K2P Channels Regulate Presynaptic Organisation through a Membrane Potential-Independent Mechanism

Loss of twk-40 function in Caenorhabditis elegans causes excessive presynaptic protein accumulation, while twk-40 gain-of-function depletes presynaptic components and impairs synaptic transmission.

• Why it matters: It addresses how neuronal ion channels organize presynaptic structure without relying on membrane excitability pathways.
• What they did: The study used twk-40 loss- and gain-of-function mutants and compared them with transporter mutations affecting intracellular potassium and sodium channel mutations affecting membrane excitability. It also tested dependence on PYK-1 and three transcription factors.
• The result: Cytoplasmic potassium promotes presynaptic assembly via a PYK-1– and transcription-factor–dependent pathway, linking potassium homeostasis to presynaptic organization and synaptic function.

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