Abstract
BackgroundThaxtomin A (TA) is a phytotoxin produced by plant pathogenic Streptomyces spp. responsible for potato common scab. TA inhibits cellulose biosynthesis in expanding plant tissues and is essential for disease induction. Auxin treatment of various plant tissues has been repeatedly demonstrated to inhibit TA toxicity and to reduce common scab. This work utilises Arabidopsis thaliana mutants with resistance to cellulose biosynthesis inhibitors (CBIs) to investigate the interaction between TA, other CBIs and auxins.ResultsThree CBI resistant A. thaliana mutants; txr1-1 (tolerance to TA), ixr1-1 (tolerance to isoxaben - IXB) and KOR1 (cellulose deficiency), showed no altered root growth response to treatment with natural or synthetic auxins, nor with the auxin efflux transport inhibitor 2,3,5-Triiodobenzoic acid (TIBA). However, all mutants had significantly enhanced tolerance to 1-napthylphthalamic acid (NPA), another auxin efflux transport inhibitor, which blocks polar auxin transport at a site distinct from TIBA. NPA tolerance of txr1-1 and ixr1-1 was further supported by electrophysiological analysis of net H+ fluxes in the mature, but not elongation zone of roots. All three mutants showed increased tolerance to IXB, but only txr1-1 showed tolerance to TA. No mutant showed enhanced tolerance to a third CBI, dichlobenil (DCB).ConclusionsWe have demonstrated that plant tolerance to TA and IXB, as well as cell wall synthesis modifications in roots, have resulted in specific co-resistance to NPA but not TIBA. This suggests that CBI resistance has an impact on polar auxin efflux transport processes associated with the NPA binding protein. We also show that NPA inhibitory response in roots occurs in the mature root zone but not the elongation zone. Responses of mutants to CBIs indicate a similar, but not identical mode of action of TA and IXB, in contrast to DCB.
Highlights
Thaxtomin A (TA) is a phytotoxin produced by plant pathogenic Streptomyces spp. responsible for potato common scab
Mutant screening against various auxin sources Consistent with previous studies [23], aux1-7 had enhanced resistance to both 2,4-D (P = 0.0004, F = 15.6) and Indole-3-acetic acid (IAA) (P < 0.0001, F = 35.4), but not to 1-naphthalene acetic acid (NAA) (P = 0.81, F = 0.06), when compared to root growth by 50% (RG50) value of the wild type (WT) control (Figure 1)
All mutant lines and the WT control examined showed equivalent root growth suppression when treated with various concentrations of the auxin transport inhibitor, Triiodobenzoic acid (TIBA) (Figure 2B)
Summary
Thaxtomin A (TA) is a phytotoxin produced by plant pathogenic Streptomyces spp. responsible for potato common scab. TA inhibits cellulose biosynthesis in expanding plant tissues and is essential for disease induction. Auxin treatment of various plant tissues has been repeatedly demonstrated to inhibit TA toxicity and to reduce common scab. This work utilises Arabidopsis thaliana mutants with resistance to cellulose biosynthesis inhibitors (CBIs) to investigate the interaction between TA, other CBIs and auxins. Thaxtomin A (TA) is the major phytotoxin produced by pathogenic Streptomyces spp. responsible for common scab, a globally important disease of potato [1]. TA inhibits cellulose biosynthesis in expanding plant tissues and its production is essential for disease induction [2,3,4]. The TXR1 gene is involved in a cellular transport system and mutations in this gene in Arabidopsis thaliana txr lead to a decrease in toxin sensitivity, most likely due to reduced toxin uptake [15]
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