Charged Residues between the Selectivity Filter and S6 Segments Contribute to the Permeation Phenotype of the Sodium Channel
نویسندگان
چکیده
The deep regions of the Na(+) channel pore around the selectivity filter have been studied extensively; however, little is known about the adjacent linkers between the P loops and S6. The presence of conserved charged residues, including five in a row in domain III (D-III), hints that these linkers may play a role in permeation. To characterize the structural topology and function of these linkers, we neutralized the charged residues (from position 411 in D-I and its homologues in D-II, -III, and -IV to the putative start sites of S6) individually by cysteine substitution. Several cysteine mutants displayed enhanced sensitivities to Cd(2+) block relative to wild-type and/or were modifiable by external sulfhydryl-specific methanethiosulfonate reagents when expressed in TSA-201 cells, indicating that these amino acids reside in the permeation pathway. While neutralization of positive charges did not alter single-channel conductance, negative charge neutralizations generally reduced conductance, suggesting that such charges facilitate ion permeation. The electrical distances for Cd(2+) binding to these residues reveal a secondary "dip" into the membrane field of the linkers in domains II and IV. Our findings demonstrate significant functional roles and surprising structural features of these previously unexplored external charged residues.
منابع مشابه
Second-hit kinetic perturbations reveal structural features of the domain IV S6 segment associated with fast inactivation
Methods In order to reveal structural features of the domain IV S6 segment (DIV-S6) relevant to FI, we produced serial replacements by cysteines of residues 1575–1591 in DIVS6 of the rNaV1.4 channel ("first hit"). Furthermore, a critical residue within the selectivity filter of the rNaV1.4 channel, K1237, was replaced by the negatively charged glutamate ("second hit"). Previously, this mutation...
متن کاملStructural basis of ion permeation gating in Slo2.1 K+ channels
The activation gate of ion channels controls the transmembrane flux of permeant ions. In voltage-gated K(+) channels, the aperture formed by the S6 bundle crossing can widen to open or narrow to close the ion permeation pathway, whereas the selectivity filter gates ion flux in cyclic-nucleotide gated (CNG) and Slo1 channels. Here we explore the structural basis of the activation gate for Slo2.1...
متن کاملTail End of the S6 Segment: Role in Permeation in Shaker Potassium Channels
The permeation pathway in voltage-gated potassium channels has narrow constrictions at both the extracellular and intracellular ends. These constrictions might limit the flux of cations from one side of the membrane to the other. The extracellular constriction is the selectivity filter, whereas the intracellular bundle crossing is proposed to act as the activation gate that opens in response to...
متن کاملTopology of the selectivity filter of a TRPV channel: rapid accessibility of contiguous residues from the external medium.
The transient receptor potential type V5 (TRPV5) channel is a six-transmembrane domain ion channel that is highly selective to Ca(2+). To study the topology of the selectivity filter using the substituted cysteine accessibility method (SCAM), cysteine mutants at positions 541-547 were studied as heterotetramers using dimeric constructs that couple the control channel in tandem with a cysteine-b...
متن کاملProbing the role of negatively charged amino acid residues in ion permeation of skeletal muscle ryanodine receptor.
Sequence comparison suggests that the ryanodine receptors (RyRs) have pore architecture similar to that of the bacterial K+ channel KcsA. The lumenal loop linking the two most C-terminal transmembrane spanning segments in the RyRs has a predicted pore helix and an amino acid motif (GGGIG) similar to the selectivity filter (TVGYG) of KcsA identified by x-ray analysis. The RyRs have many negative...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- The Journal of General Physiology
دوره 115 شماره
صفحات -
تاریخ انتشار 2000