The gram-positive plant pathogen Rhodococcus fascians provokes leafy gall formation on a wide range of plants through secretion of signal molecules that interfere with the hormone balance of the host. Crucial virulence genes are located on a linear plasmid, and their expression is tightly controlled. A mutant with a mutation in a chromosomal locus that affected virulence was isolated. The mutation was located in gene vicA, which encodes a malate synthase and is functional in the glyoxylate shunt of the Krebs cycle. VicA is required for efficient in planta growth in symptomatic, but not in normal, plant tissue, indicating that the metabolic requirement of the bacteria or the nutritional environment in plants or both change during the interaction. We propose that induced hyperplasia on plants represents specific niches for the causative organisms as a result of physiological alterations in the symptomatic tissue. Hence, such interaction could be referred to as metabolic habitat modification.The outcome of a plant-pathogen interaction results from the complex action of a whole set of genes, from both host and pathogen. The tools used by pathogens to provoke plant diseases are often well characterized, and a wide array of pathogenic approaches has been described, ranging from destructive to subtle strategies. The most destructive interactions are often lethal for the plant and result from the bacterial secretion of extracellular cell wall-degrading enzymes that literally digest the plant (for instance, soft rots by Pantoea species [1]) or from the obstruction of transport tissues leading to wilting (such as for Ralstonia solanacearum [23], Pantoea stewartii [28], and Corynebacterium species [29,46]). A more subtle approach consists of disrupting the plant's hormone balance, resulting in the formation of hyperplasia without killing the host (such as crown galls by Agrobacterium tumefaciens [26] and galls by Pantoea agglomerans pv. gypsophilae [30] and Pseudomonas savastanoi pv. savastanoi [58]).The most obvious reason why bacteria seek interaction with plants is nutrition. For the necrogenic pathogens, this nutritional benefit is clear. On the other hand, A. tumefaciens transfers a discrete piece of its tumor-inducing (Ti) plasmid, the T-DNA, which carries genes responsible for hormone and opine synthesis, to the plant nucleus (47). Opines are novel compounds whose structure depends on the bacterial strain that induces the crown gall. Only this strain carries the catabolic genes specific for that type of opine on its Ti plasmid (14). Hence, the bacterium that invests its energy into genetically transforming its host is rewarded in terms of specific nutritional compounds. However, for other hyperplasia-inducing bacteria such a benefit is not evident.Rhodococcus fascians (20) belongs to the latter class of pathogens. It is a gram-positive actinomycete with a very broad host range, encompassing both monocots and dicots (3, 53). It is a well-adapted epiphyte and grows on the surface of the plant as well as inside tissues...