Abstract
Mechanisms underlying plant non-host resistance to Xanthomonas oryzae pv. oryzicola (Xoc), the pathogen causing rice leaf streak disease, are largely unknown. Cyclic nucleotide-gated ion channels (CNGCs) are calcium-permeable channels that are involved in various biological processes including plant resistance. In this study, functions of two tomato CNGC genes SlCNGC1 and SlCNGC14 in non-host resistance to Xoc were analyzed. Silencing of SlCNGC1 and SlCNGC14 in tomato significantly enhanced Xoc-induced hypersensitive response (HR) and non-host resistance, demonstrating that both SlCNGC1 and SlCNGC14 negatively regulate non-host resistance related HR and non-host resistance to Xoc in tomato. Silencing of SlCNGC1 and SlCNGC14 strikingly increased Xoc-induced callose deposition and strongly promoted both Xoc-induced and flg22-elicited H2O2, indicating that these two SlCNGCs repress callose deposition and ROS accumulation to attenuate non-host resistance and PAMP-triggered immunity (PTI). Importantly, silencing of SlCNGC1 and SlCNGC14 apparently compromised cytosolic Ca2+ accumulation, implying that SlCNGC1 and SlCNGC14 function as Ca2+ channels and negatively regulate non-host resistance and PTI-related responses through modulating cytosolic Ca2+ accumulation. SlCNGC14 seemed to play a stronger regulatory role in the non-host resistance and PTI compared to SlCNGC1. Our results reveal the contribution of CNGCs and probably also Ca2+ signaling pathway to non-host resistance and PTI.
Highlights
Each pathogen has its own host range
Our data in this study strongly indicate that SlCNGC1 and SlCNGC14 function as Ca2+ channels and negatively regulate tomato non-host resistance to X. oryzae pv. oryzicola (Xoc) through modulating Reactive oxygen species (ROS) accumulation and callose deposition
SlCNGC14-silenced aequorin transgenic plants strongly decreased with the peak value drop to only 97 and 39 relative luminescence (RLU), respectively (Figure 4). This result indicates that SlCNGC1 and SlCNGC14 function as Ca2+ channels and negatively regulate non-host resistance and pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) through modulating cytosolic Ca2+
Summary
Non-host resistance is triggered when a non-adapted pathogen attempts to infect a plant species outside of its host range. Non-host resistance is widely occurring, durable and broad-spectrum to non-adapted pathogens and is highly potential to be exploited in crop resistance engineering (Schulze-Lefert and Panstruga, 2011; Senthil-Kumar and Mysore, 2013). It has been clear that plant non-host resistance utilizes both preformed and induced defense mechanisms and frequently elicites hypersensitive response (HR). The induced non-host resistance is elicited after the preformed defense is overcome. As observed for host resistance, pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI) are often initiated in this layer of defense (Niks and Marcel, 2009; Senthil-Kumar and Mysore, 2013). The mechanisms underlying plant non-host resistance are far from well understood
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