Dataset Information

Tripartite symbiosis formed by Pisum sativum, rhizobia and mycorrhiza: Implications for the symbionts, the host plant and the pathogenic fungi

ABSTRACT: Ascochyta blight causes severe losses in field pea production and the search for resistance traits towards the causal agent Didymella pinodes is of particular importance to farmers. Various microsymbionts are reported to shape the plants´ immune response. However, regardless their contribution to resistance, they are hardly included in experimental designs. In this project, the bi-directional effect of the symbionts´ (rhizobia, mycorrhiza) and the leaf proteome/metabolome of two field pea cultivars with varying resistance levels towards D. pinodes is delineated.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Pisum Sativum (garden Pea)

TISSUE(S): Plant Cell, Leaf

SUBMITTER: Reinhard Turetschek

LAB HEAD: Stefanie Wienkoop

PROVIDER: PXD005861 | Pride | 2017-03-15

REPOSITORIES: Pride

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Key metabolic traits of Pisum sativum maintain cell vitality during Didymella pinodes infection: cultivar resistance and the microsymbionts' influence.

Turetschek Reinhard R Desalegn Getinet G Epple Tamara T Kaul Hans-Peter HP Wienkoop Stefanie S

Journal of proteomics 20170306

Ascochyta blight causes severe losses in field pea production and the search for resistance traits towards the causal agent Didymella pinodes is of particular importance for farmers. Various microsymbionts have been reported to shape the plants' immune response. However, regardless their contribution to resistance, they are hardly included in experimental designs. We delineate the effect of symbionts (rhizobia, mycorrhiza) on the leaf proteome and metabolome of two field pea cultivars with varyi ...[more]

PMID: 28268116

Similar Datasets

Project description:Ascochyta blight (AB) is a devastating and aggressive disease of field peas caused by multiple pathogens and the occurrence of the combinations of these pathogens forms a disease complex of which Peyronellaea pinodes, is the most aggressive. AB symptoms include necrotic lesions on all above ground parts of the plant, which can reduce crop yield by up to 70% and result in major economic losses globally. Crop resistance to the disease is reported to be quantitative and, although several genes have been reported to be AB response genes in Spanish pea genotypes, the lines or genotypes of the Australian field pea breeding program have not been investigated. Plants have specialized defence mechanisms that enable them respond to pathogen invasion, and this involves a cascade of genes which are differentially regulated upon infection. In this study, the time-course gene expression profiles of four Australian field pea genotypes including commercial varieties, known to have varying levels of AB resistance were investigated in response to P. pinodes infection. Infected and control plants at 0, 6, 24, 48, 72 and 96HPI were sampled for RNA seq. Mapping of transcriptome sequencing data against the field pea genome resulted in about the identification of c. 6,700 differentially expressed genes. Of the 21 AB resistance genes reported in previously published studies, only seven were present on the list of DEGs generated in this study. No significant pattern was identified in gene expression for the seven genes to differentiate resistant from susceptible genotypes. However, four key genes i.e., disease response protein, malate dehydrogenase, isoflavone 2 hydrogenase and Isoflavone reductase were shown to be associated with suppression of AB disease phenotype after 96HPI. Furthermore, GO functional annotation revealed several genes associated with defence including genes associated with the Salicylic acid pathway, reactive oxygen species, programmed cell death and hypersensitive response. Although the overall result showed a lack of strong resistance in the Australian pea genotypes as well as the fact that disease suppression does not directly equal resistance, we however were able to identify potential candidates that could be pyramided from exotic material into the breeding program to assess for improved resistance.

Project description:Objectives: Development of daptomycin resistance (DAPR) in Staphylococcus aureus is associated with clinical treatment failures. Mechanism(s) of such resistance has not been clearly defined. Methods: We studied an isogenic daptomycin-susceptible (DAPS) and daptomycin-resistant (DAPR) S. aureus strain pair (616; 701) from a patient with relapsing endocarditis during daptomycin treatment, using comparative transcriptomic and proteomic techniques. Results. Minor differences in genome content were found between strains by DNA hybridization. Transcriptomic analyses identified a number of genes differentially expressed in important functional categories: cell division, metabolism of bacterial envelopes and global regulation. Of note, the DAPR isolate exhibited reduced expression of the major cell wall autolysis gene coincident with upregulation of genes involved in wall teichoic acid production. Using quantitative (q)RT-PCR on gene cadre putatively involved in cationic peptide resistance, we formulated a putative regulatory network compatible with microarray data-sets, mainly implicating bacterial envelopes. Of interest, qRT-PCR of this same gene cadre from two distinct isogenic DAPS/DAPR clinical strain pairs revealed evidence of other strain dependent networks operative in the DAPR phenotype. Comparative proteomics of 616 vs 701 revealed differential abundance of proteins in various functional categories including: cell-wall associated targets and biofilm-formation proteins. Phenotypically, strains 616 and 701 showed major differences in ability to develop bacterial biofilms in presence of the antibacterial lipid, oleic acid. Conclusions: Compatible with previous in vitro observations, in vivo acquired DAPR in S. aureus is a complex, multistep phenomenon allowing for: i) strain dependent phenotypes; ii) transcriptome adaptation; and iii) modification of lipid and protein content of cellular envelopes. Daptomycin suceptible strain vs daptomycin non suceptible strain after daptomycin treatment

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