Abstract
Potato plants treated with the pathogen-associated molecular pattern Pep-13 mount salicylic acid- and jasmonic acid-dependent defense responses, leading to enhanced resistance against Phytophthora infestans, the causal agent of late blight disease. Recognition of Pep-13 is assumed to occur by binding to a yet unknown plasma membrane-localized receptor kinase. The potato genes annotated to encode the co-receptor BAK1, StSERK3A and StSERK3B, are activated in response to Pep-13 treatment. Transgenic RNAi-potato plants with reduced expression of both SERK3A and SERK3B were generated. In response to Pep-13 treatment, the formation of reactive oxygen species and MAP kinase activation, observed in wild type plants, is highly reduced in StSERK3A/B-RNAi plants, suggesting that StSERK3A/B are required for perception of Pep-13 in potato. In contrast, defense gene expression is induced by Pep-13 in both control and StSERK3A/B-depleted plants. Altered morphology of StSERK3A/B-RNAi plants correlates with major shifts in metabolism, as determined by untargeted metabolite profiling. Enhanced levels of hydroxycinnamic acid amides, typical phytoalexins of potato, in StSERK3A/B-RNAi plants are accompanied by significantly decreased levels of flavonoids and steroidal glycoalkaloids. Thus, altered metabolism in StSERK3A/B-RNAi plants correlates with the ability of StSERK3A/B-depleted plants to mount defense, despite highly decreased early immune responses.
Highlights
Perception of pathogen or microbe-associated molecular patterns (PAMPs/MAMPs) in plants by plasma membrane pattern recognition receptors (PRRs) initiates the activation of immune responses, leading to the formation of reactive oxygen species (ROS), MAP kinase activation and transcriptional reprogramming[1]
In contrast to Arabidopsis, which has five members of the somatic embryogenesis receptor kinases (SERKs) gene family, only three members, SERK1, SERK3A and SERK3B, were reported for tomato (Solanum lycopersicum)[6,7]. While both SERK3A or SERK3B are important for defense against root knot nematodes and nonpathogenic Pseudomonas syringae pv. tomato (Pst) DC3000 hrcC, a role for defense against pathogenic Pst DC3000 was demonstrated by virus-induced gene silencing for SERK3B, but not SERK3A7
In subsequent qRT-PCR analyses, primers were used, which are predicted to amplify both StSERK3A and StSERK3B transcripts. These analyses revealed significantly enhanced StSERK3A/B transcript levels in Pep-13-infiltrated potato leaves four hours after treatment, which declined after 24 hours (Fig. 1B)
Summary
Perception of pathogen or microbe-associated molecular patterns (PAMPs/MAMPs) in plants by plasma membrane pattern recognition receptors (PRRs) initiates the activation of immune responses, leading to the formation of reactive oxygen species (ROS), MAP kinase activation and transcriptional reprogramming[1]. In contrast to Arabidopsis, which has five members of the SERK gene family, only three members, SERK1, SERK3A and SERK3B, were reported for tomato (Solanum lycopersicum)[6,7]. While both SERK3A or SERK3B are important for defense against root knot nematodes and nonpathogenic Pseudomonas syringae pv. The receptor-like protein ELICITIN RESPONSE (ELR) from a wild potato associates with SERK3A from Solanum tuberosum and confers elicitin recognition and enhanced resistance against P. infestans[9]. Infiltration of Pep-13 into potato leaves leads to the accumulation of salicylic acid, jasmonic acid and hydrogen peroxide, as well as to defense gene activation, hypersensitive cell death and enhanced resistance to P. infestans infection[13]. Defense gene expression was induced by Pep-13 in StSERK3A/B-depleted plants
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