scholarly journals Mechanism of Long-Range Chromosome Motion Triggered by Gene Activation

2020 ◽  
Vol 52 (3) ◽  
pp. 309-320.e5 ◽  
Author(s):  
Anqi Wang ◽  
Janhavi A. Kolhe ◽  
Nate Gioacchini ◽  
Imke Baade ◽  
William M. Brieher ◽  
...  
2006 ◽  
Vol 23 (4) ◽  
pp. 619
Author(s):  
Yugong Ho ◽  
Felice Elefant ◽  
Stephen A. Liebhaber ◽  
Nancy E. Cooke

Transcription ◽  
2017 ◽  
Vol 8 (4) ◽  
pp. 261-267 ◽  
Author(s):  
Christopher M. Vockley ◽  
Ian C. McDowell ◽  
Antony M. D'Ippolito ◽  
Timothy E. Reddy
Keyword(s):  

2021 ◽  
Author(s):  
Tirso Pons ◽  
Francois Serra ◽  
Florencio Pazos ◽  
Alfonso Valencia ◽  
Carlos Martinez-A

Chromatin structure and organization has a key role in gene expression regulation. Here, we integrated ChIP-seq, RNA-seq, Hi-C, epigenetic, and cancer-related mutations data to get insight into the role of Death Inducer Obliterator gene (Dido1) in RNA pol II (RNAPII) transcription and chromatin structure regulation. Analysis of ChIP-seq data of DIDO3, the largest protein isoform of Dido1, revealed binding-sites overlap about 70% with RNAPII and H3K36me3 in the mouse genome, but also significant overlap 10-30% with Polycomb, CTCF, H3K4me3, and H3K27ac. Based on this analysis we propose that DIDO3 PHD domain interacts with H3K36me3 posttranslational modification. Integrating multi-omics data we describe how DIDO3 potentially recruit several transcription factors, including RNAPII, and also regulates genes transcribing those same transcription factors. DIDO3 regulation of the genes traduced into proteins to which it binds puts DIDO3 in the center of intricate feedback loops. We showed, by using data from a DIDO3 mutant, that DIDO3 C-terminus is responsible for most of these transcriptional regulation, and is also implicated in other very important pathways by regulating genes encoding for Polycomb-accessory proteins, subunits of the SWI/SNF chromatin remodelling, or Set1/COMPASS chromatin modifier complexes. These multi-protein complexes control gene activation or silencing and also play a role in tumour development. DIDO3 C-terminus region and splice-site for alternative DIDO2/DIDO3 protein isoforms tended to accumulate recurrent truncating mutations identified in the TCGA Pan-Cancer dataset. We hypothesize that deregulation of DIDO3, as it happens with large epigenetic complexes and long-range interactions, leads to cell differentiation deficiency and cancer development. Overall, we propose here a molecular mechanism by which DIDO3, favour RNAPII pausing and long-range chromatin interactions.


2005 ◽  
Vol 286 (2) ◽  
pp. 629-636 ◽  
Author(s):  
Qi Chen ◽  
Lan Lin ◽  
Sheryl Smith ◽  
Qing Lin ◽  
Jumin Zhou

Development ◽  
2009 ◽  
Vol 136 (16) ◽  
pp. 2803-2813 ◽  
Author(s):  
A. I. Hagemann ◽  
X. Xu ◽  
O. Nentwich ◽  
M. Hyvonen ◽  
J. C. Smith
Keyword(s):  

2021 ◽  
Author(s):  
Andres Tapia del Fierro ◽  
Bianca den Hamer ◽  
Natasha Jansz ◽  
Kelan Chen ◽  
Tamara Beck ◽  
...  

The interplay between 3D chromatin architecture and gene silencing is incompletely understood. Here, we report a novel point mutation in the non-canonical SMC protein SMCHD1 that enhances its silencing capacity at endogenous developmental targets and at the facioscapulohumeral muscular dystrophy associated macro-array, D4Z4. Heightened SMCHD1 silencing perturbs developmental Hox gene activation, causing a homeotic transformation in mice. Paradoxically, the mutant SMCHD1 appears to enhance insulation against another epigenetic regulator complex, PRC2, while depleting long range chromatin interactions akin to what is observed in the absence of SMCHD1. These data suggest that SMCHD1′s role in long range chromatin interactions is not directly linked to gene silencing or insulating the chromatin, refining the model for how the different levels of SMCHD1-mediated chromatin regulation interact to bring about gene silencing in normal development and disease.


2002 ◽  
Vol 9 (2) ◽  
pp. 291-302 ◽  
Author(s):  
Yugong Ho ◽  
Felice Elefant ◽  
Nancy Cooke ◽  
Stephen Liebhaber

2017 ◽  
Author(s):  
Nezha S. Benabdallah ◽  
Iain Williamson ◽  
Robert S. Illingworth ◽  
Shelagh Boyle ◽  
Graeme R. Grimes ◽  
...  

AbstractEnhancers are critical regulators of gene expression and can be located far from their target gene. It is widely assumed that mechanisms of enhancer action involve reorganization of three-dimensional chromatin architecture, but this is poorly understood. Here we identify a novel mechanism of long-range enhancer associated chromatin reorganization. At the Sonic hedgehog (Shh) locus we observe large-scale decompaction of chromatin between Shh and its brain enhancers in neural progenitor cells. We show that the chromatin unfolding is dependent on activation of the enhancers, not the promoter, is impeded by chromatin-bound proteins located between the enhancer and promoter, and is mediated by the recruitment of Poly (ADP-Ribose) Polymerase 1. We suggest that large-scale chromatin decompaction, analogous to the inducible puffs in Drosophila polytene chromosomes, represents a new mechanism of chromatin reorganization coupled to long-range gene activation from mammalian enhancers and that seems incompatible with a chromatin-looping model of enhancer-promoter communication


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