听觉毛细胞角质板和连接处的 F-肌动蛋白受 ADF 和 cofilin 的调控,以实现正常的立体纤毛束模式化和维持。

Jamis McGrath, Katelin Hawbaker, Benjamin J Perrin
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引用次数: 0

摘要

听觉毛细胞将声音引起的内耳振动转化为神经信号,其正常功能依赖于多种肌动蛋白群。立体纤毛是围绕线性交联 F-肌动蛋白核心形成的机械感觉突起。它们固定在主要由随机定向的肌动蛋白丝组成的角质板上。第三种肌动蛋白群存在于毛细胞连接处附近,由平行和分枝的细丝组成。肌动蛋白解聚因子(ADF)和cofilin-1(CFL1)蛋白能分解肌动蛋白丝,是调节立体纤毛中F-肌动蛋白所必需的,但它们对角质板和交界处肌动蛋白群的影响尚不清楚。在这里,我们发现 ADF 和 CFL1 的缺失会破坏立体纤毛有序成束的模式,而且这种表型与角质板和交界肌动蛋白群的发育缺陷相关。ADF/CFL1 在成熟细胞中继续调节这些肌动蛋白群,这对于长期维持毛细胞形态是必要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
F-actin in the cuticular plate and junctions of auditory hair cells is regulated by ADF and cofilin to allow for normal stereocilia bundle patterning and maintenance.

Auditory hair cells, which convert sound-induced vibrations in the inner ear into neural signals, depend on multiple actin populations for normal function. Stereocilia are mechanosensory protrusions formed around a core of linear, crosslinked F-actin. They are anchored in the cuticular plate, which predominantly consists of randomly oriented actin filaments. A third actin population is found near hair cell junctions, consisting of both parallel and branched filaments. Actin depolymerizing factor (ADF) and cofilin-1 (CFL1) proteins disassemble actin filaments and are required to regulate F-actin in stereocilia, but their effect on cuticular plate and junctional actin populations is unclear. Here, we show that loss of ADF and CFL1 disrupts the patterning of stereocilia into orderly bundles and that this phenotype correlates with defective development of the cuticular plate and junctional actin populations. ADF/CFL1 continue to regulate these actin populations in mature cells, which is necessary for long-term maintenance of hair cell morphology.

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