Chromatin organization at the nuclear periphery as revealed by image analysis of structured illumination microscopy data

Fišerová, Jindřiška; Efenberková, Michaela; Sieger, Tomáš; Maninová, Miloslava; Uhlířová, Jana; Hozák, Pavel

doi:10.1242/dev.156224

Cited by 3 publications

(3 citation statements)

References 16 publications

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“…Our research showed that the PCL2 gene upregulated H3K4me2 and down-regulated H3K9me2, which does not seem to explain that these two changes are directly related to cell proliferation. But studies have shown that in specific cell cycles, the modification of H3K4me2 and H3K9me2 is related to chromatin inhibition [34]. Therefore, the mechanism that PCL2 alters the methylation of histone sites and the changes in cell fate caused by changes in these histone sites will be our future investigation.…”

Section: Discussionmentioning

confidence: 94%

Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells

Wang

Gao

et al. 2020

J Neurooncol

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Introduction The Polycomb group (PcG) is an important family of transcriptional regulators that controls growth and tumorigenesis. The PcG mainly consists of two complexes, PRC1 and Polycomb Repressive Complex 2 (PRC2). Polycomb-like 2 (PCL2) is known to interact with the PRC2 protein. The role of PCL2 in the development and progression of glioma is unclear. Methods We use The Cancer Genome Atlas (TCGA) database to detect the expression of PCL2 in various tumors. 117 cases of clinical glioma (WHOI-IV) were collected, and PCL2 expression and localization were detected by immunohistochemical staining. Glioma cells U87/U251 were infected with overexpressed and interfered PCL2. CCK8 assay, colony formation assay, EdU method, cell cycle and apoptosis were used to detect cell proliferation and apoptosis. Western blot was used to detect the expression of PRC2-related core proteins. After DZNeP intervention, PRC2 protein expression was again measured to discuss the mechanism of PCL2 action. Results TCGA database results and immunohistochemical staining results suggest that PCL2 is highly expressed in gliomas. We found that the PCL2 gene promoted tumor cell proliferation, enhanced the colony formation ability, and increased S phase in the cell cycle. The overexpression of PCL2 upregulated the expression levels of EZH2 and EED (two core members of PRC2), decreased the expression of SUZ12, increased the level of H3K27 trimethylation (H3K27me3), H3K4 dimethylation (H3K4me2), and decreased H3K9 dimethylation (H3K9me2). The result after interfering with PCL2 was the opposite. Conclusions As an important accessory protein of PRC2, PCL2 can not only change the expression of PRC2 components, but also affect the expression level of Histone methylation. Therefore, PCL2 may be an important hub for regulating the synergy among PRC2 members. This study revealed PCL2 as a new target for tumor research and open up a new avenue for future research in glioma.

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Section: Discussionmentioning

confidence: 94%

Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells

Wang

Gao

et al. 2020

J Neurooncol

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“…The fact that nuclear periphery is enriched in condensed heterochromatin, justifies the association of H3K9me3 marks in K97E aggregates. Though lamins at the periphery are known to recruit condensed heterochromatin [57] however, reports have mentioned the existence histone marks for active chromatin near the nuclear pore complexes (NPC) [58].…”

Section: Discussionmentioning

confidence: 99%

Alteration of epigenetic landscape by lamin A mutations: Hallmark of Dilated Cardiomyopathy

Banerjee

Sengupta

2020

Preprint

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Mutations in lamin A have been reported to be associated with over 16 human diseases including dilated cardiomyopathy (DCM). We have focused on three such DCM causing mutants of lamin A which have to address the contribution of lamins in the pathogenesis of DCM at molecular level. We have elucidated the effect of these mutants for the first time on the epigenetic landscape of a myogenic fibroblast cell line C2C12. C2C12 cells expressing these mutant proteins exhibited alterations in some histone modification marks like H3K4me3, H3K9me3, H3K27me3, H3K36me3 and RNA Polymerase II activity compared to its wild type variants. This report paves the way for further studies involving epigenetic regulation in laminopathies which would be an important step in explaining the molecular mechanism and pathophysiology of the diseases like dilated cardiomyopathy.

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“…Euchromatin is generally less condensed, rich in GC content and histone modifications indicative of active transcription, such as H3K4me3, H3K27ac, H4K8ac and H4K16ac (Lawrence et al, 2016). Genomic regions embedded in euchromatin tend to be positioned centrally in the nucleus, apart from nuclear pore regions (Fišerová et al, 2017) located at the nuclear membrane. In contrast, heterochromatin is more compacted, thereby less accessible, largely transcriptionally inactive and decorated with H3K9me3 (facultative heterochromatin) and H3K27me3 (constitutive heterochromatin) histone marks (Penagos-Puig & Furlan-Magaril, 2020).…”

Section: Table Of Contents Introductionmentioning

confidence: 99%

Chromatin reorganization, signaling responses and non-coding RNA regulators in homeostasis and senescence

Josipović¹

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In mammalian cells, a relatively limited fraction of genetic information is utilized in a variety of ways to give rise to distinct cellular phenotypes. Thus, the genotype essentially acts as input for multilayered regulatory networks, which coordinate cellular activities and ultimately shape cell identity and function. Early studies, focusing on individual components of such regulatory networks, have unraveled core principles of cellular functions. Therein, individual, or small groups of genes are regulated by a defined set of locally acting factors. The idea of such individual regulatory units persists, despite new experimental and computational evidence pointing to extensively intertwined "pan-genomic" regulatory networks. In such emerging models, intricate cellular traits originate from numerous interactions, and the mutual dependencies between distinct regulatory units are further governed by such factors as 3D chromatin architecture, noncoding RNA, and even regulatory crosstalk between cells. Therefore, understanding the mechanisms of accurate spatiotemporal regulation of gene expression requires not only elucidating the roles of individual factors at local nodes, but also their contribution to a collective pan-genomic network.In light of such a view, I combined genomics and functional studies in primary human cells to study the regulatory modes of three diverse molecular factors in the context of cellular homeostasis. In Chapter 1, I examine the contribution of active RNA polymerase II (RNA Pol II) in the intricate process of setting up chromatin organization following exit from mitosis. In Chapter 2, I examine the role of HMGB1 as an architectural and RNA-binding factor mediating key events in cells exiting homeostatic cell cycle progression to enter replicative senescence. In Chapter 3, I explore the regulatory potential of two circRNAs, circCAMSAP1 and circRAB3IP, in navigating the regulation of cell cycle progression and inflammation in human cells. Taken together, these three layers of genomic regulation -via RNA Pol II transcription, a dual-function transcription factor, and a pair of circular non-coding RNAs -exemplify the idea of multi-layered regulation of pan-genomic networks inside human cells.

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Chromatin organization at the nuclear periphery as revealed by image analysis of structured illumination microscopy data

Cited by 3 publications

References 16 publications

Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells

Polycomb-like 2 regulates PRC2 components to affect proliferation in glioma cells

Alteration of epigenetic landscape by lamin A mutations: Hallmark of Dilated Cardiomyopathy

Chromatin reorganization, signaling responses and non-coding RNA regulators in homeostasis and senescence

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