The bacterial genus Burkholderia consists of more than 100 species isolated from a bewildering
array of niches. Many of them are closely interacting with a growing list of hosts from different
eukaryotic kingdoms. These interactions are often beneficial but Burkholderia can be pathogenic
for their fungal, plant or/and animal host. Curiously, virulence towards particular hosts is not a
phylogenetic trait. Plant and human pathogens are found throughout the different genomic clades,
with close relatives being non-pathogenic. Moreover, known virulence factors are poorly conserved
within the Burkholderia genomes indicating that horizontal gene transfer has been key to turn
particular species into pathogens. Despite the lack of clear genomic traits among pathogenic
Burkholderia, one common feature of species that are linked to human disease (cepacia syndrome,
melloidosis) seems to be the ability to intervene with host defense mechanisms. Though the exact
manner by which this occurs is quite distinct in the different species, all are related to degradation
or inactivation of immune and antimicrobial proteins via extracellular proteases or amidases. This
project aims to undertake comparative genomics, phenotypic analyses, proteomics and mutagenic
studies in a large selection of Burkholderia strains from the Ugent Laboratory of Microbiology
collection to investigate whether these protein families are indeed key to the ability of Burkholderia
to become pathogens.