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The Pseudomonas syringae pv. tomato Type III Effector HopM1 Suppresses Arabidopsis Defenses Independent of Suppressing Salicylic Acid Signaling and of Targeting AtMIN7

Overview of attention for article published in PLOS ONE, December 2013
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Title
The Pseudomonas syringae pv. tomato Type III Effector HopM1 Suppresses Arabidopsis Defenses Independent of Suppressing Salicylic Acid Signaling and of Targeting AtMIN7
Published in
PLOS ONE, December 2013
DOI 10.1371/journal.pone.0082032
Pubmed ID
Authors

Anju Gangadharan, Mysore-Venkatarau Sreerekha, Justin Whitehill, Jong Hyun Ham, David Mackey

Abstract

Pseudomonas syringae pv tomato strain DC3000 (Pto) delivers several effector proteins promoting virulence, including HopM1, into plant cells via type III secretion. HopM1 contributes to full virulence of Pto by inducing degradation of Arabidopsis proteins, including AtMIN7, an ADP ribosylation factor-guanine nucleotide exchange factor. Pseudomonas syringae pv phaseolicola strain NPS3121 (Pph) lacks a functional HopM1 and elicits robust defenses in Arabidopsis thaliana, including accumulation of pathogenesis related 1 (PR-1) protein and deposition of callose-containing cell wall fortifications. We have examined the effects of heterologously expressed HopM1Pto on Pph-induced defenses. HopM1 suppresses Pph-induced PR-1 expression, a widely used marker for salicylic acid (SA) signaling and systemic acquired resistance. Surprisingly, HopM1 reduces PR-1 expression without affecting SA accumulation and also suppresses the low levels of PR-1 expression apparent in SA-signaling deficient plants. Further, HopM1 enhances the growth of Pto in SA-signaling deficient plants. AtMIN7 contributes to Pph-induced PR-1 expression. However, HopM1 fails to degrade AtMIN7 during Pph infection and suppresses Pph-induced PR-1 expression and callose deposition in wild-type and atmin7 plants. We also show that the HopM1-mediated suppression of PR-1 expression is not observed in plants lacking the TGA transcription factor, TGA3. Our data indicate that HopM1 promotes bacterial virulence independent of suppressing SA-signaling and links TGA3, AtMIN7, and other HopM1 targets to pathways distinct from the canonical SA-signaling pathway contributing to PR-1 expression and callose deposition. Thus, efforts to understand this key effector must consider multiple targets and unexpected outputs of its action.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 48 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 2%
Germany 1 2%
Unknown 46 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 14 29%
Researcher 10 21%
Student > Bachelor 4 8%
Student > Master 3 6%
Student > Doctoral Student 2 4%
Other 4 8%
Unknown 11 23%
Readers by discipline Count As %
Agricultural and Biological Sciences 19 40%
Biochemistry, Genetics and Molecular Biology 13 27%
Environmental Science 1 2%
Nursing and Health Professions 1 2%
Social Sciences 1 2%
Other 0 0%
Unknown 13 27%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 07 December 2013.
All research outputs
#20,211,690
of 22,733,113 outputs
Outputs from PLOS ONE
#173,182
of 194,037 outputs
Outputs of similar age
#266,897
of 306,486 outputs
Outputs of similar age from PLOS ONE
#4,354
of 5,039 outputs
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