A meet-up of two second messengers: the c-di-AMP receptor DarB controls (p)ppGpp synthesis in Bacillus subtilis

Larissa Krüger, Christina Herzberg, Dennis Wicke, Heike Bähre, Jana L. Heidemann, Achim Dickmanns, Kerstin Schmitt, Ralf Ficner and Jörg Stülke ()
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Larissa Krüger: Georg-August-University Göttingen
Christina Herzberg: Georg-August-University Göttingen
Dennis Wicke: Georg-August-University Göttingen
Heike Bähre: Research Core Unit Metabolomics, Hannover Medical School
Jana L. Heidemann: Georg-August-University Göttingen
Achim Dickmanns: Georg-August-University Göttingen
Kerstin Schmitt: Georg-August-University Göttingen
Ralf Ficner: Georg-August-University Göttingen
Jörg Stülke: Georg-August-University Göttingen

Nature Communications, 2021, vol. 12, issue 1, 1-12

Abstract: Abstract Many bacteria use cyclic di-AMP as a second messenger to control potassium and osmotic homeostasis. In Bacillus subtilis, several c-di-AMP binding proteins and RNA molecules have been identified. Most of these targets play a role in controlling potassium uptake and export. In addition, c-di-AMP binds to two conserved target proteins of unknown function, DarA and DarB, that exclusively consist of the c-di-AMP binding domain. Here, we investigate the function of the c-di-AMP-binding protein DarB in B. subtilis, which consists of two cystathionine-beta synthase (CBS) domains. We use an unbiased search for DarB interaction partners and identify the (p)ppGpp synthetase/hydrolase Rel as a major interaction partner of DarB. (p)ppGpp is another second messenger that is formed upon amino acid starvation and under other stress conditions to stop translation and active metabolism. The interaction between DarB and Rel only takes place if the bacteria grow at very low potassium concentrations and intracellular levels of c-di-AMP are low. We show that c-di-AMP inhibits the binding of DarB to Rel and the DarB–Rel interaction results in the Rel-dependent accumulation of pppGpp. These results link potassium and c-di-AMP signaling to the stringent response and thus to the global control of cellular physiology.

Date: 2021
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-21306-0

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DOI: 10.1038/s41467-021-21306-0

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