170 Acetylation patterns of histone H3K27 in aged pig oocytes

2022 ◽  
Vol 34 (2) ◽  
pp. 323
Author(s):  
K. Sprungl ◽  
H. Arena ◽  
S. Reynolds ◽  
B. Whitaker
Keyword(s):  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rupalatha Maddala ◽  
Junyuan Gao ◽  
Richard T. Mathias ◽  
Tylor R. Lewis ◽  
Vadim Y. Arshavsky ◽  
...  

AbstractS100A4, a member of the S100 family of multifunctional calcium-binding proteins, participates in several physiological and pathological processes. In this study, we demonstrate that S100A4 expression is robustly induced in differentiating fiber cells of the ocular lens and that S100A4(−/−) knockout mice develop late-onset cortical cataracts. Transcriptome profiling of lenses from S100A4(−/−) mice revealed a robust increase in the expression of multiple photoreceptor- and Müller glia-specific genes, as well as the olfactory sensory neuron-specific gene, S100A5. This aberrant transcriptional profile is characterized by corresponding increases in the levels of proteins encoded by the aberrantly upregulated genes. Ingenuity pathway network and curated pathway analyses of differentially expressed genes in S100A4(−/−) lenses identified Crx and Nrl transcription factors as the most significant upstream regulators, and revealed that many of the upregulated genes possess promoters containing a high-density of CpG islands bearing trimethylation marks at histone H3K27 and/or H3K4, respectively. In support of this finding, we further documented that S100A4(−/−) knockout lenses have altered levels of trimethylated H3K27 and H3K4. Taken together, our findings suggest that S100A4 suppresses the expression of retinal genes during lens differentiation plausibly via a mechanism involving changes in histone methylation.


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.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Jay F Sarthy ◽  
Michael P Meers ◽  
Derek H Janssens ◽  
Jorja G Henikoff ◽  
Heather Feldman ◽  
...  

Lysine 27-to-methionine (K27M) mutations in the H3.1 or H3.3 histone genes are characteristic of pediatric diffuse midline gliomas (DMGs). These oncohistone mutations dominantly inhibit histone H3K27 trimethylation and silencing, but it is unknown how oncohistone type affects gliomagenesis. We show that the genomic distributions of H3.1 and H3.3 oncohistones in human patient-derived DMG cells are consistent with the DNAreplication-coupled deposition of histone H3.1 and the predominant replication-independent deposition of histone H3.3. Although H3K27 trimethylation is reduced for both oncohistone types, H3.3K27M-bearing cells retain some domains, and only H3.1K27M-bearing cells lack H3K27 trimethylation. Neither oncohistone interferes with PRC2 binding. Using Drosophila as a model, we demonstrate that inhibition of H3K27 trimethylation occurs only when H3K27M oncohistones are deposited into chromatin and only when expressed in cycling cells. We propose that oncohistones inhibit the H3K27 methyltransferase as chromatin patterns are being duplicated in proliferating cells, predisposing them to tumorigenesis.


2018 ◽  
Vol 131 (12) ◽  
pp. jcs215525 ◽  
Author(s):  
Ye Zhang ◽  
Jian-Feng Chang ◽  
Jin Sun ◽  
Lu Chen ◽  
Xiao-Mei Yang ◽  
...  

Theranostics ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 361-378
Author(s):  
Yan Jiang ◽  
Chan Xiang ◽  
Fan Zhong ◽  
Yang Zhang ◽  
Liyan Wang ◽  
...  

2019 ◽  
Vol 39 (8) ◽  
pp. 4179-4184
Author(s):  
NADEZHDA ROMANCHIKOVA ◽  
PETERIS TRAPENCIERIS

2018 ◽  
Vol 10 (441) ◽  
pp. eaao4680 ◽  
Author(s):  
Timothy L. Lochmann ◽  
Krista M. Powell ◽  
Jungoh Ham ◽  
Konstantinos V. Floros ◽  
Daniel A. R. Heisey ◽  
...  

2018 ◽  
Author(s):  
Barbara H. Rath ◽  
Isabella Waung ◽  
Kevin Camphausen ◽  
Philip Tofilon
Keyword(s):  

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