Stereocilia on auditory sensory cells are actin-based protrusions that mechanotransduce sound into an electrical signal. These stereocilia are arranged into a bundle with three rows of increasing length to form a staircase-like morphology that is required for hearing. Stereocilia in the shorter rows, but not the tallest row, are mechanotransducing because they have force-sensitive channels localized at their tips. The onset of mechanotransduction during mouse postnatal development refines stereocilia length and width. However, it is unclear how actin is differentially regulated between stereocilia in the tallest row of the bundle and the shorter, mechanotransducing rows. Here, we show actin turnover is increased at the tips of mechanotransducing stereocilia during bundle maturation. Correspondingly, from birth to postnatal day 6, these stereocilia had increasing amounts of available actin barbed ends, where monomers can be added or lost readily, as compared with the non-mechanotransducing stereocilia in the tallest row. The increase in available barbed ends depended on both mechanotransduction and MYO15 or EPS8, which are required for the normal specification and elongation of the tallest row of stereocilia. We also found that loss of the F-actin-severing proteins ADF and cofilin-1 decreased barbed end availability at stereocilia tips. These proteins enriched at mechanotransducing stereocilia tips, and their localization was perturbed by the loss of mechanotransduction, MYO15, or EPS8. Finally, stereocilia lengths and widths were dysregulated in Adf and Cfl1 mutants. Together, these data show that actin is remodeled, likely by a severing mechanism, in response to mechanotransduction.

听觉感觉细胞上的立体纤毛是基于肌动蛋白的突起，可将声音机械转变成电信号。这些静纤毛排列成三排，长度逐渐增加，形成听力所需的阶梯状形态。较短行中的立体纤毛具有机械传导作用，但最高行中则不然，因为它们的尖端具有力敏感通道。小鼠出生后发育过程中机械转导的开始细化了静纤毛的长度和宽度。然而，目前尚不清楚肌动蛋白在束最高行的静纤毛和较短的机械传导行之间是如何差异调节的。在这里，我们表明肌动蛋白周转在束成熟过程中在机械传导静纤毛的尖端增加。相应地，从出生到出生后第 6 天，这些静纤毛具有越来越多的可用肌动蛋白带刺末端，与最高行中的非机械传导静纤毛相比，单体可以很容易地添加或丢失。可用刺端的增加取决于机械转导和 MYO15 或 EPS8，这是最高一排静纤毛的正常规格和伸长所必需的。我们还发现，F-肌动蛋白切断蛋白 ADF 和 cofilin-1 的缺失降低了静纤毛尖端的倒刺末端可用性。这些蛋白质在机械转导静纤毛尖端富集，并且它们的定位因机械转导、MYO15 或 EPS8 的缺失而受到干扰。最后， Adf和Cfl1突变体中静纤毛的长度和宽度失调。总之，这些数据表明，肌动蛋白可能通过切断机制来重塑，以响应力转导。