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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2013
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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) |
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Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 |
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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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