The extremely halophilic archaeon Halobacterium salinarum R1 responds to potassium limitation by expression of the K+-transporting KdpFABC P-type ATPase and by a decrease in intracellular K+.

Halobacterium species balance high external osmolality by the accumulation of almost equimolar amounts of KCl. Thus, steady K(+) supply is a vital prerequisite for life of these extreme halophiles. So far, K(+) is reported to enter the halobacterial cell only passively by use of potential-driven uniporters. However, the genome of both the extreme halophilic archaeon Halobacterium sp. NRC-1 and H. salinarum R1 comprises one single gene cluster containing the genes kdpFABC coding for homologs of the bacterial ATP-driven K(+) uptake system KdpFABC, together with an additional ORF so far annotated as cat3 in Halobacterium sp. NRC-1 and as UspA protein in H. salinarum R1 (the ORF is only referred to as cat3 in the following). Deletion of the kdpFABCcat3 genes led to a reduced ability to grow under limiting K(+) concentrations, whereas real-time RT-PCR measurements revealed cat3-dependent high expression rates of the Kdp system in case of external K(+) depletion. Synthesis of the KdpFABC complex enables H. salinarum R1 to grow under extreme potassium-limiting conditions of >20 microM K(+). These results provide the first experimental evidence of an ATP-driven K(+) uptake system in Halobacterium. Moreover, H. salinarum R1 was shown to further adapt to K(+) limitation by a significant decrease of the intracellular K(+) level, which suggests a rather complex mechanism of K(+) homeostasis, in which the adaptation of cellular K(+) concentrations and the concomitant transcriptional regulation of genes coding for a high-affinity ATP-driven K(+) uptake system ensure the essential potassium supply under limiting conditions.