Interphase chromosome conformation is specified by distinct folding programs inherited via mitotic chromosomes or through the cytoplasm

Allana Schooley, Sergey V Venev, Vasilisa Aksenova, Emily Navarrete, Mary Dasso, Job Dekker
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Abstract

Identity-specific interphase chromosome conformation must be re-established each time a cell divides. To understand how interphase folding is inherited, we developed an experimental approach that physically segregates mediators of G1 folding that are intrinsic to mitotic chromosomes from cytoplasmic factors. Proteins essential for nuclear transport, RanGAP1 and Nup93, were degraded in pro-metaphase arrested DLD-1 cells to prevent the establishment of nucleo-cytoplasmic transport during mitotic exit and isolate the decondensing mitotic chromatin of G1 daughter cells from the cytoplasm. Using this approach, we discover a transient folding intermediate entirely driven by chromosome-intrinsic factors. In addition to conventional compartmental segregation, this chromosome-intrinsic folding program leads to prominent genome-scale microcompartmentalization of mitotically bookmarked and cell type-specific cis-regulatory elements. This microcompartment conformation is formed during telophase and subsequently modulated by a second folding program driven by factors inherited through the cytoplasm in G1. This nuclear import-dependent folding program includes cohesin and factors involved in transcription and RNA processing. The combined and inter-dependent action of chromosome-intrinsic and cytoplasmic inherited folding programs determines the interphase chromatin conformation as cells exit mitosis.
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通过有丝分裂染色体或细胞质遗传的不同折叠程序规定了染色体间期的构象
每次细胞分裂都必须重新建立具有特异性的间期染色体构象。为了了解间期折叠是如何遗传的,我们开发了一种实验方法,将有丝分裂染色体固有的 G1 期折叠介质与细胞质因子进行物理分离。在原分裂期停滞的 DLD-1 细胞中降解了核运输所必需的蛋白质 RanGAP1 和 Nup93,以防止在有丝分裂出期建立核-胞质运输,并将 G1 子细胞的有丝分裂染色质从胞质中分离出来。利用这种方法,我们发现了一种完全由染色体内在因子驱动的瞬时折叠中间体。除了传统的区室分离外,这种染色体组内生折叠程序还导致有丝分裂标记和细胞类型特异性顺式调控元件的基因组尺度微区室化。这种微室构象在端期形成,随后由 G1 期通过细胞质遗传的因子驱动的第二个折叠程序进行调节。这种依赖核导入的折叠程序包括凝聚素以及参与转录和 RNA 处理的因子。染色体固有折叠程序和细胞质遗传折叠程序的共同作用和相互依赖决定了细胞在有丝分裂后期的染色质构象。
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