Abstract
Microbial necrosis and ethylene-inducing peptide 1 (Nep1)-like proteins (NLPs) act as cytolytic toxins and immunogenic patterns in plants. Our previous work shows that cytolytic NLPs (i.e., PyolNLP5 and PyolNLP7) from the biocontrol agent Pythium oligandrum enhance plant resistance against Phytophthora pathogens by inducing the expression of plant defensins. However, the relevance between PyolNLP-induced necrosis and plant resistance activation is still unclear. Here, we find that the necrosis-inducing activity of PyolNLP5 requires amino acid residues D127 and E129 within the conserved “GHRHDLE” motif. However, PyolNLP5-mediated plant disease resistance is irrelevant to its necrosis-inducing activity and the accumulation of reactive oxygen species (ROS). Furthermore, we reveal the positive role of non-cytotoxic PyolNLPs in enhancing plant resistance against Phytophthora pathogens and the fugal pathogen Sclerotinia sclerotiorum. Similarly, non-cytotoxic PyolNLPs also activate plant defense in a cell death-independent manner and induce defensin expression. The functions of non-cytotoxic PyolNLP13/14 rely on their conserved nlp24-like peptide pattern. Synthetic Pyolnlp24s derived from both cytotoxic and non-cytotoxic PyolNLPs can induce plant defensin expression. Unlike classic nlp24, Pyolnlp24s lack the ability of inducing ROS burst in plants with the presence of Arabidopsis nlp24 receptor RLP23. Taken together, our work demonstrates that PyolNLPs enhance plant resistance in an RLP23-independent manner, which requires the conserved nlp24-like peptide pattern but is uncoupled with ROS burst and cell death.
Highlights
Millions of years of coevolution of plants and microbial pathogens have shaped the antagonistic ability of both parties
Multiple sequence alignment analysis found that these five PyolNLPs were very conserved (Supplementary Figure 1), and evolutionary analysis found that they were all located in Group 1 (Supplementary Figure 2)
We further examined whether the non-cytotoxic PyolNLP13/14 could activate plant immunity responses by testing their effect on the expression of six defense-related N. benthamiana genes, including NbPTI5 and NbCyp71D20 involved in PTI, salicylic acid (SA)-dependent ENHANCED DISEASE SUSCEPTIBILITY 1 (NbEDS1) and NbPR1, and ETHYLENE INSENSITIVE 3 (NbEIN3) and PLANT DEFENSIN 1.2 (NbPDF1.2) involved in jasmonic acid and ethylene signaling pathways
Summary
Millions of years of coevolution of plants and microbial pathogens have shaped the antagonistic ability of both parties. Their interactions upgrade both pathogen invasion approaches and plant defense mechanisms (Jones and Dangl, 2006; Ottmann et al, 2009). The bacterial PAMP elongation factor thermo unstable (EF-Tu) is recognized by Arabidopsis LRR-RLK EFR via its conserved N-terminal N-acetylated epitope elf (Zipfel et al, 2006). The subsequent immune activation after PRR-RLK/RLP recognition is referred to as MAMP- or PAMP-triggered immunity (MTI or PTI), which leads to the rise of cytosolic Ca2+ level, production of extracellular reactive oxygen species (ROS) and activation of mitogen-activated protein kinase (MAPK) cascades (Couto and Zipfel, 2016). MTI/PTI, ROS accumulation and the downstream signaling cascades trigger various defense mechanisms to defend pathogen invasion (Poland et al, 2009; Yang and Fernando, 2021)
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