Ligand-receptor interactions guide axon navigation and dendrite arborization. Mechanical forces also influence guidance choices. However, the nature of such mechanical stimulations, the mechanosensor identity, and how they interact with guidance receptors are unknown. Here, we demonstrate that mechanosensitive DEG/ENaC channels are required for dendritic arbor morphogenesis in Caenorhabditis elegans. Inhibition of DEG/ENaC channels causes reduced dendritic outgrowth and branching in vivo, a phenotype that is alleviated by overexpression of the mechanosensitive channels PEZO-1/Piezo or YVC1/TrpY1. DEG/ENaCs trigger local Ca²⁺ transients in growing dendritic filopodia via activation of L-type voltage-gated Ca²⁺ channels. Anchoring of filopodia by dendrite ligand-receptor complexes is required for the mechanical activation of DEG/ENaC channels. Therefore, mechanosensitive channels serve as a checkpoint for appropriate chemoaffinity by activating Ca²⁺ transients required for neurite growth.

配体-受体相互作用指导轴突导航和树突树枝状化。机械力也会影响导向选择。然而，这种机械刺激的性质、机械传感器的身份以及它们如何与引导受体相互作用是未知的。在这里，我们证明了秀丽隐杆线虫的树突乔木形态发生需要机械敏感的 DEG/ENaC 通道。DEG/ENaC 通道的抑制导致体内树突生长和分支减少，这种表型可通过机械敏感通道 PEZO-1/Piezo 或 YVC1/TrpY1 的过表达而得到缓解。DEG/ENaCs通过激活 L 型电压门控 Ca ^{2+在生长的树突丝状伪足中触发局部 Ca 2+瞬变}渠道。DEG/ENaC 通道的机械激活需要树突配体-受体复合物锚定丝状伪足。因此，机械敏感通道通过激活神经突生长所需的Ca ²⁺瞬变作为适当化学亲和力的检查点。