Abstract

BackgroundUnderstanding how plants and pathogens modulate gene expression during the host-pathogen interaction is key to uncovering the molecular mechanisms that regulate disease progression. Recent advances in sequencing technologies have provided new opportunities to decode the complexity of such interactions. In this study, we used an RNA-based sequencing approach (RNA-seq) to assess the global expression profiles of the wheat yellow rust pathogen Puccinia striiformis f. sp. tritici (PST) and its host during infection.ResultsWe performed a detailed RNA-seq time-course for a susceptible and a resistant wheat host infected with PST. This study (i) defined the global gene expression profiles for PST and its wheat host, (ii) substantially improved the gene models for PST, (iii) evaluated the utility of several programmes for quantification of global gene expression for PST and wheat, and (iv) identified clusters of differentially expressed genes in the host and pathogen. By focusing on components of the defence response in susceptible and resistant hosts, we were able to visualise the effect of PST infection on the expression of various defence components and host immune receptors.ConclusionsOur data showed sequential, temporally coordinated activation and suppression of expression of a suite of immune-response regulators that varied between compatible and incompatible interactions. These findings provide the framework for a better understanding of how PST causes disease and support the idea that PST can suppress the expression of defence components in wheat to successfully colonize a susceptible host.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2684-4) contains supplementary material, which is available to authorized users.

Highlights

  • Understanding how plants and pathogens modulate gene expression during the host-pathogen interaction is key to uncovering the molecular mechanisms that regulate disease progression

  • Three biological replicates were used to generate a total of 27 poly(A) enriched cDNA libraries, which were sequenced on the Illumina HiSeq 2000 platform

  • Less than 1 % of reads mapped to the Puccinia striiformis f. sp. tritici (PST)-130 reference genome at 1, 2, and 3 dpi, similar to the results observed in the uninoculated plant control (Additional file 1: Table S1)

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Summary

Introduction

Understanding how plants and pathogens modulate gene expression during the host-pathogen interaction is key to uncovering the molecular mechanisms that regulate disease progression. Perception of pathogen-associated molecular patterns by pattern recognition receptors at the plant cell surface causes activation of basal defence responses [1]. Pathogens suppress these basal defence responses by secreting an array of effector proteins from specialized feeding structures, called haustoria in filamentous pathogens [2]. In resistant plant genotypes, plant immune receptors (resistance proteins) recognize these effector proteins and activate a second wave of defence responses. This second wave includes localised cell death, known as the hypersensitive response

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