Flexoelectricity Driven Fano Resonance in Slotted Carbon Nanotubes for Decoupled Multifunctional Sensing

Multifunctionality, interference-free signal readout, and quantum effect are important considerations for flexible sensors equipped within a single unit towards further miniaturization. To address these criteria, we present the slotted carbon nanotube (CNT) junction features tunable Fano resonance driven by flexoelectricity, which could serve as an ideal multimodal sensory receptor. Based on extensive ab initio calculations, we find that the effective Fano factor can be used as a temperature-insensitive extrinsic variable for sensing the bending strain, and the Seebeck coefficient can be used as a strain-insensitive intrinsic variable for detecting temperature. Thus, this dual-parameter permits simultaneous sensing of temperature and strain without signal interference. We further demonstrate the applicability of this slotted junction to ultrasensitive chemical sensing which enables precise determination of donor-type, acceptor-type, and inert molecules. This is due to the enhancement or counterbalance between flexoelectric and chemical gating. Flexoelectric gating would preserve the electron–hole symmetry of the slotted junction whereas chemical gating would break it. As a proof-of-concept demonstration, the slotted CNT junction provides an excellent quantum platform for the development of multistimuli sensation in artificial intelligence at the molecular scale.

Calmodulin-Connexin Partnership in Gap Junction Channel Regulation-Calmodulin-Cork Gating Model

In the past four decades numerous findings have indicated that gap junction channel gating is mediated by intracellular calcium concentrations ([Ca2+i]) in the high nanomolar range via calmodulin (CaM). We have proposed a CaM-based gating model based on evidence for a direct CaM role in gating. This model is based on the following: CaM inhibitors and the inhibition of CaM expression to prevent chemical gating. A CaM mutant with higher Ca2+ sensitivity greatly increases gating sensitivity. CaM co-localizes with connexins. Connexins have high-affinity CaM-binding sites. Connexin mutants paired to wild type connexins have a higher gating sensitivity, which is eliminated by the inhibition of CaM expression. Repeated trans-junctional voltage (Vj) pulses progressively close channels by the chemical/slow gate (CaM’s N-lobe). At the single channel level, the gate closes and opens slowly with on-off fluctuations. Internally perfused crayfish axons lose gating competency but recover it by the addition of Ca-CaM to the internal perfusion solution. X-ray diffraction data demonstrate that isolated gap junctions are gated at the cytoplasmic end by a particle of the size of a CaM lobe. We have proposed two types of CaM-driven gating: “Ca-CaM-Cork” and “CaM-Cork”. In the first, the gating involves Ca2+-induced CaM activation. In the second, the gating occurs without a [Ca2+]i rise.

Bio-inspired artificial ion channels: from physical to chemical gating

Artificial ion channels mimicking the intelligent gating functions of biological ion channels are highly desirable for label-free sensing, on-demand delivery and controllable separation. There have been huge advances in fabricating...

Nanobubble-controlled nanofluidic transport

Nanofluidic platforms offering tunable material transport are applicable in biosensing, chemical detection, and filtration. Prior studies have achieved selective and controllable ion transport through electrical, optical, or chemical gating of complex nanostructures. Here, we mechanically control nanofluidic transport using nanobubbles. When plugging nanochannels, nanobubbles rectify and occasionally enhance ionic currents in a geometry-dependent manner. These conductance effects arise from nanobubbles inducing surface-governed ion transport through interfacial electrolyte films residing between nanobubble surfaces and nanopipette walls. The nanobubbles investigated here are mechanically generated, made metastable by surface pinning, and verified with cryogenic transmission electron microscopy. Our findings are relevant to nanofluidic device engineering, three-phase interface properties, and nanopipette-based applications.

Calmodulin-Cork Model of Gap Junction Channel Gating—One Molecule, Two Mechanisms

The Calmodulin-Cork gating model is based on evidence for the direct role of calmodulin (CaM) in channel gating. Indeed, chemical gating of cell-to-cell channels is sensitive to nanomolar cytosolic calcium concentrations [Ca2+]i. Calmodulin inhibitors and inhibition of CaM expression prevent chemical gating. CaMCC, a CaM mutant with higher Ca2+-sensitivity greatly increases chemical gating sensitivity (in CaMCC the NH2-terminal EF-hand pair (res. 9–76) is replaced by the COOH-terminal pair (res. 82–148). Calmodulin colocalizes with connexins. Connexins have high-affinity CaM binding sites. Several connexin mutants paired to wild-type connexins have a high gating sensitivity that is eliminated by inhibition of CaM expression. Repeated transjunctional voltage (Vj) pulses slowly and progressively close a large number of channels by the chemical/slow gate (CaM lobe). At the single-channel level, the chemical/slow gate closes and opens slowly with on-off fluctuations. The model proposes two types of CaM-driven gating: “Ca-CaM-Cork” and “CaM-Cork”. In the first, gating involves Ca2+-induced CaM-activation. In the second, gating takes place without [Ca2+]i rise. The Ca-CaM-Cork gating is only reversed by a return of [Ca2+]i to resting values, while the CaM-Cork gating is reversed by Vj positive at the gated side.

Calmodulin-Mediated Regulation of Gap Junction Channels

Evidence that neighboring cells uncouple from each other as one dies surfaced in the late 19th century, but it took almost a century for scientists to start understanding the uncoupling mechanism (chemical gating). The role of cytosolic free calcium (Ca2+i) in cell–cell channel gating was first reported in the mid-sixties. In these studies, only micromolar [Ca2+]i were believed to affect gating—concentrations reachable only in cell death, which would discard Ca2+i as a fine modulator of cell coupling. More recently, however, numerous researchers, including us, have reported the effectiveness of nanomolar [Ca2+]i. Since connexins do not have high-affinity calcium sites, the effectiveness of nanomolar [Ca2+]i suggests the role of Ca-modulated proteins, with calmodulin (CaM) being most obvious. Indeed, in 1981 we first reported that a CaM-inhibitor prevents chemical gating. Since then, the CaM role in gating has been confirmed by studies that tested it with a variety of approaches such as treatments with CaM-inhibitors, inhibition of CaM expression, expression of CaM mutants, immunofluorescent co-localization of CaM and gap junctions, and binding of CaM to peptides mimicking connexin domains identified as CaM targets. Our gating model envisions Ca2+-CaM to directly gate the channels by acting as a plug (“Cork” gating model), and probably also by affecting connexin conformation.