Neural cell fate in rca1 and cycA mutants:: the roles of intrinsic and extrinsic factors in asymmetric division in the Drosophila central nervous system
Neural cell fate in rca1 and cycA mutants:: the roles of intrinsic and extrinsic factors in asymmetric division in the Drosophila central nervous system
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DOI：
10.1016/s0925-4773(99)00190-2
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发表时间：
1999-11-01
影响因子：
2.6
通讯作者：
Patel, NH
中科院分区：
文献类型：
--
作者：
Lear, BC;Skeath, JB;Patel, NH
在缺乏细胞周期蛋白A（RCAL）或细胞周期蛋白A的果蝇胚胎的中枢神经系统（CNS）中，我们观察到几个神经节母细胞（GMC）无法分裂。尽管GMC通常会产生两个获得不同命运（“ A/B”）的兄弟姐妹神经元，但非个人GMC仅以其后代之一（'B'）的方式进行区分。在合子麻木的突变体中，兄弟姐妹神经元的命运改变（“ a/b”至“ a/a”）很少发生，或者在某些兄弟姐妹对中不会发生。我们已经确定，母体和合子麻木的耗竭会导致兄弟姐妹神经元获得均衡的命运（'a/a'），其表达能力几乎完整。实际上，麻木的突变胚胎，我们也观察到几个GMC中的二元细胞命运变化（b'to'a'）。最后，我们已经证明了中胚层中三角洲的表达足以达到两个兄弟姐妹的命运。我们的结果表明，要获得差异化同胞神经元命运，绝对需要内在的决定因素麻木。虽然还需要外部因素缺口和三角洲才能达到这两个命运，但我们的结果表明可以从兄弟姐妹对以外接收Delta信号。 （c）1999 Elsevier Science Ireland Ltd.保留所有权利。
In the central nervous system (CNS) of Drosophila embryos lacking regulator of cyclin A (rcal) or cyclin A, we observe that several ganglion mother cells (GMCs) fail to divide. Whereas GMCs normally produce two sibling neurons that acquire different fates ('A/B'), nondividing GMCs differentiate exclusively in the manner of one of their progeny ('B'). In zygotic numb mutants, sibling neuron fate alterations ('A/B' to 'A/A') occur infrequently or do not occur in some sibling pairs; we have determined that depletion of both maternal and zygotic numb causes sibling neurons to acquire equalized fates ('A/A') with near-complete expressivity. In real, numb mutant embryos, we observe binary cell fate changes ('B' to 'A') in several GMCs as well. Finally, we have demonstrated that expression of Delta in the mesoderm is sufficient to attain both sibling fates. Our results indicate that the intrinsic determinant Numb is absolutely required to attain differential sibling neuron fates. While the extrinsic factors Notch and Delta are also required to attain both fates, our results indicate that Delta signal can be received from outside the sibling pair. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.