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The Phytophthora nucleolar effector Pi23226 targets host ribosome biogenesis to induce necrotrophic cell death. | LitMetric

The Phytophthora nucleolar effector Pi23226 targets host ribosome biogenesis to induce necrotrophic cell death.

Plant Commun

Plant Immunity Research Center, Seoul National University, Seoul 08826, Republic of Korea; Plant Genomics and Breeding Institute, Department of Agriculture, Forestry and Bioresources, College of Agriculture and Life Science, Seoul National University, Seoul 08826, Republic of Korea. Electronic address:

Published: September 2023

AI Article Synopsis

  • Pathogen effectors, particularly from Phytophthora infestans, manipulate plant immune responses by targeting various organelles, including the nucleolus, which shows signs of stress during infection.
  • The study found that the effector Pi23226 causes cell death and nucleolar inflation, while its homolog Pi23015 does not have these effects, highlighting a specific role for Pi23226 in the infection process.
  • Additionally, Pi23226 binds to ribosomal RNA precursors, disrupts protein translation, and ultimately boosts the pathogen's ability to infect the host plant, shedding light on the nucleolus's role in plant-pathogen interactions.

Article Abstract

Pathogen effectors target diverse subcellular organelles to manipulate the plant immune system. Although the nucleolus has emerged as a stress marker and several effectors are localized in the nucleolus, the roles of nucleolar-targeted effectors remain elusive. In this study, we showed that Phytophthora infestans infection of Nicotiana benthamiana results in nucleolar inflation during the transition from the biotrophic to the necrotrophic phase. Multiple P. infestans effectors were localized in the nucleolus: Pi23226 induced cell death in N. benthamiana and nucleolar inflation similar to that observed in the necrotrophic stage of infection, whereas its homolog Pi23015 and a deletion mutant (Pi23226ΔC) did not induce cell death or affect nucleolar size. RNA immunoprecipitation and individual-nucleotide-resolution UV crosslinking and immunoprecipitation sequencing analysis indicated that Pi23226 bound to the 3' end of 25S rRNA precursors, resulting in accumulation of unprocessed 27S pre-rRNAs. The nucleolar stress marker NAC082 was strongly upregulated under Pi23226-expressing conditions. Pi23226 subsequently inhibited global protein translation in host cells by interacting with ribosomes. Pi23226 enhanced P. infestans pathogenicity, indicating that Pi23226-induced ribosome malfunction and cell death were beneficial for pathogenesis in the host. Our results provide evidence for the molecular mechanism underlying RNA-binding effector activity in host ribosome biogenesis and lead to new insights into the nucleolar action of effectors in pathogenesis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10504586PMC
http://dx.doi.org/10.1016/j.xplc.2023.100606DOI Listing

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