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Long-term consequences of Sox9 depletion on inner ear development.

机译:SOX9消耗对内耳发展的长期后果。

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摘要

The transcription factor Sox9 has been implicated in inner ear formation in several species. To investigate the long-term consequences of Sox9 depletion on inner ear development we analyzed the inner ear architecture of Sox9-depleted Xenopus tadpoles generated by injection of increasing amounts of Sox9 morpholino antisense oligonucleotides. We found that Sox9-depletion resulted in major defects in the development of vestibular structures, semicircular canals and utricle, while the ventrally located saccule was less severely affected in these embryos. Consistent with this phenotype, we observed a specific loss of the dorsal expression of Wnt3a expression in the otic vesicle of Sox9 morphants, associated with an increase in cell death and a reduction in cell proliferation in the region of the presumptive otic epithelium. We propose that, in addition to its early role in placode specification, Sox9 is also required for the maintenance of progenitors in the otic epithelium.
机译:转录因子Sox9在几种物种中涉及内耳形成。 为了研究SOX9耗尽对内耳发展的长期后果,我们分析了通过注射增加量的SOX9甲嘧啶反义寡核苷酸产生的SOX9耗尽的外耳蝌蚪的内耳结构。 我们发现SOX9-Fepleion导致前庭结构,半圆形运河和utricle的发育中的主要缺陷,而介口的囊状在这些胚胎中较小地受到严重影响。 与这种表型一致,我们观察到在SOX9 Morphants的Otc囊泡中的Wnt3a表达的含量表达的特异性丧失,与药物死亡的增加和推定肠溶液区域区域中细胞增殖的降低相关。 我们提出,除了在Placode规范中的早期作用之外,SOX9还需要维持肠溶液中的祖细胞。

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