# PurK, N5-Carboxyaminoimidazole Ribonucleotide Synthetase, an Exocrine Protein Induced by Potato Plants, Influences the Virulence Through Motility Modulation in Pectobacterium brasiliense NJAU180

## TL;DR

A protein called PurK, produced by a potato pathogen, helps the bacteria infect plants by boosting movement and suppressing plant defenses.

## Contribution

PurK is identified as a novel extracellular protein in Pectobacterium brasiliense that modulates virulence through motility and immune suppression, independent of its role in purine biosynthesis.

## Key findings

- PurK is a plant-induced extracellular protein in Pectobacterium brasiliense that significantly reduces virulence when deleted.
- PurK promotes bacterial motility by modulating flagellar gene transcription and suppresses plant callose deposition.
- PurK triggers hypersensitive responses and upregulates PTI marker genes in host plants, but its effects are independent of purine biosynthesis.

## Abstract

Bacterial pathogens secrete effector proteins that suppress plant immune responses and facilitate infection. This study focuses on Pectobacterium brasiliense NJAU180, a bacterial pathogen causing severe blackleg disease in potato plants in Inner Mongolia, China. Using exoproteomic analysis, plant-induced extracellular proteins were identified by comparing culture supernatants from P. brasiliense NJAU180 grown in minimal medium (MM) alone and in the presence of aseptically grown potato plantlets at an early growth stage (OD600 ≈ 0.5). The results reveal PurK as a novel plant-induced extracellular protein, and deletion of purK markedly reduces virulence. PurK, N5-carboxyaminoimidazole ribonucleotide synthetase, is a key enzyme in de novo purine biosynthesis. Its impact on virulence is distinct from the conventional production of plant cell wall–degrading enzymes: PurK promotes motility by modulating transcription of flagellar genes, acting through its three domains as an integrated unit to infect successfully. Extracellularly detected PurK suppresses callose deposition, a PAMP-triggered immunity (PTI)-like defense, while it also triggers a strong hypersensitive response and upregulates expression of PTI marker genes such as PR2 and WRKY7 when secreted into the host plant. Although PurK interacts specifically with PurE, our data indicate that PurK’s pathogenic effects operate independently of purine biosynthesis. This study reveals a reliable experimental model for more accurate assessment of microbe–plant interactions and highlights new functional roles for PurK in P. brasiliense NJAU180 pathogenesis and identifies potential targets for disease control strategies.