The University of Queensland, Queensland Brain Institute, Clem Jones Centre for Ageing Dementia Research, Brisbane, Queensland 4072, Australia.
The University of Queensland, Queensland Brain Institute, Brisbane, Queensland 4072, Australia.
Mol Cell Neurosci. 2017 Oct;84:112-118. doi: 10.1016/j.mcn.2017.04.003. Epub 2017 May 22.
Bulk endocytosis allows stimulated neurons to take up a large portion of the presynaptic plasma membrane in order to regenerate synaptic vesicle pools. Actin, one of the most abundant proteins in eukaryotic cells, plays an important role in this process, but a detailed mechanistic understanding of the involvement of the cortical actin network is still lacking, in part due to the relatively small size of nerve terminals and the limitation of optical microscopy. We recently discovered that neurosecretory cells display a similar, albeit much larger, form of bulk endocytosis in response to secretagogue stimulation. This allowed us to identify a novel highly dynamic role for the acto-myosin II cortex in generating constricting rings that precede the fission of nascent bulk endosomes. In this review we focus on the mechanism underpinning this dramatic switch in the organization and function of the cortical actin network. We provide additional experimental data that suggest a role of tropomyosin Tpm3.1 and Tpm4.2 in this process, together with an emerging model of how actin controls bulk endocytosis.
胞吞作用使受刺激的神经元能够摄取大部分突触前细胞膜，以再生突触小泡池。肌动蛋白是真核细胞中最丰富的蛋白质之一，在这个过程中起着重要作用，但由于神经末梢相对较小和光学显微镜的限制，皮质肌动蛋白网络的参与的详细机制仍不清楚。我们最近发现，神经分泌细胞在受到分泌刺激时会表现出类似的、但更大的胞吞作用形式。这使我们能够识别肌动球蛋白皮层在生成收缩环中的新的高度动态作用，该收缩环先于新生胞吞体的裂变。在这篇综述中，我们重点介绍了皮质肌动蛋白网络的组织和功能发生这种戏剧性转变的机制。我们提供了额外的实验数据，表明原肌球蛋白 Tpm3.1 和 Tpm4.2 在这个过程中起作用，以及肌动蛋白如何控制胞吞作用的新兴模型。
