4.7 Article

Transcriptional profile of AvrRpt2EA-mediated resistance and susceptibility response to Erwinia amylovora in apple

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SCIENTIFIC REPORTS
卷 11, 期 1, 页码 -

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NATURE PORTFOLIO
DOI: 10.1038/s41598-021-88032-x

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  1. Projekt DEAL
  2. Deutsche Forschungsgemeinschaft (DFG) [AOBJ 577770, 611951]

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This study identified 211 differentially expressed genes in the response of apple to the bacterial pathogen Erwinia amylovora, with a focus on the activation of heat-shock response genes in the susceptible reaction. The potential roles of genes involved in the formation of flavonoids and terpenoids, ribosome-inactivating enzymes, and transcription factors in resistance to the pathogen were also highlighted.
Most of the commercial apple cultivars are highly susceptible to fire blight, which is the most devastating bacterial disease affecting pome fruits. Resistance to fire blight is described especially in wild Malus accessions such as M. x robusta 5 (Mr5), but the molecular basis of host resistance response to the pathogen Erwinia amylovora is still largely unknown. The bacterial effector protein AvrRpt2(EA) was found to be the key determinant of resistance response in Mr5. A wild type E. amylovora strain and the corresponding avrRpt2(EA) deletion mutant were used for inoculation of Mr5 to induce resistance or susceptible response, respectively. By comparison of the transcriptome of both responses, 211 differentially expressed genes (DEGs) were identified. We found that heat-shock response including heat-shock proteins (HSPs) and heat-shock transcription factors (HSFs) are activated in apple specifically in the susceptible response, independent of AvrRpt2(EA). Further analysis on the expression progress of 81 DEGs by high-throughput real-time qPCR resulted in the identification of genes that were activated after inoculation with E. amylovora. Hence, a potential role of these genes in the resistance to the pathogen is postulated, including genes coding for enzymes involved in formation of flavonoids and terpenoids, ribosome-inactivating enzymes (RIPs) and a squamosa promoter binding-like (SPL) transcription factor.

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