Abstract

The Actinomycete Rhodococcus fascians causes the leafy gall syndrome, an infectious plant disease that affects a wide range of plants, primarily dicotyledonous herbs. The syndrome is associated with delayed senescence, loss of apical dominance, activation of dormant axillary meristems, and formation of multiple inflorescences, leading to a stunted and bushy plant appearance. A major breakthrough in the elucidation of the virulence strategy of this pathogen was the discovery of a linear virulence plasmid, pFiD188 for R.fascians strain D188. Upon perception of a compatible host plant, an autoregulatory mechanism mediated by the att operon directs a switch in the bacterial life style from a harmless epiphyte into a pathogenic endophyte and, concomitantly, activates gene expression of the fas operon that encodes a cytokinin biosynthesis pathway. A mixture of five cytokinins determines the cytokinin activity of R.fascians that directly affects plant responses and development. Moreover, the bacterial cytokinins stimulate the host to produce auxins and polyamines, that function as accessory signals to aid in symptom development. The plant reacts against the developmental hijacking by R.fascians by activating a set of counteracting measures that ultimately results in a delicate balance, allowing a long-lasting biotrophic interaction.

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