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首页> 外文期刊>Cell and Tissue Research >Lmx1a is required for segregation of sensory epithelia and normal ear histogenesis and morphogenesis
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Lmx1a is required for segregation of sensory epithelia and normal ear histogenesis and morphogenesis

机译：Lmx1a是感觉上皮分离和正常耳朵组织发生与形态发生所必需的

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At embryonic day 8.5, the LIM-homeodomain factor Lmx1a is expressed throughout the otic placode but becomes developmentally restricted to non-sensory epithelia of the ear (endolymphatic duct, ductus reuniens, cochlea lateral wall). We confirm here that the ears of newborn dreher (Lmx1a dr) mutants are dysmorphic. Hair cell markers such as Atoh1 and Myo7 reveal, for the first time, that newborn Lmx1a mutants have only three sensory epithelia: two enlarged canal cristae and one fused epithelium comprising an amalgamation of the cochlea, saccule, and utricle (a “cochlear-gravistatic” endorgan). The enlarged anterior canal crista develops by fusion of horizontal and anterior crista, whereas the posterior crista fuses with an enlarged papilla neglecta that may extend into the cochlear lateral wall. In the fused endorgan, the cochlear region is distinguished from the vestibular region by markers such as Gata3, the presence of a tectorial membrane, and cochlea-specific innervation. The cochlea-like apex displays minor disorganization of the hair and supporting cells. This contrasts with the basal half of the cochlear region, which shows a vestibular epithelium-like organization of hair cells and supporting cells. The dismorphic features of the cochlea are also reflected in altered gene expression patterns. Fgf8 expression expands from inner hair cells in the apex to most hair cells in the base. Two supporting cell marker proteins, Sox2 and Prox1, also differ in their cellular distribution between the base and the apex. Sox2 expression expands in mutant canal cristae prior to their enlargement and fusion and displays a more diffuse and widespread expression in the base of the cochlear region, whereas Prox1 is not detected in the base. These changes in Sox2 and Prox1 expression suggest that Lmx1a expression restricts and sharpens Sox2 expression, thereby defining non-sensory and sensory epithelium. The adult Lmx1a mutant organ of Corti shows a loss of cochlear hair cells, suggesting that the long-term maintenance of hair cells is also disrupted in these mutants.
机译：在胚胎的第8.5天，LIM同源结构域因子Lmx1a在整个听觉斑块中表达，但在发育上仅限于耳朵的非感觉上皮细胞（内淋巴管，肾小管，耳蜗侧壁）。我们在这里证实，新生儿德雷尔（Lmx1a dr ）突变体的耳朵是畸形的。毛细胞标记（例如Atoh1和Myo7）首次揭示，新生的Lmx1a突变体仅具有三个感觉上皮：两个扩大的管cr和一个融合的上皮，其中包括耳蜗，球囊和囊的融合（“ （endorgan）。扩大的前管cr通过水平和前cr的融合而发展，而后cr与扩大的乳头状缺损融合，该乳头缺损可能延伸到耳蜗侧壁。在融合的内器官中，耳蜗区域与前庭区域的区别在于标记物，例如Gata3，存在的盖膜和耳蜗特异性神经支配。耳蜗状的先端显示出毛发和支持细胞的轻微混乱。这与耳蜗区域的基底一半形成对比，后者显示了毛细胞和支持细胞的前庭上皮样组织。耳蜗的畸变特征也反映在改变的基因表达模式中。 Fgf8表达从先端的内部毛细胞扩展到基部的大多数毛细胞。两种支持细胞标记蛋白，Sox2和Prox1，在碱基和先端之间的细胞分布也不同。 Sox2的表达在其扩大和融合之前在突变的cr中扩展，并在耳蜗区域的底部显示出更加分散和广泛的表达，而在底部未检测到Prox1。 Sox2和Prox1表达的这些变化表明Lmx1a表达限制并增强了Sox2表达，从而定义了非感觉上皮和感觉上皮。 Corti的成年Lmx1a突变器官显示出耳蜗毛细胞的丢失，这表明在这些突变体中，毛细胞的长期维持也受到了破坏。

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