Medeiros Nelson A, Burnette Dylan T, Forscher Paul
Interdepartmental Neuroscience Program, Yale University, New Haven, CT 06520, USA.
Nat Cell Biol. 2006 Mar;8(3):215-26. doi: 10.1038/ncb1367. Epub 2006 Feb 26.
Retrograde actin flow works in concert with cell adhesion to generate traction forces that are involved in axon guidance in neuronal growth cones. Myosins have been implicated in retrograde flow, but identification of the specific myosin subtype(s) involved has been controversial. Using fluorescent speckle microscopy (FSM) to assess actin dynamics, we report that inhibition of myosin II alone decreases retrograde flow by 51% and the remaining flow can be almost fully accounted for by the 'push' of plus-end actin assembly at the leading edge of the growth cone. Interestingly, actin bundles that are associated with filopodium roots elongated by approximately 83% after inhibition of myosin II. This unexpected result was due to decreased rates of actin-bundle severing near their proximal (minus or pointed) ends which are located in the transition zone of the growth cone. Our study reveals a mechanism for the regulation of actin-bundle length by myosin II that is dependent on actin-bundle severing, and demonstrate that retrograde flow is a steady state that depends on both myosin II contractility and actin-network treadmilling.
肌动蛋白逆行流与细胞黏附协同作用,产生参与神经元生长锥轴突导向的牵引力。肌球蛋白与逆行流有关,但所涉及的特定肌球蛋白亚型的鉴定一直存在争议。利用荧光斑点显微镜(FSM)评估肌动蛋白动力学,我们发现仅抑制肌球蛋白II可使逆行流减少51%,剩余的流几乎可以完全由生长锥前缘正端肌动蛋白组装的“推动”来解释。有趣的是,在抑制肌球蛋白II后,与丝状伪足根部相关的肌动蛋白束延长了约83%。这一意外结果是由于位于生长锥过渡区的肌动蛋白束近端(负端或尖端)附近的肌动蛋白束切断速率降低所致。我们的研究揭示了一种由肌球蛋白II调节肌动蛋白束长度的机制,该机制依赖于肌动蛋白束切断,并证明逆行流是一种依赖于肌球蛋白II收缩性和肌动蛋白网络踏车行为的稳态。