Nature | 突破传统模型——内源振荡器塑造神经细胞命运，保证神经元仅生成一根轴突

TL;DR - A Nature paper from Frank Bradke's team (German Center for Neurodegenerative Diseases) shows that neuronal polarity — why a neuron grows exactly one axon — is driven by an intrinsic, soma-originated cytoskeletal oscillator rather than growth cones sensing external cues. This overturns the dominant extracellular-guidance model and names actomyosin contractility as a target for axon repair.

• Soma, not growth cone, is the control hub: live-cell imaging and embryonic brain slices show immature neurites undergo periodic alternating extension/retraction, with only one neurite elongating at a time, driven by ARP2/3-generated actin waves originating in the cell body — independent of extracellular guidance signals.
• ARP2/3 vs. myosin II antagonism: the actin wave first retracts all neurites; when it stochastically enters one neurite tip, local ARP2/3 weakens myosin-driven contraction and permits microtubule extension, giving that neurite axonal advantage. Myosin II acts as a global growth inhibitor, and ARP2/3 has position-dependent bidirectional function — reconciling previously contradictory results.
• Genetic and rescue evidence: ARP3 knockout abolishes actin waves and blocks axon formation; myosin inhibition rescues the knockout phenotype, indicating excessive actomyosin contraction is the core barrier to axon growth. The selected neurite eventually becomes ARP2/3-independent and grows continuously; the rest become dendrites.
• Significance: explains why neurons form a single axon despite a growth-factor-rich developmental environment, and proposes actomyosin contractility as a molecular target for spinal cord injury and neurodegenerative axon regeneration.