Identification of the auditory hair cell mechano-electrical transduction (hcMET) channel has been a major focus in the hearing research field since the 1980s, when direct mechanical gating of a transduction channel was proposed [23]. To this day, the molecular identity of this channel remains controversial. However, many of the hcMET-channel's properties have been characterized including: pore properties, calcium dependent ion permeability, rectification, and single channel conductance. At this point, elucidating the molecular identity of the hcMET-channel will provide new tools for understanding the mechanotransduction process. This review discusses the significance of identifying the hcMET-channel, the difficulties associated with that task, as well as the establishment of clear criteria for this identification. Finally, we discuss potential candidate channels in light of these criteria.

Mammalian carotid body arterial chemoreceptors function as an early warning system for hypoxia, triggering acute life-saving arousal and cardiorespiratory reflexes. To serve this role, carotid body glomus cells are highly sensitive to decreases in oxygen availability. While the mitochondria and plasma membrane signaling proteins have been implicated in oxygen sensing by glomus cells, the mechanism underlying their mitochondrial sensitivity to hypoxia compared to other cells is unknown. Here, we identify HIGD1C, a novel hypoxia-inducible gene domain factor isoform, as an electron transport chain Complex IV-interacting protein that is almost exclusively expressed in the carotid body and is therefore not generally necessary for mitochondrial function. Importantly, HIGD1C is required for carotid body oxygen sensing and enhances Complex IV sensitivity to hypoxia. Thus, we propose that HIGD1C promotes exquisite oxygen sensing by the carotid body, illustrating how specialized mitochondria can be used as sentinels of metabolic stress to elicit essential adaptive behaviors.

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Hair cell mechanosensitivity resides in the sensory hair bundle, an apical protrusion of actin-filled stereocilia arranged in a staircase pattern. Hair bundle deflection activates mechano-electric transduction (MET) ion channels located near the tops of the shorter rows of stereocilia. The elicited macroscopic current is shaped by the hair bundle motion so that the mode of stimulation greatly influences the cell’s output. We present data quantifying the displacement of the whole outer hair cell bundle using high-speed imaging when stimulated with a fluid jet. We find a spatially non-uniform stimulation that results in splaying, where the hair bundle expands apart. Based on modeling, the splaying is predominantly due to fluid dynamics with a small contribution from hair bundle architecture. Additionally, in response to stimulation, the hair bundle exhibited a rapid motion followed by a slower motion in the same direction (creep) that is described by a double exponential process. The creep is consistent with originating from a linear passive system that can be modeled using two viscoelastic processes. These viscoelastic mechanisms are integral to describing the mechanics of the mammalian hair bundle.

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