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Abstract

Bacterial contact-dependent growth inhibition (CDI) is involved in processes such as biofilm formation, adhesion to host cells, and intra-species competition. CDI are described in many pathogenic bacteria, e.g. Enterobacteria, Pseudomonas and Burkholderia species. Previously characterized CDI loci minimally encode an extracellular CdiA protein, CdiB transporter and immunity protein CdiI. The toxin encoded at the C-terminus of CdiA causes contact-dependent cell death in the bacteria lacking the cognate CdiI immunity protein. We have identified multiple CdiA and CdiB homologs in Ralstonia solanacearum, an aggressive soil-borne pathogen that causes wilting disease in diverse plants. An unusually large number of putative CDI loci was found in R. solanacearum strains. The putative CDI loci exhibit both conservation and patterns of recent recombination events overlapping with cdiA and cdiI, indicative of increased diversification at toxin-immunity domains. Loci cluster into four families. Each of the investigated R. solanacearum strains has at least one putative CDI locus from each family. Members of different families vary in their positions in the genome, duplication number and locus architecture. Interestingly, three of the families have locus architecture typical for Burkholderia spp. and one family has an Enterobacteria-like CDI locus architecture. We are currently investigating how strains that share or vary in putative CDI loci perform in direct competition in vitro and in planta using co-culturing and co-infection assays combined with ddPCR quantification. This work will contribute to our understanding of how CDI systems mediate pathogenicity and interbacterial interactions in Ralstonia solanacearum.