0000000000447184
AUTHOR
Stephanie Nilkens
Bacterial sensor kinases using Fe–S cluster binding PAS or GAF domains for O2sensing
[4Fe-4S](2+) clusters are used by very diverse types of bacterial sensors for response to oxygen, including DNA-binding proteins of the CRP/FNR family and sensor kinases like NreB. In NreB the cluster is bound by an input domain of the PAS type. The [4Fe-4S](2+) cluster of NreB responds to O(2) by degradation to a [2Fe-2S](2+) cluster which is labile and decomposes. NreB constitutes together with AirS the NreB/AirS family of bacterial sensor kinases that contain PAS or GAF domains for binding of [4Fe-4S](2+) or [2Fe-2S](2+) clusters and oxygen sensing. The NreB/AirS family is related to the FixL sensor kinases that use hemeB binding PAS domains for oxygen sensing.
The NreA Protein Functions as a Nitrate Receptor in the Staphylococcal Nitrate Regulation System
Staphylococci are able to use nitrate as an alternative electron acceptor during anaerobic respiration. The regulation of energy metabolism is dependent on the presence of oxygen and nitrate. Under anaerobic conditions, staphylococci employ the nitrate regulatory element (Nre) for transcriptional activation of genes involved in reduction and transport of nitrate and nitrite. Of the three proteins that constitute the Nre system, NreB has been characterized as an oxygen sensor kinase and NreC has been characterized as its cognate response regulator. Here, we present structural and functional data that establish NreA as a new type of nitrate receptor. The structure of NreA with bound nitrate w…
Nitrate/oxygen co-sensing by an NreA/NreB sensor complex ofStaphylococcus carnosus
In Staphylococci maximal induction of nitrate reductase (narGHJI genes) requires anaerobic conditions, the presence of nitrate, and the NreABC regulatory system. Aerobic regulation is effected by the NreB/NreC two-component system. The role of the nitrate receptor NreA in nitrate induction and its relation to aerobic regulation was analysed in Staphylococcus carnosus. Nitrate induction of a narG-lip reporter gene required presence of NreB/NreC. When nreA was deleted, nitrate was no longer required for maximal induction, suggesting that NreA is a nitrate regulated inhibitor of NreB/NreC. In vitro, NreA and mutant NreA(Y95A) decreased NreB phosphorylation in part or completely, which was due …