The object of this paper is to review the electronic conductance in double quantum well systems. These are quantum well structures in which electrons are confined in the z direction by large band gap material barrier layers, yet form a free two-dimensional Fermi gas within the sandwiched low band gap material layers in the x–y plane. Aspects related to the conductance in addition to the research progress made since the inception of such systems are included. While the review focuses on the tunnelling conductance properties of double quantum well devices, the longitudinal conductance is also discussed. Double quantum well systems are a more recent generation of structures whose precursors are the well known double-barrier resonant tunnelling systems. Thus, they have electronic signatures such as negative differential resistance, in addition to resonant tunnelling, whose behaviours depend on the wavefunction coupling between the quantum wells. As such, the barrier which separates the quantum wells can be tailored in order to provide better control of the device’s electronic properties over their single well ancestors.

Higher affinity for TnI explains how troponin C (TnC) carrying a causative hypertrophic cardiomyopathy mutation, TnCA8V, sensitizes muscle cells to Ca2+. Muscle fibers reconstituted with TnCA8V require ~2.3-fold less [Ca2+] to achieve 50% maximum-tension compared to fibers reconstituted with wild-type TnC (TnCWT). Binding measurements rule out a significant change in N-terminus Ca2+-affinity of isolated TnCA8V, and TnCA8V binds the switch-peptide of troponin-I (TnIsp) ~1.6-fold more strongly than TnCWT; thus we model the TnC-TnIsp interaction as competing with the TnI-actin interaction. Tension data are well-fit by a model constrained to conditions in which the affinity of TnCA8V for TnIsp is 1.5-1.7-fold higher than that of TnCWT at all [Ca2+]. Mean ATPase rates of reconstituted cardiac myofibrils is greater for TnCA8V than TnCWT at all [Ca2+], with statistically significant differences in the means at higher [Ca2+]. To probe TnC-TnI interaction in low Ca2+, displacement of bis-ANS from TnI was monitored as a function of TnC. Whereas Ca2+-TnCWT displaces significantly more bis-ANS than Mg2+-TnCWT, Ca2+-TnCA8V displaces probe equivalently to Mg2+-TnCA8V and Ca2+-TnCWT, consistent with stronger Ca2+-independent TnCA8V-TnIsp. A Matlab program for computing theoretical activation is reported. Our work suggests that contractility is constantly above normal in hearts made hypertrophic by TnCA8V.

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Cooperative activation of striated muscle by calcium is based on the movement of tropomyosin described by the steric blocking theory of muscle contraction. Presently, the Hill model stands alone in reproducing both myosin binding data and a sigmoidal-shaped curve characteristic of calcium activation (Hill TL (1983) Two elementary models for the regulation of skeletal muscle contraction by calcium. Biophys J 44: 383–396.). However, the free myosin is assumed to be fixed by the muscle lattice and the cooperative mechanism is based on calcium-dependent interactions between nearest neighbor tropomyosin subunits, which has yet to be validated. As a result, no comprehensive model has been shown capable of fitting actual tension data from striated muscle. We show how variable free myosin is a selective advantage for activating the muscle and describe a mechanism by which a conformational change in tropomyosin propagates free myosin given constant total myosin. This mechanism requires actin, tropomyosin, and filamentous myosin but is independent of troponin. Hence, it will work equally well with striated, smooth and non-muscle contractile systems. Results of simulations with and without data are consistent with a strand of tropomyosin composed of ∼20 subunits being moved by the concerted action of 3–5 myosin heads, which compares favorably with the predicted length of tropomyosin in the overlap region of thick and thin filaments. We demonstrate that our model fits both equilibrium myosin binding data and steady-state calcium-dependent tension data and show how both the steepness of the response and the sensitivity to calcium can be regulated by the actin-troponin interaction. The model simulates non-cooperative calcium binding both in the presence and absence of strong binding myosin as has been observed. Thus, a comprehensive model based on three well-described interactions with actin, namely, actin-troponin, actin-tropomyosin, and actin-myosin can explain the cooperative calcium activation of striated muscle.

The reversal of flagellar motion (switching) results from the interaction between a switch complex of the flagellar rotor and a torque-generating stationary unit, or stator (motor unit). To explain the steeply cooperative ligand-induced switching, present models propose allosteric interactions between subunits of the rotor, but do not address the possibility of a reaction that stimulates a bidirectional motor unit to reverse direction of torque. During flagellar motion, the binding of a ligand-bound switch complex at the dwell site could excite a motor unit. The probability that another switch complex of the rotor, moving according to steady-state rotation, will reach the same dwell site before that motor unit returns to ground state will be determined by the independent decay rate of the excited-state motor unit. Here, we derive an analytical expression for the energy coupling between a switch complex and a motor unit of the stator complex of a flagellum, and demonstrate that this model accounts for the cooperative switching response without the need for allosteric interactions. The analytical result can be reproduced by simulation when (1) the motion of the rotor delivers a subsequent ligand-bound switch to the excited motor unit, thereby providing the excited motor unit with a second chance to remain excited, and (2) the outputs from multiple independent motor units are constrained to a single all-or-none event. In this proposed model, a motor unit and switch complex represent the components of a mathematically defined signal transduction mechanism in which energy coupling is driven by steady-state and is regulated by stochastic ligand binding. Mathematical derivation of the model shows the analytical function to be a general form of the Hill equation (Hill AV (1910) The possible effects of the aggregation of the molecules of haemoglobin on its dissociation curves. J Physiol 40: iv–vii).