Abstract
BackgroundFusarium wilt, caused by the fungal pathogen Fusarium oxysporum f. sp. cubense tropical race 4 (Foc TR4), is considered the most lethal disease of Cavendish bananas in the world. The disease can be managed in the field by planting resistant Cavendish plants generated by somaclonal variation. However, little information is available on the genetic basis of plant resistance to Foc TR4. To a better understand the defense response of resistant banana plants to the Fusarium wilt pathogen, the transcriptome profiles in roots of resistant and susceptible Cavendish banana challenged with Foc TR4 were compared.ResultsRNA-seq analysis generated more than 103 million 90-bp clean pair end (PE) reads, which were assembled into 88,161 unigenes (mean size = 554 bp). Based on sequence similarity searches, 61,706 (69.99%) genes were identified, among which 21,273 and 50,410 unigenes were assigned to gene ontology (GO) categories and clusters of orthologous groups (COG), respectively. Searches in the Kyoto Encyclopedia of Genes and Genomes Pathway database (KEGG) mapped 33,243 (37.71%) unigenes to 119 KEGG pathways. A total of 5,008 genes were assigned to plant-pathogen interactions, including disease defense and signal transduction. Digital gene expression (DGE) analysis revealed large differences in the transcriptome profiles of the Foc TR4-resistant somaclonal variant and its susceptible wild-type. Expression patterns of genes involved in pathogen-associated molecular pattern (PAMP) recognition, activation of effector-triggered immunity (ETI), ion influx, and biosynthesis of hormones as well as pathogenesis-related (PR) genes, transcription factors, signaling/regulatory genes, cell wall modification genes and genes with other functions were analyzed and compared. The results indicated that basal defense mechanisms are involved in the recognition of PAMPs, and that high levels of defense-related transcripts may contribute to Foc TR4 resistance in banana.ConclusionsThis study generated a substantial amount of banana transcript sequences and compared the defense responses against Foc TR4 between resistant and susceptible Cavendish bananas. The results contribute to the identification of candidate genes related to plant resistance in a non-model organism, banana, and help to improve the current understanding of host-pathogen interactions.
Highlights
Fusarium wilt, caused by the fungal pathogen Fusarium oxysporum f. sp. cubense tropical race 4 (Foc TR4), is considered the most lethal disease of Cavendish bananas in the world
After the reads were assembled into contigs, scaffolds and clusters successively, they were analyzed for unigenes, of which more than 90,000 were present in ‘Brazilan’ and more than 100,000 in ‘Nongke No 1’ (Table 2)
In Musa, we found that cyclic nucleotide gated channels (CNGCs) 1, CNGC 5 and CNGC 6 changed after pathogen-associated molecular pattern (PAMP) perception, which suggested that there is a fundamental difference in the Ca2+ influx mechanism between banana and Arabidopsis
Summary
Fusarium wilt, caused by the fungal pathogen Fusarium oxysporum f. sp. cubense tropical race 4 (Foc TR4), is considered the most lethal disease of Cavendish bananas in the world. Fusarium wilt, caused by the fungal pathogen Fusarium oxysporum f. Cubense tropical race 4 (Foc TR4), is considered the most lethal disease of Cavendish bananas in the world. To a better understand the defense response of resistant banana plants to the Fusarium wilt pathogen, the transcriptome profiles in roots of resistant and susceptible Cavendish banana challenged with Foc TR4 were compared. The crop is threatened by Fusarium wilt, a fungal disease considered to be one of the most destructive in agricultural history [1,2]. Known as Panama disease, is caused by the soil borne fungus, Fusarium oxysporum f. The pathogen infects banana roots, colonizes and occludes the xylem vessels, and causes a reddish-brown discoloration of the rhizome and pseudostem. Once the soil is infested with Foc, susceptible cultivars cannot be successfully replanted for up to 30 years [3]
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