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由肌动蛋白和肌球蛋白驱动的周向和轴向张力的偶联影响体内轴突直径。

Coupled circumferential and axial tension driven by actin and myosin influences in vivo axon diameter.

机构信息

Department of Mechanical Science and Engineering, University of Illinois at Urbana-Champaign, Urbana, IL, USA.

Department of Electrical and Computer Engineering, University of Illinois at Urbana-Champaign, Urbana, IL, USA.

出版信息

Sci Rep. 2017 Oct 27;7(1):14188. doi: 10.1038/s41598-017-13830-1.

DOI:10.1038/s41598-017-13830-1
PMID:29079766
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5660205/
Abstract

It has long been known that neuronal axons are contractile. They actively maintain rest tension along the longitudinal direction both in vitro and in vivo. Here we show evidence that embryonic drosophila axons also actively maintain contractility/tension along the circumferential direction. We used confocal microscopy and spatial light interference microscopy to monitor axonal diameter along their length. We observed a decrease in diameter when microtubules are disrupted and an increase in diameter when actin filaments or myosin II are disrupted. Interestingly, active diameter reduction occurred consistently when axons were subjected to manipulations known to increase axial tension, suggesting that tension can be coupled in the axial and circumferential direction. This is further supported by the remarkably similar time constants for diameter reduction and rest tension increase of slackened axons. We infer that the actomyosin-driven circumferential contraction/hoop tension applies a squeezing force on the microtubule bundle of the axons. This hoop tension is balanced by the restoring force of the microtubule bundle. Therefore, axonal diameter increased when actin/myosin disrupting drugs relaxed the hoop tension and decreased when microtubule disrupting drug relaxed the restoring force. Circumferential tension thus can regulate axonal diameter and volume, as well as potentially microtubules alignment, inter-tubular spacing, and, by extension, axonal transport.

摘要

长期以来,人们一直知道神经元轴突是可收缩的。它们在体外和体内都能主动维持沿纵向的静息张力。在这里,我们提供证据表明,胚胎果蝇轴突也能主动维持沿圆周方向的收缩/张力。我们使用共聚焦显微镜和空间光干涉显微镜来监测沿轴突长度的轴突直径。当微管被破坏时,我们观察到直径减小,当肌动蛋白丝或肌球蛋白 II 被破坏时,直径增加。有趣的是,当轴突受到已知会增加轴向张力的操作时,主动直径减小始终发生,这表明张力可以在轴向和圆周方向上耦合。这进一步得到了松弛轴突的直径减小和静息张力增加的时间常数非常相似的支持。我们推断,肌动球蛋白驱动的圆周收缩/箍张力对轴突的微管束施加挤压力。这种箍张力由微管束的恢复力平衡。因此,当肌动蛋白/肌球蛋白破坏药物放松箍张力时,轴突直径增加,而当微管破坏药物放松恢复力时,轴突直径减小。因此,圆周张力可以调节轴突的直径和体积,以及潜在的微管排列、管间间距,并通过延伸调节轴突运输。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/53ec674f1d3f/41598_2017_13830_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/1cd6bf7e80f7/41598_2017_13830_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/51c5ee6fe3f1/41598_2017_13830_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/7511a341bc08/41598_2017_13830_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/8c6934848d69/41598_2017_13830_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/ab985abfd9dc/41598_2017_13830_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/53ec674f1d3f/41598_2017_13830_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/1cd6bf7e80f7/41598_2017_13830_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/51c5ee6fe3f1/41598_2017_13830_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/7511a341bc08/41598_2017_13830_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/8c6934848d69/41598_2017_13830_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/ab985abfd9dc/41598_2017_13830_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bf5/5660205/53ec674f1d3f/41598_2017_13830_Fig6_HTML.jpg

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Actin dynamics provides membrane tension to merge fusing vesicles into the plasma membrane.肌动蛋白动态为融合囊泡与质膜融合提供膜张力。
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