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The Signal Transfer from the Receptor NpSRII to the Transducer NpHtrII Is Not Hampered by the D75N Mutation

Published inBiophysical journal, vol. 100, no. 9, p. 2275-2282
Publication date2011-05
Abstract

Sensory rhodopsin II (NpSRII) is a phototaxis receptor of Natronomonas pharaonis that performs its function in complex with its cognate transducer (NpHtrII). Upon light activation NpSRII triggers by means of NpHtrII a signal transduction chain homologous to the two component system in eubacterial chemotaxis. The D75N mutant of NpSRII, which lacks the blue-shifted M intermediate and therefore exhibits a significantly faster photocycle compared to the wild-type, mediates normal phototaxis responses demonstrating that deprotonation of the Schiff base is not a prerequisite for transducer activation. Using site-directed spin labeling and time resolved electron paramagnetic-resonance spectroscopy, we show that the mechanism revealed for activation of the wild-type complex, namely an outward tilt motion of the cytoplasmic part of the receptor helix F and a concomitant rotation of the transmembrane transducer helix TM2, is also valid for the D75N variant. Apparently, the D75N mutation shifts the ground state conformation of NpSRII-D75N and its cognate transducer into the direction of the signaling state.

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Citation (ISO format)
HOLTERHUES, Julia et al. The Signal Transfer from the Receptor <i>Np</i>SRII to the Transducer <i>Np</i>HtrII Is Not Hampered by the D75N Mutation. In: Biophysical journal, 2011, vol. 100, n° 9, p. 2275–2282. doi: 10.1016/j.bpj.2011.03.017
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ISSN of the journal0006-3495
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