Left-right asymmetric morphogenesis of the anterior midgut depends on the activation of a non-muscle myosin II in Drosophila.
Left-right asymmetric morphogenesis of the anterior midgut depends on the activation of a non-muscle myosin II in Drosophila.
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DOI：
10.1016/j.ydbio.2010.05.501
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发表时间：
2010-08
影响因子：
2.7
通讯作者：
T. Okumura;Hiroo Fujiwara;Kiichiro Taniguchi;Junpei Kuroda;Naotaka Nakazawa;Mitsutoshi Nakamura;Ryo Hatori;Akira Ishio;Reo Maeda;K. Matsuno
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文献类型：
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作者：
T. Okumura;Hiroo Fujiwara;Kiichiro Taniguchi;Junpei Kuroda;Naotaka Nakazawa;Mitsutoshi Nakamura;Ryo Hatori;Akira Ishio;Reo Maeda;K. Matsuno
许多动物在其内脏器官中表现出典型的左右（LR）不对称。LR轴的形成所需的后续LR不对称发展的机制是很好的理解，特别是在一些脊椎动物。然而，LR不对称形态发生的分子机制，特别是机械力是如何整合到器官的LR不对称形态发生，知之甚少。在这里，我们确定了拉链（zip），编码果蝇非肌肉肌球蛋白II（肌球蛋白II）重链，作为LR不对称发展所需的胚胎前中肠（AMG）的基因。已知肌球蛋白II在形态发生和细胞迁移期间在各种类型的细胞中直接产生机械力。我们发现，肌球蛋白II参与了两个事件中的LR不对称发展的AMG。首先，它引入了LR偏向的方向位置的环形内脏肌（CVMU）细胞，外部覆盖中肠上皮。第二，它是AMG的LR偏置旋转所必需的。我们的研究结果表明，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中起着至关重要的作用。结合以往在脊椎动物中的研究，肌球蛋白II参与LR不对称形态发生可能是进化保守的。
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.