Halorhodopsin is a light-driven chloride pump.

TLDR

The authors measured light‑induced membrane potentials, ionic fluxes, and volume changes in vesicles containing bacteriorhodopsin or halorhodopsin, revealing that bacteriorhodopsin drives proton extrusion via a proton/sodium antiport and passive chloride efflux, while halorhodopsin mediates primary inward chloride transport accompanied by passive cation uptake. Halorhodopsin functions as an inward chloride pump, producing volume increase, membrane potential, pH change, and swelling against both electrical and concentration gradients, and the data rule out a significant role for sodium, contradicting earlier claims of an outward sodium pump.

Abstract

Light-dependent membrane potentials, ionic fluxes, and volume changes were measured in two kinds of Halobacterium halobium cell envelope vesicles: one containing bacteriorhodopsin and another halorhodopsin. Bacteriorhodopsin-containing vesicles extruded protons by a primary electrogenic mechanism and an energized volume decrease was observed. This was shown to be the consequences of sodium extrusion via proton/sodium antiport (which recirculated protons) and the accompanying passive chloride extrusion. Halorhodopsin-containing vesicles, in contrast, exhibited a volume increase during illumination, apparently caused by primary inward transport of chloride, and accompanied by passive cation (sodium or potassium, and proton) uptake. It was demonstrated that the chloride transport will occur against both electrical and concentration gradients across the vesicle membrane. Moreover, chloride was required on the vesicle exterior for the light-dependent generation of membrane potential, pH change, and swelling. These observations are inconsistent with an earlier proposal that halorhodopsin is an outward directed sodium pump, but suggest very strongly that it is an inward directed chloride pump. Quantitative arguments from the present work rule out a significant role of sodium in the functioning of halorhodopsin.