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Updated: Jan 9, 2026

Identification of Post-translational Modifications of Plant Protein Complexes
Published on: February 22, 2014
The virulence function of RXLR effector PpE4 of Phytophthora parasitica is coupled with its cell death-inducing
Guiyan Huang1,2, Yanan Hu1, Nannan Lu1
1China-USA Citrus Huanglongbing Joint Laboratory, National Navel Orange Engineering Research Center, and College of Life Sciences, Gannan Normal University, Ganzhou, Jiangxi, China.
Abstract:
RXLR effectors secreted by Phytophthora pathogens are important virulence factors in suppressing plant immunity and facilitating pathogen infection. In addition to possessing a variety of functions, some RXLR effectors have been found to trigger host cell death with different underlying mechanisms. PpE4 was previously reported as a virulent RXLR effector secreted by Phytophthora parasitica and triggers cell death in various plants. However, it is uncertain whether this type of cell death promotes or restricts the colonization of this hemibiotrophic pathogen. Here, we explored the correlation between the cell death activity of PpE4 and its contribution to the infection of P. parasitica. Sequencing data revealed that PpE4 exhibited both point mutations and presence/absence polymorphisms in the P. parasitica population under positive selection. E4D, one of four alleles, lost its cell death-inducing ability, also lost its ability to increase plant susceptibility to pathogen infection. Furthermore, E4D could compromise the cell death-inducing and virulence functions of the other three PpE4 alleles. PpE4 truncated mutants deficient in cell death-inducing activity showed abolished ability to increase plant susceptibility. Finally, PpE4 was unable to increase the susceptibility of TRV-NPK plants, which showed abolished cell death. Taken together, the cell death-inducing activity of PpE4 is essential for its virulence function during colonization of hemibiotrophic pathogen, suggesting that P. parasitica exploits the cell death triggered by PpE4 to facilitate the transition from biotrophy to necrotrophy. These findings provide a new perspective for understanding the role of RXLR effectors triggered cell death in the pathogenesis of hemibiotrophic pathogens.
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