School of Fundamental Sciences, Massey University, Palmerston North, New Zealand; The MacDiarmid Institute for Advanced Materials and Nanotechnology, Wellington, New Zealand.
School of Fundamental Sciences, Massey University, Palmerston North, New Zealand.
Biophys J. 2021 Jul 6;120(13):2631-2643. doi: 10.1016/j.bpj.2021.05.017. Epub 2021 Jun 2.
Within the nucleus of the eukaryotic cell, DNA is partitioned into domains of highly condensed, transcriptionally silent heterochromatin and less condensed, transcriptionally active euchromatin. Heterochromatin protein 1α (HP1α) is an architectural protein that establishes and maintains heterochromatin, ensuring genome fidelity and nuclear integrity. Although the mechanical effects of changes in the relative amount of euchromatin and heterochromatin brought about by inhibiting chromatin-modifying enzymes have been studied previously, here we measure how the material properties of the nuclei are modified after the knockdown of HP1α. These studies were inspired by the observation that poorly invasive MCF7 breast cancer cells become more invasive after knockdown of HP1α expression and that, indeed, in many solid tumors the loss of HP1α correlates with the onset of tumor cell invasion. Atomic force microscopy (AFM), optical tweezers (OT), and techniques based on micropipette aspiration (MA) were each used to characterize the mechanical properties of nuclei extracted from HP1α knockdown or matched control MCF7 cells. Using AFM or OT to locally indent nuclei, those extracted from MCF7 HP1α knockdown cells were found to have apparent Young's moduli that were significantly lower than nuclei from MCF7 control cells, consistent with previous studies that assert heterochromatin plays a major role in governing the mechanical response in such experiments. In contrast, results from pipette-based techniques in the spirit of MA, in which the whole nuclei were deformed and aspirated into a conical pipette, showed considerably less variation between HP1α knockdown and control, consistent with previous studies reporting that it is predominantly the lamins in the nuclear envelope that determine the mechanical response to large whole-cell deformations. The differences in chromatin organization observed by various microscopy techniques between the MCF7 control and HP1α knockdown nuclei correlate well with the results of our measured mechanical responses and our hypotheses regarding their origin.
在真核细胞的核内,DNA 被分割成高度浓缩的转录沉默异染色质和较少浓缩的转录活跃常染色质域。异染色质蛋白 1α(HP1α)是一种结构蛋白,它建立和维持异染色质,确保基因组的保真度和核的完整性。尽管以前已经研究了通过抑制染色质修饰酶来改变常染色质和异染色质的相对含量所带来的机械效应,但在这里,我们测量了 HP1α 敲低后核的物质性质如何被改变。这些研究的灵感来自于这样的观察结果,即侵袭性较差的 MCF7 乳腺癌细胞在 HP1α 表达敲低后变得更具侵袭性,事实上,在许多实体瘤中,HP1α 的丢失与肿瘤细胞侵袭的发生相关。原子力显微镜(AFM)、光学镊子(OT)和基于微管吸吮(MA)的技术分别用于表征从 HP1α 敲低或匹配的对照 MCF7 细胞中提取的核的机械特性。使用 AFM 或 OT 局部压痕核,发现从 MCF7 HP1α 敲低细胞中提取的核的表观杨氏模量明显低于 MCF7 对照细胞的核,这与先前的研究一致,该研究断言异染色质在这些实验的机械响应中起主要作用。相比之下,基于 MA 精神的基于管的技术的结果,其中整个核被变形并吸入锥形管中,在 HP1α 敲低和对照之间显示出相当小的变化,这与先前的研究一致,该研究报告说,主要是核膜中的核纤层决定了对大的整个细胞变形的机械响应。在 MCF7 对照和 HP1α 敲低核之间各种显微镜技术观察到的染色质组织的差异与我们测量的机械响应的结果以及我们关于其起源的假设很好地相关。