Key result
Molecular dynamics simulations reveal that introducing the G143E mutation in KirBac1.1 causes significant widening at the helix bundle crossing gate and a twisting motion of the cytoplasmic domain.
MD simulations of KirBac1.1 mutants provide high-resolution insights into the structural rearrangements and protein-lipid interactions underlying the activation gating of Kir channels.
Structural insights from KirBac1.1 simulations warrant validation in mammalian models; leaves open relevance to human Kir channelopathies.
Prokaryotic inwardly rectifying (KirBac) potassium channels are homologous to mammalian Kir channels. Their activity is controlled by dynamical conformational changes that regulate ion flow through a central pore. Understanding the dynamical rearrangements of Kir channels during gating requires high-resolution structure information from channels crystallized in different conformations and insight into the transition steps, which are difficult to access experimentally. In this study, we use MD simulations on wild type KirBac1.1 and an activatory mutant to investigate activation gating of KirBac channels. Full atomistic MD simulations revealed that introducing glutamate in position 143 causes significant widening at the helix bundle crossing gate, enabling water flux into the cavity. Further, global rearrangements including a twisting motion as well as local rearrangements at the subunit interface in the cytoplasmic domain were observed. These structural rearrangements are similar to recently reported KirBac3.1 crystal structures in closed and open conformation, suggesting that our simulations capture major conformational changes during KirBac1.1 opening. In addition, an important role of protein-lipid interactions during gating was observed. Slide-helix and C-linker interactions with lipids were strengthened during activation gating.
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Linder et al. (2015) studied this question. G143E mutation vs. Wild type KirBac1.1 was evaluated on Conformational changes (helix bundle crossing gate widening and CTD rotation). Molecular dynamics simulations reveal that introducing the G143E mutation in KirBac1.1 causes significant widening at the helix bundle crossing gate and a twisting motion of the cytoplasmic domain.
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