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果蝇胚胎肌肉和表皮发育中Notch的自主和非自主功能。

Autonomous and nonautonomous Notch functions for embryonic muscle and epidermis development in Drosophila.

作者信息

Baker R, Schubiger G

机构信息

Department of Genetics, Unviersity of Washington, Seattle 98195, USA.

出版信息

Development. 1996 Feb;122(2):617-26. doi: 10.1242/dev.122.2.617.

DOI:10.1242/dev.122.2.617
PMID:8625813
Abstract

The Notch (N) gene encodes a cell signaling protein that mediates neuronal and epidermal determination in Drosophila embryos. N also regulates several aspects of myogenic development; embryos lacking N function have too many muscle founder cells and fail to properly differentiate somatic muscle. To identify cell-autonomous requirements for Notch function during muscle development, we expressed a Notch minigene in the mesoderm, but not in the ectoderm, of amorphic N-embryos. In these embryos, muscle founder hypertrophy is rescued, indicating that Notch is autonomously required by mesoderm cells to regulate the proper number of muscle founders. However, somatic muscle differentiation is only partially normalized, suggesting that Notch is also required in the ectoderm for proper muscle development. Additionally, mesodermal expression of Notch partially rescues epidermal development in overlying neurogenic ectoderm. This is unexpected, since previous studies suggest that Notch is autonomously required by proneural ectoderm cells for epidermal development. Mesodermal expression of a truncated Notch protein lacking the extracellular domain does not rescue ventral epidermis, suggesting that the extra-cellular domain of Notch can non-autonomously rescue epidermal development across germ layers.

摘要

Notch(N)基因编码一种细胞信号蛋白,该蛋白在果蝇胚胎中介导神经元和表皮的决定。N 还调节肌源性发育的几个方面;缺乏 N 功能的胚胎有过多的肌肉起始细胞,并且不能正确分化体壁肌肉。为了确定肌肉发育过程中 Notch 功能的细胞自主需求,我们在无义 N 基因胚胎的中胚层而非外胚层中表达了一个 Notch 小基因。在这些胚胎中,肌肉起始细胞肥大得到挽救,这表明中胚层细胞自主需要 Notch 来调节适当数量的肌肉起始细胞。然而,体壁肌肉分化仅部分恢复正常,这表明外胚层中 Notch 对于正常的肌肉发育也是必需的。此外,Notch 在中胚层的表达部分挽救了覆盖其上的神经源性外胚层中的表皮发育。这是出乎意料的,因为先前的研究表明,神经前体外胚层细胞自主需要 Notch 来进行表皮发育。缺乏细胞外结构域的截短 Notch 蛋白在中胚层的表达不能挽救腹侧表皮,这表明 Notch 的细胞外结构域可以非自主地挽救跨胚层的表皮发育。

相似文献

1
Autonomous and nonautonomous Notch functions for embryonic muscle and epidermis development in Drosophila.果蝇胚胎肌肉和表皮发育中Notch的自主和非自主功能。
Development. 1996 Feb;122(2):617-26. doi: 10.1242/dev.122.2.617.
2
Multiple roles for notch in Drosophila myogenesis.Notch在果蝇肌肉生成中的多种作用。
Dev Biol. 1998 Sep 1;201(1):66-77. doi: 10.1006/dbio.1998.8944.
3
Muscles in the Drosophila second thoracic segment are patterned independently of autonomous homeotic gene function.果蝇第二胸节中的肌肉形成模式独立于自主同源异型基因功能。
Curr Biol. 1997 Apr 1;7(4):222-7. doi: 10.1016/s0960-9822(06)00117-5.
4
Ectoderm induces muscle-specific gene expression in Drosophila embryos.外胚层诱导果蝇胚胎中肌肉特异性基因的表达。
Development. 1995 May;121(5):1387-98. doi: 10.1242/dev.121.5.1387.
5
The Drosophila neurogenic gene big brain, which encodes a membrane-associated protein, acts cell autonomously and can act synergistically with Notch and Delta.果蝇神经发生基因“大脑发达”编码一种膜相关蛋白,其作用具有细胞自主性,并且能与Notch和Delta协同发挥作用。
Development. 1997 Oct;124(19):3881-93. doi: 10.1242/dev.124.19.3881.
6
Mesodermal cell fate decisions in Drosophila are under the control of the lineage genes numb, Notch, and sanpodo.果蝇中胚层细胞命运的决定受谱系基因 numb、Notch 和 sanpodo 的控制。
Mech Dev. 1998 Jul;75(1-2):117-26. doi: 10.1016/s0925-4773(98)00098-7.
7
The Snail repressor positions Notch signaling in the Drosophila embryo.蜗牛抑制因子在果蝇胚胎中定位Notch信号通路。
Development. 2002 Apr;129(7):1785-93. doi: 10.1242/dev.129.7.1785.
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wingless is required for the formation of a subset of muscle founder cells during Drosophila embryogenesis.在果蝇胚胎发育过程中,无翅基因对于一部分肌肉起始细胞的形成是必需的。
Development. 1995 Nov;121(11):3829-37. doi: 10.1242/dev.121.11.3829.
9
Evidence for a novel Notch pathway required for muscle precursor selection in Drosophila.果蝇中肌肉前体细胞选择所需的新型Notch信号通路的证据。
Mech Dev. 1998 Dec;79(1-2):39-50. doi: 10.1016/s0925-4773(98)00170-1.
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Notch signaling patterns Drosophila mesodermal segments by regulating the bHLH transcription factor twist.Notch信号通路通过调控bHLH转录因子twist来塑造果蝇中胚层节段。
Development. 2004 May;131(10):2359-72. doi: 10.1242/dev.01113.

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