Abstract

Bacterial blight caused by Xanthomonas oryzae pv. oryzae (Xoo) is one of the most devastating diseases of rice. However, the molecular mechanism underpinning the Xoo resistance of rice is still not fully understood. Here, we report that a class II small heat shock protein gene, OsHsp18.0, whose expression was differentially induced between a resistant and a susceptible variety in response to Xoo infection, plays positive roles in both biotic and abiotic resistance. The molecular chaperone activity of OsHsp18.0 was confirmed by a bacterium-expressed glutathione S-transferase fusion protein. Overexpression of OsHsp18.0 in a susceptible rice variety significantly enhanced its resistance to multiple Xoo strains, whereas silencing of OsHsp18.0 in a resistant variety drastically increased its susceptibility. The enhanced Xoo resistance in OsHsp18.0-overexpressing lines was positively correlated with the sensitized salicylic acid-dependent defense responses. In addition to disease resistance, the OsHsp18.0 overexpressing and silencing lines exhibited enhanced and reduced tolerance, respectively, to heat and salt treatments. The subcellular localization study revealed that the green fluorescent protein-OsHsp18.0 was enriched on the nuclear envelope, suggesting a potential role of OsHsp18.0 in the nucleo-cytoplasmic trafficking. Together, our results reveal that the rice OsHsp18.0 is a positive regulator in both biotic and abiotic defense responses.

Highlights

  • All organisms produce heat shock proteins (Hsps) in response to elevation in temperature and certain other stresses[1]

  • The growth rate of bacteria Zhe[173] was significantly reduced at 7 and 11 dpi on the leaves of the transgenic lines OE-3 and OE-6 (p < 0.01) relative to on the leaves of Nipponbare (Fig. 4c). These results suggest that overexpression of OsHsp18.0 results in a broad-spectrum resistance to Xanthomonas oryzae pv. oryzae (Xoo) strains and OsHsp18.0 plays a positive role in basal resistance or PAMP-triggered immunity (PTI)

  • salicylic acid (SA) accumulation responded differently to different Xoo strains, the free SA level in OsHsp18.0-overexpressing plants was significantly increased (p < 0.05) compared with Nipponbare both before and after the infections by different Xoo strains (Fig. 6a). These results suggest that the increased level of free SA in OsHsp18.0-overexpressing plants may be responsible for the enhanced resistance to Xoo (Fig. 4)

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Summary

Introduction

All organisms produce heat shock proteins (Hsps) in response to elevation in temperature and certain other stresses[1]. Some sHsps have been demonstrated to form complexes with denatured proteins and prevent their aggregation in vitro and in vivo[2, 9, 10]. From these complexes, the target proteins are subsequently refolded by Hsp100/Hsp[70] and cochaperones in an ATP-dependent manner during the recovery phase[6, 8, 11]. The CII subfamily has a conserved N-terminal amino acid motif (DA-AMAATP) that is not found in the other cytoplasmic/nuclear sHsps[7]. The rest of six cloned Xoo R genes encode different types of proteins, indicating the functional diversity in rice–Xoo interactions[18]. Given the importance of the rice Xoo disease, there is an urgency to clone more Xoo R genes to aid in fully understanding the molecular mechanisms underpinning the resistance against Xoo

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