S ymbionts and pathogens are comparable in that they colonize eukaryotic hosts. Many pathogenic and symbiotic genetic determi- nants are located on mobile genetic elements. Horizontal gene transfer contributes to the genetic variability of or- ganisms, which drives the evolution of the microorgan- ism–host interaction. Whereas pathogenic interactions result in damage or death of the re- spective host, symbiotic inter- actions are characterized by an overall benefit (Table 1). In spite of these different out- comes, similar mechanisms of pathogenesis and sym- biosis exist in bacteria to facilitate successful col- onization of a particular niche. The most notable mechanisms include quorum sensing and the two- component regulatory systems, which allow adap- tation to the constantly changing conditions found in a new niche. Furthermore, pathogens and possibly also symbionts are able to modulate the host environ- ment by type III secretion of effector molecules that interfere directly with host cellular functions. Of equal importance is the contribution of the host, an aspect which has been difficult to address because of the lack of experimental tractability. Clearly, features such as host immunity and susceptibility play an im- portant role in the bacteria–host interaction and a full understanding of this interaction will therefore only be accomplished by taking an integrated approach. Horizontal gene transfer Genetic variability plays an important role in the evo- lution of pathogenic and symbiotic interactions. In addition to the chromosome, most prokaryotes pos- sess different classes of mobile genetic elements that allow the acquisition, loss or structural change of sometimes large regions of the bacterial genome. Horizontal gene transfer represents a powerful mechanism by which the outcome of a bacteria–host interaction can be permanently altered. Horizontal gene transfer is mediated by genomic islands, plasmids, transposons and IS elements, and phages (Table 2). Genomic islands encode functions relevant for bacteria–host interactions and are found in diverse animal and plant pathogens (where they are known as pathogenicity is- lands) and also in the sym- biont Mesorhizobium loti (a symbiosis island) 1 . Plasmids can also encode many impor- tant pathogenic determinants such as toxins, type III secre- tion systems and invasion determinants 2 . The plasmids of the aphid endosymbiont Buchnera aphidicola contain biosynthetic operons that complement the amino acid deficiency of the host 3 . The sym-plasmid of Rhizobium, which carries essential genes for symbiotic competence, might have been derived from the plant pathogen Agrobacterium tumefaciens 4 . Lysogenic phages integrated in the bacterial genome are often associated with the production of virulence factors, such as toxins, in diverse pathogens and also in the symbiont Xenorhabdus nematophilus 2,5 . There is also evidence for horizontal gene transfer of the IS element IS1312 from the plant symbiont Rhizobium meliloti to the plant pathogen A. tumefaciens 6 . Taken together, there is increasing evidence of horizontal gene transfer between animal and plant pathogens and between plant pathogens and symbionts. This suggests that horizontal gene transfer might be a mechanism by which genetic information can be ex- changed between pathogens and symbionts in general. Quorum sensing Quorum sensing describes the ability of bacteria to sense cell densities and to regulate specific sets of genes accordingly 7 . It is mediated via specific sig- nalling molecules called autoinducers (AI), which accumulate extracellularly as cell density increases. When a threshold concentration of the AI is reached, gene expression of density-dependent genes is initi- ated. Fundamental to this phenomenon are two genes, one synthesizing the AI (LuxI or a homologue) and the other serving as an AI receptor (LuxR or a homologue). Most but not all quorum-sensing mech- anisms analysed play a specific role in symbiont– or pathogen–host interactions. Quorum sensing regulates the virulence properties of various plant and animal pathogens. Examples in- clude the production of cell wall degrading enzymes and carbapenem antibiotics in the plant pathogen Traditionally, symbiotic and pathogenic interactions were considered different manifestations of the bacteria–host interaction. However, the molecular mechanisms that mediate communication between and cellular modulation of the involved partners are quite similar. With this review we aim to contribute to a reduction of the traditional gap between symbiosis and pathogenesis research. U. Hentschel*, M. Steinert and J. Hacker are in the Institut für Molekulare Infektionsbiologie, Universität Würzburg, Röntgenring, 11, D-97070 Würzburg, Germany. *tel: +49 931 312588, fax: +49 931 312578, e-mail: ute.hentschel@mail.uni-wuerzburg.de R EVIEWS TRENDS IN MICROBIOLOGY 226 VOL. 8 NO. 5 MAY 2000 0966-842X/00/$ - see front matter © 2000 Elsevier Science Ltd. All rights reserved. PII: S0966-842X(00)01758-3 Common molecular mechanisms of symbiosis and pathogenesis Ute Hentschel, Michael Steinert and Jörg Hacker