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Infection and Immunity, December 2005, p. 8353-8361, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8353-8361.2005

Whole-Genome Analyses of Speciation Events in Pathogenic Brucellae

Biosciences Directorate, Lawrence Livermore National Laboratory, Livermore, California 94551,¹ Instituto de Investigaciones Biotecnologicas, Universidad Nacional de General San Martin (IIB-INTECH-CONICET), Av. Gral. Paz 5445, P.O. Box 30, 1650 San Martin, Buenos Aires, Argentina,² Department of Biological Science, California State University, Fullerton, California 92834-6850,³ Life Sciences Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831⁴

Received 13 July 2005/ Returned for modification 15 August 2005/ Accepted 19 September 2005

Despite their high DNA identity and a proposal to group classical Brucella species as biovars of Brucella melitensis, the commonly recognized Brucella species can be distinguished by distinct biochemical and fatty acid characters, as well as by a marked host range (e.g., Brucella suis for swine, B. melitensis for sheep and goats, and Brucella abortus for cattle). Here we present the genome of B. abortus 2308, the virulent prototype biovar 1 strain, and its comparison to the two other human pathogenic Brucella species and to B. abortus field isolate 9-941. The global distribution of pseudogenes, deletions, and insertions supports previous indications that B. abortus and B. melitensis share a common ancestor that diverged from B. suis. With the exception of a dozen genes, the genetic complements of both B. abortus strains are identical, whereas the three species differ in gene content and pseudogenes. The pattern of species-specific gene inactivations affecting transcriptional regulators and outer membrane proteins suggests that these inactivations may play an important role in the establishment of host specificity and may have been a primary driver of speciation in the genus Brucella. Despite being nonmotile, the brucellae contain flagellum gene clusters and display species-specific flagellar gene inactivations, which lead to the putative generation of different versions of flagellum-derived structures and may contribute to differences in host specificity and virulence. Metabolic changes such as the lack of complete metabolic pathways for the synthesis of numerous compounds (e.g., glycogen, biotin, NAD, and choline) are consistent with adaptation of brucellae to an intracellular life-style.

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Editor: D. L. Burns

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