Pseudomonas syringae pv. syringae Uses Proteasome Inhibitor Syringolin A to Colonize from Wound Infection Sites

PLoS Pathogens

Emerson Crabill¹  Renier A. L. van der Hoorn²  Takayuki Shindo²  Markus Kaiser³  Sherry Niessen⁴  James R. Alfano⁴  Johana C. Misas-Villamil⁴  Izabella Kolodziejek⁴  Farnusch Kaschani⁵ 

[1] Center for Plant Science Innovation, University of Nebraska, Lincoln, Nebraska, United States of America;Chemical Biology Group, Department of Biology, University Duisburg-Essen, Essen, Germany;Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California, United States of America;Plant Chemetics Lab, Max Planck Institute for Plant Breeding Research, Cologne, Germany;School of Biological Sciences, University of Nebraska, Lincoln, Nebraska, United States of America

关键词: Leaves;    Immune response;    Proteasomes;    Bacteria;    Pathogen motility;    Cell death;    Immune suppression;    Bacterial growth;   

DOI  :  10.1371/journal.ppat.1003281

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

Infection of plants by bacterial leaf pathogens at wound sites is common in nature. Plants defend wound sites to prevent pathogen invasion, but several pathogens can overcome spatial restriction and enter leaf tissues. The molecular mechanisms used by pathogens to suppress containment at wound infection sites are poorly understood. Here, we studied Pseudomonas syringae strains causing brown spot on bean and blossom blight on pear. These strains exist as epiphytes that can cause disease upon wounding caused by hail, sand storms and frost. We demonstrate that these strains overcome spatial restriction at wound sites by producing syringolin A (SylA), a small molecule proteasome inhibitor. Consequently, SylA-producing strains are able to escape from primary infection sites and colonize adjacent tissues along the vasculature. We found that SylA diffuses from the primary infection site and suppresses acquired resistance in adjacent tissues by blocking signaling by the stress hormone salicylic acid (SA). Thus, SylA diffusion creates a zone of SA-insensitive tissue that is prepared for subsequent colonization. In addition, SylA promotes bacterial motility and suppresses immune responses at the primary infection site. These local immune responses do not affect bacterial growth and were weak compared to effector-triggered immunity. Thus, SylA facilitates colonization from wounding sites by increasing bacterial motility and suppressing SA signaling in adjacent tissues.

【 授权许可】

CC BY