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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Cullin-3 regulates late endosome maturation
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Cullin-3 regulates late endosome maturation

机译：Cullin-3调节晚期内体成熟

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摘要

Cullin-3 (Cul3) functions as a scaffolding protein in the Bric-a-brac, Tramtrack, Broad-complex (BTB)-Cul3-Rbx1 ubiquitin E3 ligase complex. Here, we report a previously undescribed role for Cul3 complexes in late endosome (LE) maturation. RNAi-mediated depletion of Cul3 results in a trafficking defect of two cargoes of the endoly-sosomal pathway, influenza A virus (IAV) and epidermal growth factor receptor (EGFR). IAV is able to reach an acidic endosomal compartment, coinciding with LE/lysosome (LY) markers. However, it remains trapped or the capsid is unable to uncoat after penetration into the cytosol. Similarly, activation and subsequent ubiquitination of EGFR appear normal, whereas downstream EGFR degradation is delayed and its ligand EGF accumulates in LE/LYs. Indeed, Cul3-de-pleted cells display severe morphological defects in LEs that could account for these trafficking defects; they accumulate acidic LE/LYs, and some cells become highly vacuolated, with enlarged Rab7-pos-itive endosomes. Together, these results suggest a crucial role of Cul3 in regulating late steps in the endolysosomal trafficking pathway.
机译：Cullin-3（Cul3）在Bric-a-brac，Tramtrack，宽复合体（BTB）-Cul3-Rbx1泛素E3连接酶复合体中充当支架蛋白。在这里，我们报告先前未描述的Cul3复合物在晚期内体（LE）成熟中的作用。 RNAi介导的Cul3耗竭会导致内体体途径的两类货物甲型流感病毒（IAV）和表皮生长因子受体（EGFR）的运输缺陷。 IAV能够到达酸性内体区室，与LE /溶酶体（LY）标记相吻合。然而，在渗透到细胞质中后，它仍然被捕获或衣壳不能解壳。同样，EGFR的激活和随后的泛素化似乎是正常的，而下游EGFR的降解被延迟了，其配体EGF积累在LE / LYs中。确实，耗尽Cul3的细胞在LE中显示出严重的形态学缺陷，这可以解释这些运输缺陷。它们积聚酸性LE / LYs，一些细胞变得高度空泡，并带有扩大的Rab7阳性核内体。总之，这些结果表明，Cul3在调节溶酶体运输途径的后期步骤中起着至关重要的作用。

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