Functional and structural annotation of pseudomonas chemoreceptors

Abstract

Bacteria possess different systems to sense and respond to environmental signals (Galperin, 2018). Most abundant are one-component systems (Ulrich et al., 2005), two-component systems (Stock & Zhulin, 2017) and chemosensory pathways (Porter et al., 2011). While one- and two-component systems mainly control gene expression (Stock & Zhulin, 2017, Ulrich et al., 2005), chemosensory pathways mediate chemotaxis or are associated with alternative functions (Porter et al., 2011, Wadhams & Armitage, 2004). The analysis of the increasing number of bacterial genomes shows that about half of bacteria have genes encoding chemosensory pathways (Ortega et al., 2017). The central element of a chemosensory pathway is the ternary complex formed by chemoreceptors, the CheA autokinase and the CheW coupling proteins (Wadhams & Armitage, 2004). Ligand mediated stimulation of the chemoreceptor causes an alteration of CheA activity that in turn modulates transphosphorylation to CheY that in its phosphorylated form binds to the flagellar motor causing ultimately chemotaxis (Wadhams & Armitage, 2004). The chemoreceptor typically is composed by a periplasmic ligand binding domain, a transmembrane module and a cytoplasmic signaling domain (Parkinson et al., 2015). The function and signals recognized of most chemoreceptors are unknown. The results presented in this thesis increase the knowledge about the chemotactic chemosensory pathways, reveal the signals sensed and cast light into the sensing mechanisms, which is important information to understand important physiological processes such as bacterial migration, colonization, infection and virulence. Future work will determine the potential application of this knowledge, for instance the determination of the role of these chemoreceptors in the promotion of plant root colonization or infection. The demonstration that chemoreceptors respond to chemoeffectors and structurally related antagonists may be a potential strategy to interfere specifically with chemotaxis and virulence.