Opus: University of Bath Online Publication Store Leukocyte Tyrosine Kinase Functions in Pigment Cell Development-猫眼课题宝

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S. S. Lopes-S.;X. Y. Yang;J. Carney;A. R. Rauch;G.-J Jacoby;A. S. Hurst;R. Johnson;S. L. Ward;A. Kelsh;S. S. Lopes-S.;Xueyan a;Yang;Jeanette Mü Ller;T. Carney;Anthony R. McAdow;Gerd-Jörg Rauch;A. Jacoby;L. Hurst;Mariana Delfino-Machín;P. Haffter;R. Geisler;Stephen L. Johnson;A. Ward;R. Kelsh;Greg Barsh;Stanford

此版本根据出版商政策提供。请仅引用使用上述参考文献的出版版本。发育生物学中的一个基本问题是多能性前体如何选择特定的命运。神经嵴细胞（NCC）是多能的，但驱动特定命运选择的机制仍然不完全清楚。Sox10是NCC中神经细胞和黑素细胞的特异性所必需的。像sox10突变体，斑马鱼阴暗的突变体缺乏iridophores，我们已经提出，sox10和阴暗的iridophores规格从NCC所需的。我们使用不同的方法，shady编码斑马鱼白细胞酪氨酸激酶（LTK）。细胞移植研究表明Ltk在虹膜细胞谱系内自主发挥作用。与此一致，ltk在NCC的子集中表达，然后被限制于虹膜细胞谱系。标记分析揭示了ltk突变体中虹膜细胞特化的主要缺陷。我们没有看到神经嵴细胞向其他色素细胞命运转移的证据，一些NCC随后因凋亡而丢失。这些特征也是sox10突变体中神经嵴细胞表型的特征，这使我们研究了sox10突变体中的虹膜细胞。正如预期的那样，sox10突变体在后期基本上缺乏虹膜标记。此外，sox10突变体出乎意料地比野生型同胞显示出更多的ltk表达细胞。这些细胞保持在迁移前的位置，并表达sox10，但不是最早的神经嵴标记，可能代表多能，但部分限制，祖细胞。总之，我们已经发现了一种新的信号通路在NCC的发展，并证明命运规格的虹膜作为第一个确定的作用LTK。版权所有：这是一篇开放获取的文章，根据知识共享署名许可证的条款分发，该许可证允许在任何媒体上不受限制地使用，分发和复制，前提是原作者和来源被记入。

This version is made available in accordance with publisher policies. Please cite only the published version using the reference above. Abstract A fundamental problem in developmental biology concerns how multipotent precursors choose specific fates. Neural crest cells (NCCs) are multipotent, yet the mechanisms driving specific fate choices remain incompletely understood. Sox10 is required for specification of neural cells and melanocytes from NCCs. Like sox10 mutants, zebrafish shady mutants lack iridophores; we have proposed that sox10 and shady are required for iridophore specification from NCCs. We show using diverse approaches that shady encodes zebrafish leukocyte tyrosine kinase (Ltk). Cell transplantation studies show that Ltk acts cell-autonomously within the iridophore lineage. Consistent with this, ltk is expressed in a subset of NCCs, before becoming restricted to the iridophore lineage. Marker analysis reveals a primary defect in iridophore specification in ltk mutants. We saw no evidence for a fate-shift of neural crest cells into other pigment cell fates and some NCCs were subsequently lost by apoptosis. These features are also characteristic of the neural crest cell phenotype in sox10 mutants, leading us to examine iridophores in sox10 mutants. As expected, sox10 mutants largely lacked iridophore markers at late stages. In addition, sox10 mutants unexpectedly showed more ltk-expressing cells than wild-type siblings. These cells remained in a premigratory position and expressed sox10 but not the earliest neural crest markers and may represent multipotent, but partially-restricted, progenitors. In summary, we have discovered a novel signalling pathway in NCC development and demonstrate fate specification of iridophores as the first identified role for Ltk. Copyright: ß 2008 Lopes et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Opus: University of Bath Online Publication Store Leukocyte Tyrosine Kinase Functions in Pigment Cell Development

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