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首页> 外文期刊>Aging cell. >Gene expression modulation by the linker of nucleoskeleton and cytoskeleton complex contributes to proteostasis
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Gene expression modulation by the linker of nucleoskeleton and cytoskeleton complex contributes to proteostasis

机译：通过核骨骨骼和细胞骨架复合体的接头的基因表达调节有助于蛋白质

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Cellular mechanisms that act in concert to maintain protein homeostasis (proteostasis) are vital for organismal functionality and survival. Nevertheless, subsets of aggregation‐prone proteins form toxic aggregates (proteotoxicity) that in some cases, underlie the development of neurodegenerative diseases. Proteotoxic aggregates are often deposited in the vicinity of the nucleus, a process that is cytoskeleton‐dependent. Accordingly, cytoskeletal dysfunction contributes to pathological hallmarks of various neurodegenerative diseases. Here, we asked whether the linker of nucleoskeleton and cytoskeleton (LINC) complex, which bridges these filaments across the nuclear envelope, is needed for the maintenance of proteostasis. Employing model nematodes, we discovered that knocking down LINC components impairs the ability of the worm to cope with proteotoxicity. Knocking down anc‐1 , which encodes a key component of the LINC complex, modulates the expression of transcription factors and E3 ubiquitin ligases, thereby affecting the rates of protein ubiquitination and impairing proteasome‐mediated protein degradation. Our results establish a link between the LINC complex, protein degradation, and neurodegeneration‐associated proteotoxicity.
机译：与关键组织以维持蛋白质稳态（蛋白质）的细胞机制对于有机体功能和生存至关重要。然而，聚集 - 易蛋白的亚群形成有毒聚集体（蛋白质毒性），在某些情况下，利于神经变性疾病的发展。蛋白毒毒性聚集体通常沉积在核附近，是依赖于细胞骨架的过程。因此，细胞骨骼功能障碍有助于各种神经变性疾病的病理标志。在这里，我们询问核心骨骼和细胞骨架（LINC）复合物的链接剂是否需要在核包封上桥接这些长丝，用于维持蛋白质。采用模型线虫，我们发现敲击锌组件损害了蠕虫应对蛋白毒性的能力。敲击ANC-1，其编码LINC复合物的关键组分，调节转录因子和E3泛素连接酶的表达，从而影响蛋白质泛素化和损伤蛋白酶体介导的蛋白质降解的速率。我们的结果建立了LINC复杂，蛋白质降解和神经变性相关的蛋白毒性之间的联系。

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