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首页> 外文期刊>Cytoskeleton >Restoration of Cytoskeletal and Membrane Tethering Defects but Not Defects in Membrane Trafficking in the Intestinal Brush Border of Mice Lacking Both Myosin Ia and Myosin VI
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Restoration of Cytoskeletal and Membrane Tethering Defects but Not Defects in Membrane Trafficking in the Intestinal Brush Border of Mice Lacking Both Myosin Ia and Myosin VI

机译：恢复缺少肌球蛋白Ia和肌球蛋白VI的小鼠肠刷边界中的细胞骨架和膜栓系缺陷，但不是膜运输中的缺陷。

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摘要

Myosin Ia (Myo1a), the most prominent plus-end directed motor and myosin VI (Myo6) the sole minus-end directed motor, together exert opposing tension between the microvillar (MV) actin core and the apical brush border (BB) membrane of the intestinal epithelial cell (IEC). Mice lacking Myo1a or Myo6 each exhibit a variety of defects in the tethering of the BB membrane to the actin cytoskeleton. Double mutant (DM) mice lacking both myosins revealed that all the defects observed in either the Myo1a KO or Snell's waltzer (sv/sv) Myo6 mutant mouse are absent. In isolated DM BBs, Myo1a crosslinks between MV membrane and MV actin core are absent but the gap (which is lost in Myo1a KO) between the MV core and membrane is maintained. Several myosins including Myo1c, d, and e and Myo5a are ectopically recruited to the BB. Consistent with the restoration of membrane tethering defects by one or more of these myosins, upward ATP-driven shedding of the BB membrane, which is blocked in the Myo1a KO, is restored in the DM BB. However, Myo1a or Myo6 dependent defects in expression of membrane proteins that traffic between the BB membrane and endosome (NaPi2b, NHE3, CFTR) are not restored. Compared to controls, Myo1a KO, sv/sv mice exhibit moderate and DM high levels of hypersensitivity to dextran sulfate sodium-induced colitis. Consistent with Myo1a and Myo6 playing critical roles in maintaining IEC integrity and response to injury, DM IECs exhibit increased numbers of apoptotic nuclei, above that reported for Myo1a KO. (C) 2015 Wiley Periodicals, Inc.
机译：肌球蛋白Ia（Myo1a）是最突出的正向负向运动电机，而肌球蛋白VI（Myo6）是唯一的负向正向运动电机，共同在微绒毛（MV）肌动蛋白核心与根尖刷缘（BB）膜之间施加相反的张力肠上皮细胞（IEC）。缺乏Myo1a或Myo6的小鼠在BB膜与肌动蛋白细胞骨架的束缚中均表现出多种缺陷。缺少两种肌球蛋白的双突变体（DM）小鼠表明，在Myo1a KO或Snell's waltzer（sv / sv）Myo6突变体小鼠中均未观察到所有缺陷。在分离的DM BB中，不存在MV膜和MV肌动蛋白核心之间的Myo1a交联，但保持了MV核心和膜之间的间隙（在Myo1a KO中丢失）。包括Myo1c，d和e以及Myo5a在内的几种肌球蛋白被异位地募集到BB。与这些肌球蛋白中的一种或多种恢复膜束缚缺陷相一致，在DM BB中恢复了被Myo1a KO阻断的ATP驱动的BB膜向上脱落。但是，无法恢复在BB膜和内体（NaPi2b，NHE3，CFTR）之间运输的膜蛋白表达中的Myo1a或Myo6依赖性缺陷。与对照组相比，Myo1a KO，sv / sv小鼠对硫酸葡聚糖钠诱导的结肠炎表现出中等和DM高水平的超敏反应。与Myo1a和Myo6在维持IEC完整性和对损伤的反应中起关键作用一致，DM IECs的凋亡核数目增加，高于Myo1a KO报道的数目。 （C）2015年Wiley Periodicals，Inc.

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