Epithelial dynamics shed light on the mechanisms underlying ear canal defects.
Epithelial dynamics shed light on the mechanisms underlying ear canal defects.
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DOI：
10.1242/dev.194654
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发表时间：
2020-12-14
期刊：
影响因子：
--
通讯作者：
Tucker AS
中科院分区：
文献类型：
--
作者：
Fons JM;Mozaffari M;Malik D;Marshall AR;Connor S;Greene NDE;Tucker AS
由于声波无法到达中耳，耳道发育缺陷会导致严重的听力损失。在这里，我们揭示了控制人类运河发育的新机制，并首次强调了运河关闭和重新开放的复杂系统。这些过程可能会在突变小鼠和外植体培养中受到干扰，模仿与耳道闭锁相关的缺陷。运河的较表层部分由开放的主要运河形成，该运河关闭然后重新打开。相比之下，运河的较深部分由随后打开的延伸的实心门板形成。原发根管的闭合和融合与周皮的丧失有关，Grhl3突变小鼠的周皮形成失败与根管的过早闭合有关。相反，抑制周皮细胞死亡会导致闭合停滞。一旦关闭，根管就会以波状重新打开，这是由上皮的终末分化触发的。了解根管发育中涉及的这些复杂过程有助于揭示根管闭锁的根本原因。 我们揭示了控制耳道发育的新机制，并首次强调了耳道关闭和重新打开的复杂系统。
Defects in ear canal development can cause severe hearing loss as sound waves fail to reach the middle ear. Here, we reveal new mechanisms that control human canal development and highlight for the first time the complex system of canal closure and reopening. These processes can be perturbed in mutant mice and in explant culture, mimicking the defects associated with canal atresia. The more superficial part of the canal forms from an open primary canal that closes and then reopens. In contrast, the deeper part of the canal forms from an extending solid meatal plate that opens later. Closure and fusion of the primary canal was linked to loss of periderm, with failure in periderm formation in Grhl3 mutant mice associated with premature closure of the canal. Conversely, inhibition of cell death in the periderm resulted in an arrest of closure. Once closed, re-opening of the canal occurred in a wave, triggered by terminal differentiation of the epithelium. Understanding these complex processes involved in canal development sheds light on the underlying causes of canal atresia. We reveal new mechanisms that control development of the ear canal and highlight for the first time the complex system of canal closure and reopening.
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作者：
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DOI：
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发表时间：
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期刊：
ANATOMY AND EMBRYOLOGY
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