PpTOR, a Major Factor Associated with Phytophthora parasitica Virulence, Serves as a Candidate RNAi Target for Disease Control
TL;DR
It is demonstrated that the conserved eukaryotic kinase TOR (target of rapamycin) is essential for both growth and pathogenicity in P. parasitica, establishing PpTOR as a global regulator of pathogenicity and validate PpTOR as a promising target for RNA-based disease control strategies.
Abstract
Phytophthora parasitica is a devastating oomycete pathogen that causes significant crop losses worldwide. Identifying master regulators of its virulence is crucial for the development of novel control strategies. Here, we demonstrate that the conserved eukaryotic kinase TOR (target of rapamycin) is essential for both growth and pathogenicity in P. parasitica. Transcriptomic analysis revealed that PpTOR inhibition broadly reprograms the transcriptome of P. parasitica, notably leading to the downregulation of numerous PpRxLR and PpCRN effector genes. Among these genes, the overexpression of PpRxLR3 increased plant susceptibility to P. parasitica by affecting jasmonic acid biosynthesis and signaling. On the basis of the crucial role of PpTOR, we evaluated its potential as a target for intervention. Host-induced gene silencing (HIGS) of PpTOR in Nicotiana benthamiana conferred strong resistance to P. parasitica, which was associated with the downregulation of the expression of PpTOR and key effector genes during P. parasitica infection. Furthermore, small RNA sequencing confirmed the production of PpTOR-specific siRNAs in HIGS plants. Exogenous application of synthetic siRNAs targeting PpTOR effectively reduced P. parasitica virulence. Our findings establish PpTOR as a global regulator of pathogenicity and validate PpTOR as a promising target for RNA-based disease control strategies.