Description:
Pseudomonas species employ complex, dynamic signalling networks to fine-tune their responses to changing environments, with regulation occurring at every stage in the processing of genetic information. Post-transcriptional control of protein abundance is a crucial element of this regulatory network, and forms a particular focus of my lab. As part of our ongoing research into the signalling pathways that control Pseudomonas plant-association, we identified the post-transcriptional regulator RimK, which influences the transition between active and sessile lifestyles in both pathogenic and commensal microbes.
RimK is an ATP-dependent glutamyl ligase that adds glutamate residues to the C-terminus of ribosomal protein RpsF. This in turn induces specific changes in ribosome function and translational output. RimK activity is under complex, multifactorial control; by the bacterial second messenger cyclic-di-GMP (cdG), a cdG phosphodiesterase (RimA), and a polyglutamate-specific protease (RimB). Deletion of rimK affects phenotypes including attachment, motility and cytotoxicity, compromising rhizosphere colonisation by the soil bacterium P. fluorescens and infection by the pathogens P. syringae and P. aeruginosa.
In P. fluorescens, deletion of rimK leads to reduced levels of the key translational regulator Hfq. In turn, lowered Hfq abundance induces specific downstream changes to the bacterial proteome, with significant increases in ABC transporters and stress response proteins observed for both ?rimK and ?hfq. We propose that the RimABK/cdG system represents a novel mechanism for translational regulation, whereby dynamic, post-translational ribosome modification is used to convert environmental signals into rapid changes in translational output and adaptive remodeling of the bacterial proteome.
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