Poster
Sonja Beiter
Max Planck Institute for Biology
Tübingen, Baden-Wurttemberg, Germany
Rekha Gopalan-Nair
Postdoctoral researcher
Max Planck Institute for Biology
Tübingen, Baden-Wurttemberg, Germany
Daria Evseeva
Max Planck Institute for Biology
Tübingen, Baden-Wurttemberg, Germany
Hazal Ergelen
The M3 Research Center
Tübingen, Baden-Wurttemberg, Germany
Ana Rita Brochado
Interfaculty Institute of Microbiology and Infection Medicine
Tübingen, Baden-Wurttemberg, Germany
Martina Airoldi
Interfaculty Institute of Microbiology and Infection Medicine
Tübingen, Baden-Wurttemberg, Germany
Honour McCann
Max Planck Institute for Biology
Tübingen, Baden-Wurttemberg, Germany
Pathogens compete with other microbes for access to scarce nutrients and hosts alike. Bacterial contact-dependent growth inhibition (CDI) systems mediate interbacterial recognition and antagonism via the export of long extracellular proteins (CdiA) with C-terminal toxin domains. Delivery of the toxin occurs after CdiA receptor-dependent binding to the recipient cell. The growth of the recipient cell is inhibited unless it encodes the cognate neutralizing immunity protein (CdiI). The cdiA and cdiI genes are encoded in a single locus along with the transporter cdiB. The plant pathogen Ralstonia pseudosolanacearum harbors six to ten CDI loci per genome, a dramatic amplification compared to the one to two CDI loci per genome in E. coli and Burkholderia spp., where CDI is well characterized. This amplification may enable diverse interbacterial interactions. This project aimed to identify which of the six putative CDI loci in the model strain R. pseudosolanacearum GMI1000 are critical for interbacterial competition. I established a high-throughput competition assay and performed pairwise competitions between CDI locus deletion mutants and the wildtype strain. Results showed two CDI loci exhibit reduced fitness in competition with the wildtype strain. Mutant complementation with a cognate immunity gene restored fitness. This work provides insight into a molecular mechanism underlying competitive interactions in the rhizosphere and phyllosphere alike.