Pseudomonas syringae pv. syringae uses proteasome inhibitor syringolin A to colonize from wound infection sites.

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 infec...

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Autores principales: Johana C Misas-Villamil, Izabella Kolodziejek, Emerson Crabill, Farnusch Kaschani, Sherry Niessen, Takayuki Shindo, Markus Kaiser, James R Alfano, Renier A L van der Hoorn
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Publicado: Public Library of Science (PLoS) 2013
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Acceso en línea:https://doaj.org/article/17e0158d36c04a6d98f9c38f88400e9d
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spelling oai:doaj.org-article:17e0158d36c04a6d98f9c38f88400e9d2021-11-18T06:05:50ZPseudomonas syringae pv. syringae uses proteasome inhibitor syringolin A to colonize from wound infection sites.1553-73661553-737410.1371/journal.ppat.1003281https://doaj.org/article/17e0158d36c04a6d98f9c38f88400e9d2013-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23555272/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Infection 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.Johana C Misas-VillamilIzabella KolodziejekEmerson CrabillFarnusch KaschaniSherry NiessenTakayuki ShindoMarkus KaiserJames R AlfanoRenier A L van der HoornPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 9, Iss 3, p e1003281 (2013)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Johana C Misas-Villamil
Izabella Kolodziejek
Emerson Crabill
Farnusch Kaschani
Sherry Niessen
Takayuki Shindo
Markus Kaiser
James R Alfano
Renier A L van der Hoorn
Pseudomonas syringae pv. syringae uses proteasome inhibitor syringolin A to colonize from wound infection sites.
description 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.
format article
author Johana C Misas-Villamil
Izabella Kolodziejek
Emerson Crabill
Farnusch Kaschani
Sherry Niessen
Takayuki Shindo
Markus Kaiser
James R Alfano
Renier A L van der Hoorn
author_facet Johana C Misas-Villamil
Izabella Kolodziejek
Emerson Crabill
Farnusch Kaschani
Sherry Niessen
Takayuki Shindo
Markus Kaiser
James R Alfano
Renier A L van der Hoorn
author_sort Johana C Misas-Villamil
title Pseudomonas syringae pv. syringae uses proteasome inhibitor syringolin A to colonize from wound infection sites.
title_short Pseudomonas syringae pv. syringae uses proteasome inhibitor syringolin A to colonize from wound infection sites.
title_full Pseudomonas syringae pv. syringae uses proteasome inhibitor syringolin A to colonize from wound infection sites.
title_fullStr Pseudomonas syringae pv. syringae uses proteasome inhibitor syringolin A to colonize from wound infection sites.
title_full_unstemmed Pseudomonas syringae pv. syringae uses proteasome inhibitor syringolin A to colonize from wound infection sites.
title_sort pseudomonas syringae pv. syringae uses proteasome inhibitor syringolin a to colonize from wound infection sites.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/17e0158d36c04a6d98f9c38f88400e9d
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