Genome Organisation and Function in the Cell Nucleus. Edited by Karsten Rippe.

ChemBioChem ◽  
2012 ◽  
Vol 13 (15) ◽  
pp. 2302-2303
Author(s):  
Randall H. Morse
Acta Naturae ◽  
2017 ◽  
Vol 9 (4) ◽  
pp. 42-51
Author(s):  
S. S. Ryabichko ◽  
◽  
A. N. Ibragimov ◽  
L. A. Lebedeva ◽  
E. N. Kozlov ◽  
...  

2021 ◽  
Author(s):  
Michael Chiang ◽  
Chris A. Brackley ◽  
Davide Marenduzzo ◽  
Nick Gilbert

2021 ◽  
Vol 41 ◽  
pp. 73-89
Author(s):  
AJ Hayes ◽  
◽  
J Melrose

Perlecan is a modular, multifunctional heparan sulphate-proteoglycan (HS-PG) that is present in the pericellular and wider extracellular matrix of connective tissues. In the present study, confocal microscopy was used to study perlecan distribution within intervertebral disc chondrons. Perlecan immunolabel was demonstrated intracellularly and in close association with the cell nucleus within chondrons of both the annulus fibrosus (AF) and nucleus pulposus (NP). This observation is consistent with earlier studies that have localised HS-PGs with nuclear cytoskeletal components. Nuclear HS-PGs have been proposed to transport fibroblast growth factor (FGF)-1, FGF-2 and FGFR-1 into the cell nucleus, influencing cell proliferation and the cell-cycle. Perlecan has well-known interactive properties with FGF family members in the pericellular and extracellular matrix. Perinuclear perlecan may also participate in translocation events with FGFs. The glycosaminoglycan side chains of HS-PGs can modulate chromatin structure by regulating the access of transcription factors to DNA. These mechanisms are consistent with the distribution patterns identified here and previously reported for other HS-PGs, introducing a potentially-novel arena for perlecan in gene regulation. Whilst much is known of the structure and function of perlecan in the pericellular and extracellular matrix, very little is known of any intracellular forms of perlecan. The perlecan labelling patterns described here suggest the possibility of involvement of this HS-PG in an intracrine regulatory system. Future studies should further explore this possibility and the potential for this HS-PG as a novel therapeutic target.


2005 ◽  
Vol 45 (1) ◽  
pp. 17-26 ◽  
Author(s):  
Ronald Berezney ◽  
Kishore S. Malyavantham ◽  
Artem Pliss ◽  
Sambit Bhattacharya ◽  
Raj Acharya

2019 ◽  
Vol 26 (11) ◽  
pp. R611-R626 ◽  
Author(s):  
Moray J Campbell

The 3D organization of the genome within the cell nucleus has come into sharp focus over the last decade. This has largely arisen because of the application of genomic approaches that have revealed numerous levels of genomic and chromatin interactions, including topologically associated domains (TADs). The current review examines how these domains were identified, are organized, how their boundaries arise and are regulated, and how genes within TADs are coordinately regulated. There are many examples of the disruption to TAD structure in cancer and the altered regulation, structure and function of TADs are discussed in the context of hormone responsive cancers, including breast, prostate and ovarian cancer. Finally, some aspects of the statistical insight and computational skills required to interrogate TAD organization are considered and future directions discussed.


2019 ◽  
Author(s):  
Katy A McLaughlin ◽  
Ilya M Flyamer ◽  
John P Thomson ◽  
Heidi K Mjoseng ◽  
Ruchi Shukla ◽  
...  

The DNA hypomethylation that occurs when embryonic stem cells (ESCs) are directed to the ground state of naive pluripotency by culturing in 2i conditions results in redistribution of polycomb (H3K27me3) away from its target loci. Here we demonstrate that 3D genome organisation is also altered in 2i. We found chromatin decompaction at polycomb target loci as well as loss of long-range polycomb interactions. By preventing DNA hypomethylation during the transition to the ground-state, we are able to restore the H3K27me3 distribution, and polycomb-mediated 3D genome organisation that is characteristic of primed ESCs grown in serum, to ESCs in 2i. However, these cells retain the functional characteristics of 2i ground state ESCs. Our findings demonstrate the central role of DNA methylation in shaping major aspects of 3D genome organisation but caution against assuming causal roles for the epigenome and 3D genome in gene regulation and function in ESCs.


Endocrinology ◽  
2021 ◽  
Author(s):  
Lindsey S Treviño ◽  
Daniel A Gorelick

Abstract Steroid hormones bind receptors in the cell nucleus and in the cell membrane. The most widely studied class of steroid hormone receptors are the nuclear receptors, named for their function as ligand-dependent transcription factors in the cell nucleus. Nuclear receptors, such as estrogen receptor alpha, can also be anchored to the plasma membrane, where they respond to steroids by activating signaling pathways independent of their function as transcription factors. Steroids can also bind integral membrane proteins, such as the G protein-coupled estrogen receptor. Membrane estrogen and progestin receptors have been cloned and characterized in vitro and influence the development and function of many organ systems. Membrane androgen receptors were cloned and characterized in vitro, but their function as androgen receptors in vivo is unresolved. We review the identity and function of membrane proteins that bind estrogens, progestins and androgens. We discuss evidence that membrane glucocorticoid and mineralocorticoid receptors exist, and whether glucocorticoid and mineralocorticoid nuclear receptors act at the cell membrane. In many cases, integral membrane steroid receptors act independently of nuclear steroid receptors, even though they may share a ligand.


2019 ◽  
Author(s):  
Davide Michieletto ◽  
Davide Colì ◽  
Davide Marenduzzo ◽  
Enzo Orlandini

Understanding the spatial organisation of the genome in the cell nucleus is one of the current grand challenges in biophysics. Certain biochemical – or epigenetic – marks that are deposited along the genome are thought to play an important, yet poorly understood, role in determining genome organisation and cell identity. The physical principles underlying the interplay between epigenetic dynamics and genome folding remain elusive. Here we propose and study a theory that assumes a coupling between epigenetic mark and genome densities, and which can be applied at the scale of the whole nucleus. We show that equilibrium models are not compatible with experiments and a qualitative agreement is recovered by accounting for non-equilibrium processes which can stabilise microphase separated epigenomic domains. We finally discuss the potential biophysical origin of these terms.


1980 ◽  
pp. 251-270 ◽  
Author(s):  
M. W. Berns ◽  
P. A. McNeill ◽  
S. P. Peterson ◽  
J. B. Rattner ◽  
S. Brenner ◽  
...  

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