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A Conserved Role of the Unconventional Myosin 1d in Laterality Determination

机译:非传统肌球蛋白1D在横向决定中的保守作用

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摘要

Anatomical and functional asymmetries are widespread in the animal kingdom [1,2]. In vertebrates, many visceral organs are asymmetrically placed [3]. In snails,shells and inner organs coil asymmetrically, and in Drosophila,genitalia and hindgut undergo a chiral rotation during development. The evolutionary origin of these asymmetries remains an open question [1]. Nodal signaling is widely used [4],and many,but not all,vertebrates use cilia for symmetry breaking [5]. In Drosophila, which lacks both cilia and Nodal,the unconventional myosin ID (myo1d) gene controls dextral rotation of chiral organs [6,7]. Here,we studied the role of myo1d in left-right (LR) axis formation in Xenopus. Morpholino oligomer-mediated myo1d downregulation affected organ placement in &50% of morphant tadpoles. Induction of the left-asymmetric Nodal cascade was aberrant in &70% of cases. Expression of the flow-target gene dand5 was compromised,as was flow itself,due to shorter,fewer,and non-polarized cilia at the LR organizer. Additional phenotypes pinpointed Wnt/planar cell polarity signaling and suggested that myo1d,like in Drosophila [8],acted in the context of the planar cell polarity pathway. Indeed,convergent extension of gastrula explant cultures was inhibited in myo1d morphants,and the ATF2 reporter gene for non-canonical Wnt signaling was downregulated. Finally,genetic interference experiments demonstrated a functional interaction between the core planar cell polarity signaling gene vangl2 and myo1d in LR axis formation. Thus,our data identified myo1d as a common denominator of arthropod and chordate asymmetry, in agreement with a monophyletic origin of animal asymmetry.
机译:Anathomical和功能性的不对称是动物王国的普遍[1,2]。在脊椎动物中,许多内脏器官不对称地放置[3]。在蜗牛,壳体和内脏器官卷线上不对称,在果蝇,生殖器和后果在开发期间经历手性旋转。这些不对称的进化起源仍然是一个公开的问题[1]。节点信号传导广泛使用[4],许多,但不是全部,脊椎动物使用纤毛用于对称性断裂[5]。在果蝇缺乏纤毛和节点的果蝇中,非传统的肌球蛋白ID(MyO1D)基因控制手性器官的右侧旋转[6,7]。在这里,我们研究了Xenopus左右左右(LR)轴形成的MyO1d的作用。吗啉氨基寡聚蛋白介导的Myo1d下调受影响器官放置在& 50%的Merphant Tadpoles。左不对称节点级联的诱导是在&amp中的异常中的。 70%的病例。由于LR组织者的较短,更少和非极化的纤毛,流动本身,流动靶基因丹丹5的表达受到损害。额外的表型针对WNT /平面细胞极性信号传导,并表明MyO1d在果蝇[8]中,在平面细胞极性途径的上下文中作用。实际上,在MyO1D鱼中抑制了胃肠外植物培养物的收敛延伸,并且对非规范性WNT信号传导的ATF2报告基因进行了下调。最后,遗传干扰实验证明了LR轴形成中的核心平面细胞极性信号传导基因Vangl2和MyO1d之间的功能相互作用。因此,我们的数据将Myo1d确定为节肢动物和脊索不对称的常见分母,与动物不对称的单一的血统起源一致。

著录项

  • 来源
    《Current Biology: CB》 |2018年第5期|共10页
  • 作者单位

    Univ Hohenheim Inst Zool Garbenstr 30 D-70593 Stuttgart Germany;

    Univ Hohenheim Inst Zool Garbenstr 30 D-70593 Stuttgart Germany;

    Univ Hohenheim Inst Zool Garbenstr 30 D-70593 Stuttgart Germany;

    Univ Hohenheim Inst Zool Garbenstr 30 D-70593 Stuttgart Germany;

    Univ Hohenheim Inst Zool Garbenstr 30 D-70593 Stuttgart Germany;

    Univ Hohenheim Inst Zool Garbenstr 30 D-70593 Stuttgart Germany;

    Merrimack Coll Dept Biol 315 Turnpike St N Andover MA 01845 USA;

    Univ Cote dAzur CNRS INSERM Inst Biol Valrose Parc Valrose F-06108 Nice France;

    Univ Hohenheim Inst Zool Garbenstr 30 D-70593 Stuttgart Germany;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物科学;
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