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首页> 外文期刊>Nature >Polarized endosome dynamics by spindle asymmetry during asymmetric cell division
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Polarized endosome dynamics by spindle asymmetry during asymmetric cell division

机译：极化不对称细胞分裂期间纺锤体不对称的内体动力学。

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摘要

During asymmetric division, fate determinants at the cell cortex segregate unequally into the two daughter cells. It has recently been shown that Sara (Smad anchor for receptor activation) signalling endosomes in the cytoplasm also segregate asymmetrically during asymmetric division(1,2). Biased dispatch of Sara endosomes mediates asymmetric Notch/Delta signalling during the asymmetric division of sensory organ precursors in Drosophila(1). In flies, this has been generalized to stem cells in the gut(3) and the central nervous system(1), and, in zebrafish, to neural precursors of the spinal cord(4). However, the mechanism of asymmetric endosome segregation is not understood. Here we show that the plus-end kinesin motor Klp98A targets Sara endosomes to the central spindle, where they move bidirectionally on an antiparallel array of microtubules. The microtubule depolymerizing kinesin Klp10A and its antagonist Patronin generate central spindle asymmetry. This asymmetric spindle, in turn, polarizes endosome motility, ultimately causing asymmetric endosome dispatch into one daughter cell. We demonstrate this mechanism by inverting the polarity of the central spindle by polar targeting of Patronin using nanobodies (single-domain antibodies). This spindle inversion targets the endosomes to the wrong cell. Our data uncover the molecular and physical mechanism by which organelles localized away from the cellular cortex can be dispatched asymmetrically during asymmetric division.
机译：在不对称分裂过程中，细胞皮质的命运决定因素不平等地分离为两个子细胞。最近显示，在细胞质中，Sara（受体激活的Smad锚）信号传递内体在不对称分裂过程中也不对称分离（1,2）。在果蝇的感觉器官前体的不对称分裂过程中，Sara内体的偏向调度介导了不对称的Notch / Delta信号传导（1）。在果蝇中，这已普遍化为肠道（3）和中枢神经系统（1）中的干细胞，而在斑马鱼中则为脊髓的神经前体（4）。但是，不对称内体分离的机制尚不清楚。在这里，我们显示正向驱动蛋白激酶Klp98A将Sara内体靶向到中心纺锤体，它们在反平行微管阵列上双向移动。微管解聚驱动蛋白Klp10A及其拮抗剂Patronin产生中心纺锤不对称。这种不对称的纺锤体反过来使内体的运动极化，最终导致不对称的内体向一个子细胞内分配。我们通过使用纳米抗体（单域抗体）对Patronin进行极性靶向来反转中心纺锤的极性，从而证明了这一机制。这种纺锤体倒转将内体靶向错误的细胞。我们的数据揭示了分子和物理机制，通过这些分子和物理机制，可以在不对称分裂过程中不对称地调度远离细胞皮层的细胞器。

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  • 来源
    《Nature》 |2015年第7581期|280-285|共6页
  • 作者

    Derivery Emmanuel; Seum Carole; Daeden Alicia; Loubery Sylvain; Holtzer Laurent; Juelicher Frank; Gonzalez-Gaitan Marcos;

  • 作者单位

    Univ Geneva, Fac Sci, Dept Biochem, CH-1211 Geneva, Switzerland;

    Univ Geneva, Fac Sci, Dept Biochem, CH-1211 Geneva, Switzerland;

    Univ Geneva, Fac Sci, Dept Biochem, CH-1211 Geneva, Switzerland;

    Univ Geneva, Fac Sci, Dept Biochem, CH-1211 Geneva, Switzerland;

    Univ Geneva, Fac Sci, Dept Biochem, CH-1211 Geneva, Switzerland;

    Max Planck Inst Phys Komplexer Syst, D-01187 Dresden, Germany;

    Univ Geneva, Fac Sci, Dept Biochem, CH-1211 Geneva, Switzerland;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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