MpcT is the transducer for membrane potential changes in Halobacterium salinarum

Authors

  • Matthias K. Koch,

    1. Department of Membrane Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany.
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  • Dieter Oesterhelt

    Corresponding author
    1. Department of Membrane Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany.
      E-mail oesterhe@biochem.mpg.de; Tel. (+49) 89 8578 2386; Fax (+49) 89 8578 3557.
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E-mail oesterhe@biochem.mpg.de; Tel. (+49) 89 8578 2386; Fax (+49) 89 8578 3557.

Summary

In Halobacterium salinarum mutants containing either of the light-driven ion pumps bacteriorhodopsin (H+) or halorhodopsin (Cl) as their only retinal protein, a decrease of irradiance in the absence of respiration causes a phototactic response. The conversion of the causal event, a decrease of proton motive force across the cell membrane, into a reversal of flagellar motor rotational direction was expected to involve a transducer. Via deletion analysis of all 18 known and putative halobacterial transducer (htr) genes, we found that Htr14, a methylatable membrane-bound transducer lacking an extracellular domain, mediates the biological response, which includes adaptive methylation. Based on a minimal stimulus length of 200 ms and the determined cytoplasmic buffering capacity, we conclude that the change in the membrane potential (ΔΨ), and not that of the internal pH, is the signal-generating event. Htr14 was therefore renamed to Membrane potential change Transducer, or MpcT. It is the first transducer for which the causative stimulus could be narrowed to a change in ΔΨ, as opposed to a change in pH or cellular redox state.

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