Abstract

Heat stress negatively affects barley production and under elevated temperatures defense responses to powdery mildew (Blumeria graminis f. sp. hordei, Bgh) are altered. Previous research has analyzed the effects of short-term (30 s to 2 h) heat stress, however, few data are available on the influence of long-term exposure to heat on powdery mildew infections. We simultaneously assessed the effects of short and long term heat pre-exposure on resistance/susceptibility of barley to Bgh, evaluating powdery mildew infection by analyzing symptoms and Bgh biomass with RT-qPCR in barley plants pre-exposed to high temperatures (28 and 35 °C from 30 s to 5 days). Plant defense gene expression after heat stress pre-exposure and inoculation was also monitored. Our results show that prolonged heat stress (24, 48 and 120 h) further enhanced Bgh susceptibility in a susceptible barley line (MvHV118-17), while a resistant line (MvHV07-17) retained its pathogen resistance. Furthermore, prolonged heat stress significantly repressed the expression of several defense-related genes (BAX inhibitor-1, Pathogenesis related-1b and Respiratory burst oxidase homologue F2) in both resistant and susceptible barley lines. Remarkably, heat-suppressed defense gene expression returned to normal levels only in MvHV07-17, a possible reason why this barley line retains Bgh resistance even at high temperatures.

Highlights

  • Plants are sessile organisms; a fast and efficient response to abiotic or biotic stresses is a key for their survival

  • Our results show that the expression of three plant defense-related genes (BAX inhibitor-1, Pathogenesis related 1-b and Respiratory burst oxidase homologue F2) is repressed drastically during prolonged (24, 48 and 120 h) heat stress

  • We found that pre-exposure to a prolonged heat stress (35 ◦C for 24, 48 and 120 h) enhances powdery mildew infection in the susceptible barley line MvHV118-17

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Summary

Introduction

Plants are sessile organisms; a fast and efficient response to abiotic or biotic stresses is a key for their survival. The first line of inducible plant defenses consists primarily of the pathogen-associated molecular pattern (PAMP) recognition system conferring a basal resistance (PAMP-triggered immunity, PTI) to a wide range of pathogens [1,2]. ETI is often associated with a localized programmed cell/tissue death (PCD) at infection sites called the hypersensitive response (HR) [4]. ROS like superoxide (O2− or hydrogen peroxide, H2O2) have a dual role during plant defense, as high ROS concentrations confer inhibition of invading pathogens along with PCD of infected plant cells (HR), while low ROS concentrations act as signals inducing antioxidants and pathogenesis-related (PR) genes and proteins in plant tissues adjacent to infection sites [5,6,7,8,9]. The PR1-b protein may contribute to resistance to fungal pathogens possibly by binding sterols in fungal membranes [12,13]

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