Enhanced uptake of potassium or glycine betaine or export of cyclic-di-AMP restores osmoresistance in a high cyclic-di-AMP Lactococcus lactis mutant

Betaine Wild type Osmotic shock
DOI: 10.1371/journal.pgen.1007574 Publication Date: 2018-08-03T17:23:15Z
ABSTRACT
The broadly conserved bacterial signalling molecule cyclic-di-adenosine monophosphate (c-di-AMP) controls osmoresistance via its regulation of potassium (K+) and compatible solute uptake. High levels c-di-AMP resulting from inactivation phosphodiesterase activity leads to poor growth bacteria under high osmotic conditions. To better understand how can adjust in response excessive identify signals that feed into the network, we characterised genes identified a screen for osmoresistant suppressor mutants Lactococcus ΔgdpP strain. Mutations were which increased uptake osmoprotectants, including gain-of-function mutations Kup family K+ importer (KupB) glycine betaine transporter transcriptional repressor BusR. KupB intracellular level while BusR level. In addition, was found directly bind repress expression elevated c-di-AMP. Interestingly, overactive or loss triggered accumulation, suggesting turgor pressure changes act as signal this second messenger. another group suppressors, overexpression an operon encoding EmrB multidrug resistance protein allowed cells lower their through active export. Lastly evidence is provided several are rapidly responsive environmental osmolarity changes. Taken together, work provides model containing dehydrated due osmoregulation system able sense respond cellular water stress.
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