Neurogenic phenotype of mind bomb mutants leads to severe patterning defects in the zebrafish hindbrain
Neurogenic phenotype of mind bomb mutants leads to severe patterning defects in the zebrafish hindbrain
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DOI：
10.1002/dvdy.10429
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发表时间：
2003-11-01
影响因子：
2.5
通讯作者：
Chandrasekhar, A
中科院分区：
文献类型：
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作者：
Bingham, S;Chaudhari, S;Chandrasekhar, A
斑马鱼思维炸弹（mib）突变体中Notch信号传导的失败会导致神经源性表型，其中早期分化神经元的过度产生伴随着后期分化细胞类型的丧失。我们详细描述了 mib 突变体的后脑表型。 mib 突变体中后脑鳃运动神经元 (BMN) 数量减少，但并未缺失。此外，在突变体中，BMN 簇经常在中线融合。马赛克分析表明，mib 后脑中的 BMN 模式和融合缺陷是非细胞自主产生的。突变后脑的腹中线信号传导存在缺陷，部分原因是一些中线细胞分化为神经细胞。有趣的是，虽然 mib 突变体的早期后脑模式看起来正常，但随后的菱形体特异性基因表达完全丧失。腹侧中线信号传导和菱形图案的缺陷伴随着突变后脑中神经上皮细胞的明显损失。这些观察结果表明，通过调节神经上皮细胞向神经元的分化，Notch 信号传导保留了一群非神经元细胞，这些细胞对于维持发育中的神经管的模式机制至关重要。 (C) 2003 Wiley-Liss, Inc.
Failure of Notch signaling in zebrafish mind bomb (mib) mutants results in a neurogenic phenotype where an overproduction of early differentiating neurons is accompanied by the loss of later-differentiating cell types. We have characterized in detail the hindbrain phenotype of mib mutants. Hindbrain branchiomotor neurons (BMNs) are reduced in number but not missing in mib mutants. In addition, BMN clusters are frequently fused across the midline in mutants. Mosaic analysis indicates that the BMN patterning and fusion defects in the mib hindbrain arise non-cell autonomously. Ventral midline signaling is defective in the mutant hindbrain, in part due to the differentiation of some midline cells into neural cells. Interestingly, while early hindbrain patterning appears normal in mib mutants, subsequent rhombomere-specific gene expression is completely lost. The defects in ventral midline signaling and rhombomere patterning are accompanied by an apparent loss of neuroepithelial cells in the mutant hindbrain. These observations suggest that, by regulating the differentiation of neuroepithelial cells into neurons, Notch signaling preserves a population of non-neuronal cells that are essential for maintaining patterning mechanisms in the developing neural tube. (C) 2003 Wiley-Liss, Inc.