistant diploid banana ‘TMB2X8075-7’. The markers were in qualitative linkage disequilibrium, with 13 markers linked to resistance and 88 markers associated with susceptibility to Foc race 1. Putative functions have been assigned to candidate genes through in-silico database analysis including Laccase-25 (LAC25), Homeobox-leucine zipper protein (HOX32), SWIM zinc finger family protein, Transcription factor MYB3, GDSL esterase/lipase EXL3 among others. The candidate markers and genes closely associated with resistance/susceptibility could also be used in genetic engineering or for marker-assisted selection (MAS) in breeding for Fusarium wilt resistance. The Foc race 1-banana binomial interaction of three genotypes (‘Sukali Ndiizi’ AAB, ‘Mbwazirume’ AAA and ‘TMB2X8075-7 AA) was investigated by deep sequencing of the root transcriptome to study Fusarium wilt resistance in bananas. A total of 299 million raw reads, each about 100-nucleotides long, were derived from cDNA libraries constructed at four time points: 0, 48, 96 and 192 hrs after inoculation with Foc race1. From the 10136 differentially expressed genes (DEGs), 5640 (55.7%) were uniquely up-regulated and 4496 (44.4%) uniquely down-regulated in the libraries of ‘Mbwazirume’, ‘TMB2X28075-7’ and ‘Sukali Ndiizi at 48, 96 and 192 hrs post inoculation. The DEGs were annotated with Gene Ontology (GO) terms and pathway enrichment analysis, and significant pathway categories identified included the ‘Metabolic’, ‘Ribosome’, ‘Plant–pathogen interaction’ and ‘Plant hormone signal transduction’ pathways. Salicylic acid and ethylene were stimulated in the ‘Plant hormone signal transduction’ pathways in all the three genotypes. Fifteen defence-related genes were identified as candidate genes contributing to Fusarium wilt resistance in banana. These candidate genes could be used to improve susceptible banana genotypes to enhance levels of fungal disease resistance to Foc race 1.