Abstract
The clubroot disease, caused by the obligate biotrophic protist Plasmodiophora brassicae, affects cruciferous crops worldwide. It is characterized by root swellings as symptoms, which are dependent on the alteration of auxin and cytokinin metabolism. Here, we describe that two different classes of auxin receptors, the TIR family and the auxin binding protein 1 (ABP1) in Arabidopsis thaliana are transcriptionally upregulated upon gall formation. Mutations in the TIR family resulted in more susceptible reactions to the root pathogen. As target genes for the different pathways we have investigated the transcriptional regulation of selected transcriptional repressors (Aux/IAA) and transcription factors (ARF). As the TIR pathway controls auxin homeostasis via the upregulation of some auxin conjugate synthetases (GH3), the expression of selected GH3 genes was also investigated, showing in most cases upregulation. A double gh3 mutant showed also slightly higher susceptibility to P. brassicae infection, while all tested single mutants did not show any alteration in the clubroot phenotype. As targets for the ABP1-induced cell elongation the effect of potassium channel blockers on clubroot formation was investigated. Treatment with tetraethylammonium (TEA) resulted in less severe clubroot symptoms. This research provides evidence for the involvement of two auxin signaling pathways in Arabidopsis needed for the establishment of the root galls by P. brassicae.
Highlights
The clubroot disease of the Brassicaceae is one of the most damaging diseases within this plant family [1]
The role of plant hormones during the infection of Brassicaceae roots with the obligate biotrophic protist Plasmodiophora brassicae has been studied over the decades
Among the players most likely involved in the second are potassium influx channels, which could regulate the turgor pressure within the cell in response to auxin leading to cell elongation
Summary
The clubroot disease of the Brassicaceae is one of the most damaging diseases within this plant family [1]. The infection process of plants by P. brassicae consists of two phases: (1) the primary phase, which is restricted to root hairs and (2) the secondary phase, which occurs in the cortex and stele of roots and hypocotyl and leads to abnormal development [5] During this later phase the host root responds to infection by increased cell division rates followed by hypertrophy of infected cells. The protein GH3.5 seems to play various roles in addition to the synthesis of IAA amino acid conjugates It conjugates the plant defense signal salicylic acid to amino acids [22] and is involved in the synthesis of the Arabidopsis phytoalexin camalexin [23]. Targets of both pathways were functionally investigated for their roles during disease progression
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