14-3-3 proteins are conserved, dimeric, acidic proteins that regulate multiple cellular pathways. Loss of either 14-3-3ε or 14-3-3γ leads to centrosome amplification. However, we find that while the knockout of 14-3-3ε leads to multipolar mitoses, the knockout of 14-3-3γ results in centrosome clustering and pseudo-bipolar mitoses. 14-3-3γ knockouts demonstrate compromised desmosome function and a decrease in keratin levels, leading to decreased cell stiffness and an increase in centrosome clustering. Restoration of desmosome function increased multipolar mitoses, whereas knockdown of either plakoglobin or keratin 5 led to decreased cell stiffness and increased pseudo-bipolar mitoses. These results suggest that the ability of the desmosome to anchor keratin filaments maintains cell stiffness, thus inhibiting centrosome clustering, and that phenotypes observed upon 14-3-3 loss reflect the dysregulation of multiple pathways.

中文翻译：

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桥粒功能的破坏导致具有超数中心体的 14-3-3γ 敲除细胞中中心体聚集增加

14-3-3 蛋白是保守的二聚体酸性蛋白，可调节多种细胞途径。14-3-3ε 或 14-3-3γ 的缺失导致中心体扩增。然而，我们发现虽然 14-3-3ε 的敲除会导致多极有丝分裂，但 14-3-3γ 的敲除会导致中心体聚集和假双极有丝分裂。14-3-3γ 敲除表明桥粒功能受损和角蛋白水平降低，导致细胞刚度降低和中心体聚集增加。桥粒功能的恢复增加了多极有丝分裂，而板珠蛋白或角蛋白 5 的敲低导致细胞刚度降低和假双极有丝分裂增加。这些结果表明桥粒锚定角蛋白丝的能力维持细胞刚度，从而抑制中心体聚集，