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Jarodsky, J. M.

Publications and source records attributed to Jarodsky, J. M..

3 recordsLinked to original sources

Lipids intercalate and mediate multi-channel assemblies of connexin-46/50 gap junctions

Gap junction channels enable direct electrical and metabolic exchange between adjacent cells and tissues, where they organize into dense plaques containing tens to thousands of channels. Although plaque formation is known to modulate junctional conductance, the structural basis for channel-channel organization within a membrane environment remains poorly defined. Here, we reconstitute native lens connexin-46/50 (Cx46/50) gap junction channels into MSP-based lipid nanodiscs that incorporate multiple channels to create miniature plaque-like complexes suitable for single-particle cryo-electron microscopy (cryo-EM). We determine high-resolution structures of dual-channel assemblies in two distinct configurations and find no ordered protein-protein contacts across the interface. Instead, the inter-channel space is occupied by ordered lipid density, indicating that channel packing in these assemblies is lipid mediated. These channel-channel interfaces stabilize discrete lipid populations, including an interstitial lipid intercalated between subunits and positioned near the N-terminal gating domain, suggesting a route by which channel organization could promote lipid occupancy near the pore. Additionally, we leverage this dataset to refine the Cx46/50 single-channel structure to 1.8 [A] resolution, revealing exceptional chemical detail of the pore-lining landscape in the stabilized open-state. Together, these results define principles of lipid-mediated multi-channel organization and suggest how plaque-like packing may tune gap junction function through specific lipid interactions.

biophysics↗

Reversible lipid mediated pH-gating of connexin-46/50 by cryo-EM

Gap junctions, formed by connexin proteins, establish direct electrical and metabolic coupling between cells, enabling coordinated tissue responses. These channels universally respond to intracellular pH changes, closing under acidic conditions to limit the spread of cytotoxic signals during cellular stress, such as ischemia. Using cryo-electron microscopy (cryo-EM), we uncover insights into the structural mechanism of pH-gating in native lens connexin-46/50 (Cx46/50) gap junctions. Mild acidification drives lipid infiltration into the channel pore, displacing the N-terminal (NT) domain and stabilizing pore closure. Lipid involvement is both essential and fully reversible, with structural transitions involving an ensemble of gated-states formed through non-cooperative NT domain movement as well as minor populations of a distinct destabilized open-state. These findings provide molecular insights into pH-gating dynamics, illustrating how structural changes may regulate gap junction function under cellular stress and linking Cx46/50 dysregulation to age-related cataract formation.

biophysics↗

Calcium induced N-terminal gating and pore collapse in connexin-46/50 gap junctions

Gap junctions facilitate electrical and metabolic coupling essential for tissue function. Under ischemic conditions (e.g., heart attack or stroke), elevated intracellular calcium (Ca2+) levels uncouple these cell-to-cell communication pathways to protect healthy cells from cytotoxic signals. Using single-particle cryo-EM, we elucidate details of the Ca2+-induced gating mechanism of native connexin-46/50 (Cx46/50) gap junctions. The resolved structures reveal Ca2+ binding sites within the channel pore that alter the chemical environment of the permeation pathway and induce diverse occluded and gated states through N-terminal domain remodeling. Moreover, subunit rearrangements lead to pore collapse, enabling steric blockade by the N-terminal domains, reminiscent of the "iris model" of gating proposed over four decades ago. These findings unify and expand key elements of previous gating models, providing mechanistic insights into how Ca2+ signaling regulates gap junction uncoupling and broader implications for understanding cell stress responses and tissue protection.

biophysics↗