Putative promoters within gene bodies control exon expression via TET1‐mediated H3K36 methylation

2020 ◽  
Vol 235 (10) ◽  
pp. 6711-6724
Author(s):  
Ling Ma ◽  
Tahir Muhammad ◽  
Hongyang Wang ◽  
Guangyuan Du ◽  
Ali Sakhawat ◽  
...  
PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e67448 ◽  
Author(s):  
Shijia Zhu ◽  
Guohua Wang ◽  
Bo Liu ◽  
Yadong Wang

2008 ◽  
Vol 5 (2) ◽  
Author(s):  
Dorothea Emig ◽  
Melissa S. Cline ◽  
Karsten Klein ◽  
Anne Kunert ◽  
Petra Mutzel ◽  
...  

SummaryProteins and their interactions are essential for the functioning of all organisms and for understanding biological processes. Alternative splicing is an important molecular mechanism for increasing the protein diversity in eukaryotic cells. Splicing events that alter the protein structure and the domain composition can be responsible for the regulation of protein interactions and the functional diversity of different tissues. Discovering the occurrence of splicing events and studying protein isoforms have become feasible using Affymetrix Exon Arrays. Therefore, we have developed the versatile Cytoscape plugin DomainGraph that allows for the visual analysis of protein domain interaction networks and their integration with exon expression data. Protein domains affected by alternative splicing are highlighted and splicing patterns can be compared.


2018 ◽  
Vol 8 (11) ◽  
pp. 3411-3420 ◽  
Author(s):  
Kwan Yin Lee ◽  
Mathieu Ranger ◽  
Marc D. Meneghini

2006 ◽  
Vol 27 (2) ◽  
pp. 721-731 ◽  
Author(s):  
Tiaojiang Xiao ◽  
Yoichiro Shibata ◽  
Bhargavi Rao ◽  
R. Nicholas Laribee ◽  
Rose O'Rourke ◽  
...  

ABSTRACT In yeast and other eukaryotes, the histone methyltransferase Set1 mediates methylation of lysine 4 on histone H3 (H3K4me). This modification marks the 5′ end of transcribed genes in a 5′-to-3′ tri- to di- to monomethyl gradient and promotes association of chromatin-remodeling and histone-modifying enzymes. Here we show that Ctk1, the serine 2 C-terminal domain (CTD) kinase for RNA polymerase II (RNAP II), regulates H3K4 methylation. We found that CTK1 deletion nearly abolished H3K4 monomethylation yet caused a significant increase in H3K4 di- and trimethylation. Both in individual genes and genome-wide, loss of CTK1 disrupted the H3K4 methylation patterns normally observed. H3K4me2 and H3K4me3 spread 3′ into the bodies of genes, while H3K4 monomethylation was diminished. These effects were dependent on the catalytic activity of Ctk1 but are independent of Set2-mediated H3K36 methylation. Furthermore, these effects are not due to spurious transcription initiation in the bodies of genes, to changes in RNAP II occupancy, to changes in serine 5 CTD phosphorylation patterns, or to “transcriptional stress.” These data show that Ctk1 acts to restrict the spread of H3K4 methylation through a mechanism that is independent of a general transcription defect. The evidence presented suggests that Ctk1 controls the maintenance of suppressive chromatin in the coding regions of genes by both promoting H3K36 methylation, which leads to histone deacetylation, and preventing the 3′ spread of H3K4 trimethylation, a mark associated with transcriptional initiation.


2010 ◽  
Vol 286 (10) ◽  
pp. 8361-8368 ◽  
Author(s):  
Qi Qiao ◽  
Yan Li ◽  
Zhi Chen ◽  
Mingzhu Wang ◽  
Danny Reinberg ◽  
...  

2017 ◽  
Author(s):  
Chao Lu ◽  
Simon Papillon-Cavanagh ◽  
Tenzin Gayden ◽  
Leonie G. Mikael ◽  
Denise Bechet ◽  
...  

2015 ◽  
Vol 31 (14) ◽  
pp. 2400-2402 ◽  
Author(s):  
Yarden Katz ◽  
Eric T. Wang ◽  
Jacob Silterra ◽  
Schraga Schwartz ◽  
Bang Wong ◽  
...  

2013 ◽  
Vol 58 (5) ◽  
pp. 936-948 ◽  
Author(s):  
Sonia Gandoura ◽  
Emmanuel Weiss ◽  
Pierre-Emmanuel Rautou ◽  
Magali Fasseu ◽  
Thierry Gustot ◽  
...  

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