PERINATAL LETHALITY AND DEFECTS IN HINDBRAIN DEVELOPMENT IN MICE HOMOZYGOUS FOR A TARGETED MUTATION OF THE ZINC-FINGER GENE KROX20
PERINATAL LETHALITY AND DEFECTS IN HINDBRAIN DEVELOPMENT IN MICE HOMOZYGOUS FOR A TARGETED MUTATION OF THE ZINC-FINGER GENE KROX20
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DOI：
10.1101/gad.7.11.2071
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发表时间：
1993-11-01
影响因子：
10.5
通讯作者：
GRIDLEY, T
中科院分区：
文献类型：
--
作者：
SWIATEK, PJ;GRIDLEY, T
Krox20是一个锌指基因，在脊椎动物的后脑发育过程中，在第3和第5菱节中表达。对于删除大部分Krox20基因（包括锌指DNA结合结构域）的靶向突变纯合子小鼠，出生后不久死亡。纯合突变动物的主要表型是3号和5号菱节缺失。这导致三叉神经节与面神经节和前庭神经节以及舌咽神经和迷走神经的上级神经节融合。这些融合导致这些神经节的神经根在进入脑干时发生紊乱。这些数据表明，Krox20在小鼠后脑和相关颅感觉神经节的发育过程中起着重要作用。
Krox20 is a zinc finger gene expressed in rhombomeres 3 and 5 during hindbrain development in vertebrates. Mice homozygous for a targeted mutation that deletes the majority of the Krox20 gene, including the zinc finger DNA-binding domain, died shortly after birth. The primary phenotype of the homozygous mutant animals was the loss of rhombomeres 3 and 5. This resulted in fusions of the trigeminal ganglion with the facial and vestibular ganglia, and of the superior ganglia of the glossopharyngeal and vagus nerves. These fusions resulted in a disorganization of the nerve roots of these ganglia as they entered the brain stem. These data demonstrate that Krox20 plays an essential role during development of the hindbrain and associated cranial sensory ganglia in mice.