Abstract
The production of reactive oxygen species (ROS) is a ubiquitous defense response in plants. Adapted pathogens evolved mechanisms to counteract the deleterious effects of host-derived ROS and promote infection. How plant pathogens regulate this elaborate response against ROS burst remains unclear. Using the rice blast fungus Magnaporthe oryzae, we uncovered a self-balancing circuit controlling response to ROS in planta and virulence. During infection, ROS induces phosphorylation of the high osmolarity glycerol pathway kinase MoOsm1 and its nuclear translocation. There, MoOsm1 phosphorylates transcription factor MoAtf1 and dissociates MoAtf1-MoTup1 complex. This releases MoTup1-mediated transcriptional repression on oxidoreduction-pathway genes and activates the transcription of MoPtp1/2 protein phosphatases. In turn, MoPtp1/2 dephosphorylate MoOsm1, restoring the circuit to its initial state. Balanced interactions among proteins centered on MoOsm1 provide a means to counter host-derived ROS. Our findings thereby reveal new insights into how M. oryzae utilizes a phosphor-regulatory circuitry to face plant immunity during infection.
Highlights
During co-evolution with pathogens, plants have developed an innate immune system by sensing pathogen-associated molecular patterns (PAMPs), such as flagellin and chitin produced, respectively, by bacteria and fungi (Jones and Dangl, 2006; Liu et al, 2014)
When observation was made at 60 hpi, nearly 10% of infected cells were still filled with reactive oxygen species (ROS)
These results indicated that rice elaborates ROS as a barrier to infection as early as 24 hpi, and scavenging of host ROS may be necessary for further expansion of M. oryzae during infection
Summary
During co-evolution with pathogens, plants have developed an innate immune system by sensing pathogen-associated molecular patterns (PAMPs), such as flagellin and chitin produced, respectively, by bacteria and fungi (Jones and Dangl, 2006; Liu et al, 2014). Pattern-recognition receptors (PRRs) transduce the signals to the downstream components that initiate the immune response (Boutrot and Zipfel, 2017; Zipfel, 2014), which was referred to as PAMP-triggered immunity (PTI) (Boutrot and Zipfel, 2017; Jones and Dangl, 2006) This PRR to PTI processes often involves components of MAP kinase signaling pathways, callose deposition, ROS burst, and pathogenesis related (PR) gene expression. In rice (Oryza sativa), the LysM domain of the chitin-elicitor binding protein (CEBiP) binds to chitin and associates with the bifunctional plant receptor OsCERK1 that phosphorylates the downstream receptor-like cytoplasmic kinase 185 (OsRLCK185) for the activation of PTI by causing the ROS burst (Yamaguchi et al, 2013).
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