These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Evidence for Na(+) influx via the NtpJ protein of the KtrII K(+) uptake system in Enterococcus hirae.
    Author: Kawano M, Abuki R, Igarashi K, Kakinuma Y.
    Journal: J Bacteriol; 2000 May; 182(9):2507-12. PubMed ID: 10762252.
    Abstract:
    The ntpJ gene, a cistron located at the tail end of the vacuolar-type Na(+)-ATPase (ntp) operon of Enterococcus hirae, encodes a transporter of the KtrII K(+) uptake system. We found that K(+) accumulation in the ntpJ-disrupted mutant JEM2 was markedly enhanced by addition of valinomycin at pH 10. Studies of the membrane potential (DeltaPsi; inside negative) by 3, 3'-dihexyloxacarbocyanine iodide fluorescence revealed that the DeltaPsi was hyperpolarized at pH 10 in JEM2; the DeltaPsi values of the parent strain ATCC 9790 and JEM2, estimated by determining the equilibrium distribution of K(+) or Rb(+) in the presence of valinomycin, were -118 and -160 mV, respectively. DeltaPsi generation at pH 10 was accomplished by an electrogenic Na(+) efflux via the Na(+)-ATPase, whose levels in the two strains were quite similar. Na(+) uptake driven by an artificially imposed DeltaPsi (inside negative) was missing in JEM2, suggesting that NtpJ mediates Na(+) movement in addition to K(+) movement. Finally, the growth of JEM2 arrested in K(+)-limited high-Na(+) medium at pH 10 was restored by addition of valinomycin. These results suggest that NtpJ mediates electrogenic transport of K(+) as well as Na(+), that it likely mediates K(+) and Na(+) cotransport, and that Na(+) movement via NtpJ is the major Na(+) reentry pathway at high pH values.
    [Abstract] [Full Text] [Related] [New Search]