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Mol Plant Pathol. 2016 Oct;17(8):1237-51. doi: 10.1111/mpp.12361. Epub 2016 Apr 4.

Analysis of salicylic acid-dependent pathways in Arabidopsis thaliana following infection with Plasmodiophora brassicae and the influence of salicylic acid on disease.

Author information

1
Deakin University, Faculty of Science, Engineering and Built Environment, School of Life and Environmental Science, Geelong Campus at Waurn Ponds, Vic. 3217, Australia. david.lovelock@nt.gov.au.
2
Department of Biology, Faculty of Science, University of Zagreb, Rooseveltov trg 6, 10000, Zagreb, Croatia. ivana.sola@biol.pmf.hr.
3
Institute of Botany, Technische Universität Dresden, D-01062, Dresden, Germany.
4
Department of Primary Industries, Private bag 15, Ferntree Gully DC, Vic., 3156, Australia.
5
Department of Biology, Faculty of Science, University of Zagreb, Rooseveltov trg 6, 10000, Zagreb, Croatia.
6
Department of Chemistry, Biochemistry, Technische Universität Dresden, D-01062, Dresden, Germany.
7
Deakin University, Faculty of Science, Engineering and Built Environment, School of Life and Environmental Science, Geelong Campus at Waurn Ponds, Vic. 3217, Australia.

Abstract

Salicylic acid (SA) biosynthesis, the expression of SA-related genes and the effect of SA on the Arabidopsis-Plasmodiophora brassicae interaction were examined. Biochemical analyses revealed that, in P. brassicae-infected Arabidopsis, the majority of SA is synthesized from chorismate. Real-time monitored expression of a gene for isochorismate synthase was induced on infection. SA can be modified after accumulation, either by methylation, improving its mobility, or by glycosylation, as one possible reaction for inactivation. Quantitative reverse transcription-polymerase chain reaction (qPCR) confirmed the induction of an SA methyltransferase gene, whereas SA glucosyltransferase expression was not changed after infection. Col-0 wild-type (wt) did not provide a visible phenotypic resistance response, whereas the Arabidopsis mutant dnd1, which constitutively activates the immune system, showed reduced gall scores. As dnd1 showed control of the pathogen, exogenous SA was applied to Arabidopsis in order to test whether it could suppress clubroot. In wt, sid2 (SA biosynthesis), NahG (SA-deficient) and npr1 (SA signalling-impaired) mutants, SA treatment did not alter the gall score, but positively affected the shoot weight. This suggests that SA alone is not sufficient for Arabidopsis resistance against P. brassicae. Semi-quantitative PCR revealed that wt, cpr1, dnd1 and sid2 showed elevated PR-1 expression on P. brassicae and SA + P. brassicae inoculation at 2 and 3 weeks post-inoculation (wpi), whereas NahG and npr1 showed no expression. This work contributes to the understanding of SA involvement in the Arabidopsis-P. brassicae interaction.

KEYWORDS:

Arabidopsis thaliana; Plasmodiophora brassicae; defence gene expression; salicylic acid biosynthesis; salicylic acid mutants

PMID:
26719902
DOI:
10.1111/mpp.12361
[Indexed for MEDLINE]

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