E and ID proteins regulate cell chirality and left-right asymmetric development in Drosophila.
E and ID proteins regulate cell chirality and left-right asymmetric development in Drosophila.
复制标题
E 和 ID 蛋白调节果蝇的细胞手性和左右不对称发育。
作者：
Ishibashi;T.;Hatori;R.;Maeda;R.;Nakamura;M.;Matsuyama;Y.;and Matsuno;K.
动物体内左右不对称是如何形成的是发育生物学中的一个基本问题。虽然LR不对称的机制在一些物种中得到了很好的研究，但在无脊椎动物中仍然知之甚少。我们以前表明，内在LR不对称的细胞（指定为细胞手性）驱动LR不对称的发展在theDrosophilaembryonic后肠，虽然细胞手性形成的机制仍然难以捉摸。在这里，我们发现，thefrosophila同源的Id基因，额外的macrochaetae（emc），是所需的正常LR不对称形态发生的这个器官。Id蛋白，包括Emc，已知与E-box-结合蛋白（E蛋白）相互作用并抑制E-box-结合蛋白（E蛋白），如果蝇无女儿（Da）。我们发现，daby野生型emc的抑制对于细胞手性的形成和胚胎后肠正常LR不对称发育是必不可少的。肌球蛋白ID（MyoID）编码果蝇肌球蛋白ID蛋白，已知其调节细胞手性。我们进一步表明，Emc-Da调节细胞手性形成，其中Emc在MyoID上游或平行于MyoID发挥作用。异常的Id-E蛋白调节参与各种人类疾病。我们的研究结果表明，细胞形状的缺陷可能有助于这些疾病的发病机制。
How left–right (LR) asymmetric forms in the animal body is a fundamental problem in Developmental Biology. Although the mechanisms for LR asymmetry are well studied in some species, they are still poorly understood in invertebrates. We previously showed that the intrinsic LR asymmetry of cells (designated as cell chirality) drives LR asymmetric development in theDrosophilaembryonic hindgut, although the machinery of the cell chirality formation remains elusive. Here, we found that theDrosophilahomologue of theIdgene,extra macrochaetae(emc), is required for the normal LR asymmetric morphogenesis of this organ. Id proteins, including Emc, are known to interact with and inhibit E‐box‐binding proteins (E proteins), such asDrosophilaDaughterless (Da). We found that the suppression ofdaby wild‐typeemcwas essential for cell chirality formation and for normal LR asymmetric development of the embryonic hindgut.Myosin ID(MyoID), which encodes theDrosophilaMyosin ID protein, is known to regulate cell chirality. We further showed that Emc‐Da regulates cell chirality formation, in which Emc functions upstream of or parallel to MyoID. Abnormal Id‐E protein regulation is involved in various human diseases. Our results suggest that defects in cell shape may contribute to the pathogenesis of such diseases.