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果蝇中前中肠的左右不对称形态发生依赖于非肌肉肌球蛋白 II 的激活。

Left-right asymmetric morphogenesis of the anterior midgut depends on the activation of a non-muscle myosin II in Drosophila.

机构信息

Department of Biological Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan.

出版信息

Dev Biol. 2010 Aug 15;344(2):693-706. doi: 10.1016/j.ydbio.2010.05.501. Epub 2010 May 27.

Abstract

Many animals exhibit stereotypical left-right (LR) asymmetry in their internal organs. The mechanisms of LR axis formation required for the subsequent LR asymmetric development are well understood, especially in some vertebrates. However, the molecular mechanisms underlying LR asymmetric morphogenesis, particularly how mechanical force is integrated into the LR asymmetric morphogenesis of organs, are poorly understood. Here, we identified zipper (zip), encoding a Drosophila non-muscle myosin II (myosin II) heavy chain, as a gene required for LR asymmetric development of the embryonic anterior midgut (AMG). Myosin II is known to directly generate mechanical force in various types of cells during morphogenesis and cell migration. We found that myosin II was involved in two events in the LR asymmetric development of the AMG. First, it introduced an LR bias to the directional position of circular visceral muscle (CVMU) cells, which externally cover the midgut epithelium. Second, it was required for the LR-biased rotation of the AMG. Our results suggest that myosin II in CVMU cells plays a crucial role in generating the force leading to LR asymmetric morphogenesis. Taken together with previous studies in vertebrates, the involvement of myosin II in LR asymmetric morphogenesis might be conserved evolutionarily.

摘要

许多动物的内部器官都表现出典型的左右(LR)不对称性。对于随后的 LR 不对称发育所需的 LR 轴形成机制,人们已经有了很好的理解,尤其是在一些脊椎动物中。然而,LR 不对称形态发生的分子机制,特别是机械力如何整合到器官的 LR 不对称形态发生中,仍知之甚少。在这里,我们鉴定出 zipper(zip),它编码果蝇非肌肉肌球蛋白 II(myosin II)重链,是胚胎前中肠(AMG)LR 不对称发育所必需的基因。肌球蛋白 II 已知在形态发生和细胞迁移过程中直接在各种类型的细胞中产生机械力。我们发现肌球蛋白 II 参与了 AMG 的 LR 不对称发育的两个事件。首先,它将定向位置的圆形内脏肌(CVMU)细胞引入 LR 偏置,而这些细胞外部覆盖着中肠上皮。其次,它是 AMG 的 LR 偏置旋转所必需的。我们的结果表明,CVMU 细胞中的肌球蛋白 II 在产生导致 LR 不对称形态发生的力方面发挥着关键作用。结合脊椎动物的先前研究,肌球蛋白 II 参与 LR 不对称形态发生可能在进化上是保守的。

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