Article
Biochemistry & Molecular Biology
Svetlana Sharifulina, Valentina Dzreyan, Valeria Guzenko, Svetlana Demyanenko
Summary: The study found that the levels and intracellular localization of DNMT1 and G9a proteins changed in penumbra neurons and astrocytes in the rat cerebral cortex after stroke. Inhibition of DNMT1 and G9a protected penumbra cells from apoptosis and reduced the volume of cerebral infarction induced by stroke.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Ophthalmology
Shuai Yang, Weiwei Chen, Shanshan Jin, Guangying Luo, Xia Jing, Qi Liu, Peter S. Reinach, Jia Qu, Dongsheng Yan
Summary: This study reveals the crucial role of SUV39H1 in corneal epithelial cell proliferation during wound healing, mediated by H3K9me3-dependent suppression of p27. These findings suggest that epigenetic modifiers such as SUV39H1 could be potential therapeutic approaches to accelerate corneal repair.
Article
Biochemistry & Molecular Biology
Ying Feng, Li Guo, Chen Yang, Hui Zheng, Xiao Xiao, Hanhui Ma
Summary: This study investigates the role of H3K9me3 in chromatin dynamics and genomic interactions using CRISPR-based DNA imaging. The results demonstrate that the density of H3K9me3 can dictate the stability of interactions between genomic loci and HP1a condensates.
JOURNAL OF GENETICS AND GENOMICS
(2023)
Article
Biochemistry & Molecular Biology
Amandine Barral, Gabrielle Pozo, Lucas Ducrot, Giorgio L. Papadopoulos, Sandrine Sauzet, Andrew J. Oldfield, Giacomo Cavalli, Jerome Dejardin
Summary: A study revealed the presence of dual regions with both H3K9me3 and H3K36me3 marks in mouse embryonic stem cells, which lose these marks and gain enhancer signatures upon removal of SETDB1, suggesting an important role for heterochromatin in gene control. In differentiated tissues, some of these dual domains become destabilized and enriched in enhancer marks, providing insight into heterochromatin involvement in cell identity maintenance.
Article
Multidisciplinary Sciences
Zeyang Wang, Rui Fan, Angela Russo, Filippo M. Cernilogar, Alexander Nuber, Silvia Schirge, Irina Shcherbakova, Iva Dzhilyanova, Enes Ugur, Tobias Anton, Lisa Richter, Heinrich Leonhardt, Heiko Lickert, Gunnar Schotta
Summary: Silencing of endogenous retroviruses is crucial for maintaining transcriptional and genomic integrity of cells, with DNA methylation playing a dominant role over H3K9 methylation.
NATURE COMMUNICATIONS
(2022)
Article
Developmental Biology
Saya Ichihara, Koji Nagao, Takehisa Sakaguchi, Chikashi Obuse, Takashi Sado
Summary: Stable silencing of the inactive X chromosome (Xi) in female mammals is crucial for the development of embryos and their postnatal health. SmcHD1 plays an important role in this process by facilitating the formation of H3K9me3-enriched blocks on the Xi, which in combination with H3K27me3, leads to robust heterochromatin formation. Deficiency of SmcHD1 results in the loss of H3K9me3, causing aberrant distribution of H3K27me3 on the Xi and derepression of X-inactivated genes.
Article
Biochemistry & Molecular Biology
Tushar Warrier, Chadi El Farran, Yingying Zeng, Benedict Shao Quan Ho, Qiuye Bao, Zi Hao Zheng, Xuezhi Bi, Huck Hui Ng, Derrick Sek Tong Ong, Justin Jang Hann Chu, Amartya Sanyal, Melissa Jane Fullwood, James J. Collins, Hu Li, Jian Xu, Yuin-Han Loh
Summary: SETDB1 regulates lineage-specific genes and endogenous retroviral elements through H3K9me3 deposition. In addition, it co-regulates target gene expression and genome topology with the topological regulator Cohesin at DiSCs, which are regions proximal to gene promoters involved in embryonic stem cell pluripotency and lineage development. This discovery is important for understanding the maintenance and differentiation of embryonic stem cells.
NUCLEIC ACIDS RESEARCH
(2022)
Article
Biochemistry & Molecular Biology
Jinpeng Du, Wenwei Liao, Haichuan Wang, Guimin Hou, Min Liao, Lin Xu, Jiwei Huang, Kefei Yuan, Xiangzheng Chen, Yong Zeng
Summary: This study demonstrates the essential role of MDIG in liver regeneration by regulating histone methylation to alter chromatin accessibility. MDIG deficiency results in impaired liver regeneration and delayed cell cycle progression, and it is found that MDIG regulates Myc by modifying chromatin accessibility.
SIGNAL TRANSDUCTION AND TARGETED THERAPY
(2023)
Article
Pharmacology & Pharmacy
Hsiang-i Tsai, Yanping Wu, Rui Huang, Dandan Su, Yingyi Wu, Xiaoyan Liu, Linglu Wang, Zhanxue Xu, Yuxin Pang, Chong Sun, Chao He, Fan Shu, Haitao Zhu, Dongqing Wang, Fang Cheng, Laiqiang Huang, Hongbo Chen
Summary: Mutations in the PHF6 gene are strongly associated with AML and T-ALL. PHF6 can interact with SUV39H1 to regulate rRNA transcription. Clinical mutations of PHF6 impair its ability to recruit SUV39H1, resulting in increased rRNA transcription and leukemia cell proliferation.
ACTA PHARMACEUTICA SINICA B
(2022)
Article
Oncology
Chong Wang, Tao Wang, Kang-Jing Li, Ling-Hong Hu, Yue Li, Yu-Zhong Yu, Tao Xie, Sha Zhu, Du-Jiang Fu, Yang Wang, Xian-Zi Zeng, Feng-Ping Liu, Hong Chen, Zhe-Sheng Chen, Ning-Han Feng, Jinghua Liu, Yong Jiang, Shan-Chao Zhao
Summary: The SETD4 protein plays a crucial role in prostate cancer by catalyzing histone lysine methylation and suppressing NUPR1 transcription, leading to the inhibition of Akt signaling pathway and preventing PCa development.
Article
Cell Biology
Suhila Sawesi, Sridhar A. Malkaram, Zakaria Y. Abd Elmageed, Tamer E. Fandy
Summary: This study compared the effects of curcumin and dimethoxycurcumin (DMC) on histone posttranslational modifications and enzymatic activity. It was found that both drugs had similar effects on the activity of histone lysine methyltransferase (HKMTs) and histone lysine demethylase (HKDMs) enzymes. However, the changes in histone modifications induced by the two drugs were different. These findings support the use and development of curcumin and DMC as epigenetic modifiers in cancer treatment.
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
(2022)
Article
Oncology
Jialei Sun, Na He, Weiguo Wang, Yujian Dai, Chunhui Hou, Fuliang Du
Summary: The study revealed differential gene expression between PKCi-mESC and 2i-mESC, including stem cell-related genes. Furthermore, PKCi-mESC regulated gene expression through H3K27me3 and H3K9me3 modification, which maintained stem cell self-renewal capacity.
AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH
(2022)
Article
Multidisciplinary Sciences
Rebecca A. Lee, Maggie Chang, Nicholas Yiv, Ariel Tsay, Sharon Tian, Danielle Li, Coralie Poulard, Michael R. Stallcup, Miles A. Pufall, Jen-Chywan Wang
Summary: The classical dogma of glucocorticoid-induced insulin resistance states that it is caused by the activation of certain genes. However, this study shows that glucocorticoids can also stimulate the expression of insulin-sensitizing genes. The transcriptional co-regulator EHMT2 plays a key role in this process, as it is involved in the induction of Irs2 to restrict the extent of insulin resistance caused by glucocorticoids.
NATURE COMMUNICATIONS
(2023)
Article
Clinical Neurology
Natascia Guida, Luigi Mascolo, Angelo Serani, Ornella Cuomo, Serenella Anzilotti, Paola Brancaccio, Giuseppe Pignataro, Pasquale Molinaro, Lucio Annunziato, Luigi Formisano
Summary: The study revealed that the GATA3/KMT2A complex epigenetically activates NCX3 gene transcription during ischemic preconditioning, playing a crucial role in neuroprotection.
Article
Genetics & Heredity
Laura Shapiro-Kulnane, Micah Selengut, Helen K. Salz
Summary: H3K9me3-based gene silencing is a crucial strategy for securing cell fate, but the mechanisms responsible for lineage-specific installation of this epigenetic mark are not well understood. In this study, the researchers used Drosophila female germline to investigate the molecular mechanism underlying H3K9me3 deposition onto protein coding gene phf7. The results revealed that H3K9me3 deposition requires conserved cis-regulatory elements and the involvement of a previously uncharacterized protein IDC, which directs the establishment of a sequence-specific mini domain. These findings provide insights into the mechanisms of gene silencing and the maintenance of cell identity.
