Nuclear lamins are type V intermediate filament proteins that maintain nuclear structure and function. Furthermore, Emerin - an interactor of Lamin A/C, facilitates crosstalk between the cytoskeleton and the nucleus as it also interacts with actin and Nuclear Myosin 1 (NM1). Here we show that the depletion of Lamin A/C or Emerin, alters the localization of the nuclear motor protein - Nuclear Myosin 1 (NM1) that manifests as an increase in NM1 foci in the nucleus and are rescued to basal levels upon the combined knockdown of Lamin A/C and Emerin. Furthermore, Lamin A/C-Emerin co-depletion destabilizes cytoskeletal organization as it increases actin stress fibers. This further impinges on nuclear organization, as it enhances chromatin mobility more toward the nuclear interior in Lamin A/C-Emerin co-depleted cells. This enhanced chromatin mobility was restored to basal levels either upon inhibition of Nuclear Myosin 1 (NM1) activity or actin depolymerization. In addition, the combined loss of Lamin A/C and Emerin alters the otherwise highly conserved spatial positions of chromosome territories. Furthermore, knockdown of Lamin A/C or Lamin A/C-Emerin combined, deregulates expression levels of a candidate subset of genes. Amongst these genes, both KLK10 (Chr.19, Lamina Associated Domain (LAD+)) and MADH2 (Chr.18, LAD-) were significantly repressed, while BCL2L12 (Chr.19, LAD-) is de-repressed. These genes differentially reposition with respect to the nuclear envelope. Taken together, these studies underscore a remarkable interplay between Lamin A/C and Emerin in modulating cytoskeletal organization of actin and NM1 that impinges on chromatin dynamics and function in the interphase nucleus.

中文翻译：

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Lamin A/C 和 Emerin 消耗会影响间期核中的染色质组织和动力学。

核纤层蛋白是维持核结构和功能的 V 型中间丝蛋白。此外，Emerin - Lamin A/C 的相互作用物，促进细胞骨架和细胞核之间的串扰，因为它还与肌动蛋白和核肌球蛋白 1 (NM1) 相互作用。在这里，我们表明 Lamin A/C 或 Emerin 的消耗改变了核运动蛋白 - 核肌球蛋白 1 (NM1) 的定位，表现为细胞核中 NM1 病灶的增加，并在联合击倒后恢复到基础水平Lamin A/C 和 Emerin。此外，Lamin A/C-Emerin 共消耗会破坏细胞骨架组织的稳定性，因为它会增加肌动蛋白应力纤维。这进一步影响了核组织，因为它增强了染色质在 Lamin A/C-Emerin 共耗尽细胞中更多地向核内部移动。这种增强的染色质流动性在抑制核肌球蛋白 1 (NM1) 活性或肌动蛋白解聚后恢复到基础水平。此外，Lamin A/C 和 Emerin 的组合丢失改变了染色体区域原本高度保守的空间位置。此外，联合敲除 Lamin A/C 或 Lamin A/C-Emerin 会解除对候选基因子集的表达水平的调节。在这些基因中，KLK10 (Chr.19, Lamina Associated Domain (LAD+)) 和 MADH2 (Chr.18, LAD-) 都被显着抑制，而 BCL2L12 (Chr.19, LAD-) 被去抑制。这些基因相对于核膜不同地重新定位。综合起来，