The tight junction scaffolding protein cingulin regulates neural crest cell migration.

The tight junction scaffolding protein cingulin regulates neural crest cell migration.
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DOI:
10.1002/dvdy.22735
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发表时间:
2011-10
影响因子:
2.5
通讯作者:
Taneyhill, Lisa A.
Taneyhill, Lisa A.
中科院分区:
生物学3区
文献类型:
--
作者:
Wu, Chyong-Yi;Jhingory, Sharon;Taneyhill, Lisa A.

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在脊椎动物的发育过程中,神经嵴细胞产生了多种不同的结构。这些细胞最初存在于背神经上皮中,随后获得迁移能力。虽然已有研究证明粘附连接在调节神经嵴细胞迁移中的重要性,但在这一过程中很少关注紧密连接。我们现在确定紧密连接蛋白扣带蛋白是神经嵴迁移的关键调节因子。Cingulin敲除增加迁移的神经嵴细胞结构域,这与神经管基板的破坏有关。cingulin的过度表达也增加了神经嵴细胞的迁移,并与类似的基板变化和迁移前神经嵴群体的扩大有关。Cingulin过表达导致异常的腹侧神经上皮细胞分层,这与层粘连蛋白丢失和RhoA减少有关。总之,我们的研究结果强调了扣带蛋白在神经嵴中的新功能。
Neural crest cells give rise to a diverse range of structures during vertebrate development. These cells initially exist in the dorsal neuroepithelium and subsequently acquire the capacity to migrate. Although studies have documented the importance of adherens junctions in regulating neural crest cell migration, little attention has been paid to tight junctions during this process. We now identify the tight junction protein cingulin as a key regulator of neural crest migration. Cingulin knock-down increases the migratory neural crest cell domain, which is correlated with a disruption of the neural tube basal lamina. Overexpression of cingulin also augments neural crest cell migration and is associated with similar basal lamina changes and an expansion of the premigratory neural crest population. Cingulin overexpression causes aberrant ventrolateral neuroepithelial cell delamination, which is linked to laminin loss and a decrease in RhoA. Together, our results highlight a novel function for cingulin in the neural crest.
cingulin包含球形和盘绕螺旋域,并与ZO-1,ZO-2,ZO-3和肌球蛋白相互作用。
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