Project description:Transcriptome analysis reveals the response mechanism of Frl-mediated resistance to Fusarium oxysporum f. sp. radicis-lycopersici (FORL) infection in tomato
Project description:Upon exposure to unfavorable environmental conditions, plants need to respond quickly to maintain their homeostasis. For instance, physiological, biochemical and transcriptional changes occur during plant-pathogen interaction. In the case of Vanilla planifolia Jacks., a worldwide economically important crop, it is susceptible to Fusarium oxysporum f. sp. vanillae. This pathogen causes root and stem rot in vanilla plants that lead to plant death. To investigate how vanilla plants, respond at the transcriptional level upon infection with F. oxysporum f. sp. vanillae, here we employed the RNA-Seq approach to analyze the dynamics of whole-transcriptome changes during two-time frames of the infection. Analysis of global gene expression profiles indicated that the major transcriptional change occurred at 2 dpi, in comparison to 10 dpi. Whereas 3420 genes were found with a differential expression at 2 dpi, only 839 were identified at 10 dpi. The analysis of the transcriptional profile at 2 dpi suggests that, among other responses, vanilla plants prepare to counter the infection by gathering a pool of translational regulation-related transcripts. The screening of transcriptional changes of V. planifolia Jacks upon infection by F. oxysporum f. sp. vanillae provides insights into the plant molecular response, particularly the upregulation of ribosomal proteins at early stages. Thus, we propose that the plant-pathogen interaction between V. planifolia Jacks and F. oxysporum f. sp. vanillae causes a transcriptional reprogramming coupled with a translational regulation. Altogether, this study provides the identification of molecular players that could help to fight the most damaging disease of vanilla.
Project description:Background: The fungal pathogen, Fusarium oxysporum f.sp. pisi (Fop) causes fusarium wilt in peas. Races 1, 2, 5 and 6 are responsible for the majority of the economic losses globally. These are the only races present in Australia. Molecular infection mechanisms have been studied in a few other F. oxysporum formae speciales however, there has been no Fop-pea pathosystem studies. Results: A transcriptomic study was carried out to understand the molecular pathogenicity differences between the races. Transcript analysis revealed differences in the differentially expressed genes (DEGs) in the Fop races, potentially involved in fungal pathogenicity variations. Most of the DEGs in all the races were engaged in transportation, metabolism, oxidation-reduction, translation, biosynthetic processes, signal transduction, proteolysis, among others. Race 5 expressed the most virulence-associated genes. Most genes encoding for plant cell wall degrading enzymes, CAZymes and effector-like proteins were expressed in race 2. Race 6 had expressed the least number of genes during infection. Conclusion: Fop races deploy various factors and complex strategies to mitigate host defences to facilitate colonisation. This investigation provides an overview of the putative pathogenicity genes in different Fop races during infection. These genes need to be functionally characterised to confirm their pathogenicity/virulence roles and the race-specific genes can be further explored for molecular characterisation.
Project description:Fusarium oxysporum causes Fusarium wilt syndrome in more than 120 different plant hosts, including globally important crops such as tomato, cotton, banana, melon, etc. F. oxysporum shows high host specificity in over 150 formae speciales and have been ranked in the top 10 plant fungal pathogens. Although three PMTs encoded by the pmt1, pmt2, and pmt4 are annotated in the genome of F. oxysporum, their functions have not been reported. As O-mannosylation is not found in plants, a comprehensive understanding of PMTs in F. oxysporum becomes attractive for the development of new strategy against Fusarium wilt. In order to understand the molecular mechanism of the differential functions of three PMTs, a comparative O-glycoproteome analysis of the pmt mutants were carried out.
