Tegg Robert S, Gill Warwick M, Thompson Hannah K, Davies Noel W, Ross John J, Wilson Calum R
Tasmanian Institute of Agricultural Research, University of Tasmania, New Town Research Laboratories, 13 St. John's Avenue, New Town, Tasmania 7008, Australia.
Central Science Laboratory, University of Tasmania, Private Bag 74, Hobart, Tasmania 7001, Australia.
Plant Dis. 2008 Sep;92(9):1321-1328. doi: 10.1094/PDIS-92-9-1321.
Production of the phytotoxin thaxtomin A by pathogenic Streptomyces spp. is essential for induction of common scab disease in potato. Prior studies have shown that foliar application of sublethal concentrations of 2,4-dichlorophenoxyacetic acid (2,4-D) and other auxin or auxin-like compounds significantly reduced severity and occurrence of common scab in subsequently produced tubers. However, the means of disease suppression by these compounds was not known. We confirm the disease suppressive activity of 2,4-D. Detailed tuber physiological examination showed that lenticel numbers, lenticel external dimensions, and periderm thickness and structure, physiological features believed to be critical to Streptomyces scabiei infection, were not substantially changed by 2,4-D treatments, negating a possible mechanism for disease suppression through alteration of these structures. In contrast, our studies show accumulation of 2,4-D in tubers of treated plants occurs and is associated with an enhanced tolerance to thaxtomin A. Applying 2,4-D to cultures of S. scabiei did not significantly alter in vitro growth of the pathogen. Thaxtomin A production by the pathogen was inhibited by 2,4-D, but only at the highest rate tested (1.0 mM), which is at least 200-fold more than is found in 2,4-D treated tubers. These data suggest 2,4-D has no direct effect on the pathogen or its virulence. Confirmatory evidence from studies with Arabidopsis thaliana seedlings demonstrated that the auxins 2,4-D and IAA ameliorate thaxtomin A toxicity. The evidence presented whereby auxin treatment inhibits toxicity of thaxtomin A secreted by the pathogen suggests a novel indirect means of disease suppression.
致病性链霉菌属产生植物毒素噻重氮酸A是引发马铃薯疮痂病的必要条件。先前的研究表明，叶面喷施亚致死浓度的2,4-二氯苯氧乙酸（2,4-D）以及其他生长素或类生长素化合物，能显著降低后续所产块茎上疮痂病的严重程度和发病率。然而，这些化合物抑制病害的方式尚不清楚。我们证实了2,4-D的病害抑制活性。详细的块茎生理学检查表明，皮孔数量、皮孔外部尺寸以及周皮厚度和结构（这些生理特征被认为对疮痂链霉菌感染至关重要）并未因2,4-D处理而发生实质性变化，这排除了通过改变这些结构来抑制病害的一种可能机制。相比之下，我们的研究表明，经处理植株的块茎中会积累2,4-D，且这与对噻重氮酸A的耐受性增强有关。将2,4-D应用于疮痂链霉菌培养物中，并未显著改变该病原菌的体外生长情况。该病原菌产生噻重氮酸A的过程受到2,4-D的抑制，但仅在测试的最高浓度（1.0 mM）下才出现这种情况，这一浓度至少比2,4-D处理的块茎中发现的浓度高200倍。这些数据表明，2,4-D对病原菌或其毒力没有直接影响。来自拟南芥幼苗研究的证实性证据表明，生长素2,4-D和吲哚乙酸（IAA）可减轻噻重氮酸A的毒性。生长素处理抑制病原菌分泌的噻重氮酸A毒性的证据，提示了一种新的间接病害抑制方式。
