Characterization of DNase I hypersensitive sites in the mouse 68-kDa neurofilament gene

1996 ◽  
Vol 21 (6) ◽  
pp. 713-722 ◽  
Author(s):  
Robert Kure ◽  
Tina R. Ivanov ◽  
Ian R. Brown
Genomics ◽  
1995 ◽  
Vol 29 (3) ◽  
pp. 740-750 ◽  
Author(s):  
CATHERINE POSTIC ◽  
KEVIN D. NISWENDER ◽  
JEAN-FRANCOIS DECAUX ◽  
RAMINE PARSA ◽  
KATHY D. SHELTON ◽  
...  

2020 ◽  
Vol 32 (8) ◽  
pp. 2457-2473 ◽  
Author(s):  
Jinlei Han ◽  
Pengxi Wang ◽  
Qiongli Wang ◽  
Qingfang Lin ◽  
Zhiyong Chen ◽  
...  

2007 ◽  
Vol 48 (3) ◽  
pp. 459-470 ◽  
Author(s):  
Y. Kodama ◽  
S. Nagaya ◽  
A. Shinmyo ◽  
K. Kato

2021 ◽  
Vol 209 ◽  
pp. 104223
Author(s):  
Wei Su ◽  
Fang Wang ◽  
Jiu-Xin Tan ◽  
Fu-Ying Dao ◽  
Hui Yang ◽  
...  

1991 ◽  
Vol 11 (10) ◽  
pp. 5301-5311
Author(s):  
J A Brown ◽  
S G Holmes ◽  
M M Smith

The chromatin structures of two well-characterized autonomously replicating sequence (ARS) elements were examined at their chromosomal sites during the cell division cycle in Saccharomyces cerevisiae. The H4 ARS is located near one of the duplicate nonallelic histone H4 genes, while ARS1 is present near the TRP1 gene. Cells blocked in G1 either by alpha-factor arrest or by nitrogen starvation had two DNase I-hypersensitive sites of about equal intensity in the ARS element. This pattern of DNase I-hypersensitive sites was altered in synchronous cultures allowed to proceed into S phase. In addition to a general increase in DNase I sensitivity around the core consensus sequence, the DNase I-hypersensitive site closest to the core consensus became more nuclease sensitive than the distal site. This change in chromatin structure was restricted to the ARS region and depended on replication since cdc7 cells blocked near the time of replication initiation did not undergo the transition. Subsequent release of arrested cdc7 cells restored entry into S phase and was accompanied by the characteristic change in ARS chromatin structure.


2021 ◽  
Author(s):  
Yujin Kang ◽  
Jin Kang ◽  
AeRi Kim

Super-enhancers, which consist of multiple enhancer elements, are occupied by master transcription factors and coactivators, such as Mediator, and are highly acetylated at histone H3K27. Here, we have characterized the super-enhancers in terms of DNase I hypersensitive sites (DHSs) by analyzing publicly available ChIP-seq and DNase-seq data of K562 cells and compared to the DHSs in typical enhancers. DHSs in the super-enhancers were highly marked by histone H3K4me1 than DHSs in typical enhancers. Loss of H3K4me1 by the deletion of catalytic domains in histone methyltransferases MLL3 and MLL4 remarkably decreased histone H3K27ac and histone H3 depletion at super-enhancer DHSs than at typical enhancer DHSs. The levels of enhancer RNA (eRNA) transcripts and mRNA transcripts from the putative target genes were notably reduced at and near super-enhancer DHSs than typical enhancer DHSs following H3K4me1 loss. These results indicate that histone H3K4me1 is a marker for DHSs in super-enhancers and that this modification has a more significant impact on the activation of super-enhancer DHSs than typical enhancer DHSs.


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