scholarly journals A Prokineticin-Driven Epigenetic Switch Regulates Human Epicardial Cell Stemness and Fate

Stem Cells ◽  
2018 ◽  
Vol 36 (10) ◽  
pp. 1589-1602 ◽  
Author(s):  
Rehana Qureshi ◽  
Michel Kindo ◽  
Mounia Boulberdaa ◽  
Jean-Jacques von Hunolstein ◽  
Marja Steenman ◽  
...  
Keyword(s):  
Epigenetic Switch ◽  
Epicardial Cell

scholarly journals KDM6A Lysine Demethylase Directs Epigenetic Polarity of MDSCs during Murine Sepsis

2021 ◽  
pp. 1-12
Author(s):  
Isatou Bah ◽  
Tuqa Alkhateeb ◽  
Dima Youssef ◽  
Zhi Q. Yao ◽  
Charles E. McCall ◽  
...  
Keyword(s):  
Suppressor Cells ◽  
Transcription Activation ◽  
Myeloid Derived Suppressor Cells ◽  
Molecular Processes ◽  
Epigenetic Switch ◽  
Translation Research ◽  
Non Coding Rna ◽  
Genetic Deletion ◽  
Lysine Demethylase ◽  
Long Non Coding Rna

Sepsis-induced myeloid-derived suppressor cells (MDSCs) increase mortality risk. We previously identified that long non-coding RNA Hotairm1 supports myeloid precursor shifts to Gr1<sup>+</sup>CD11b<sup>+</sup> MDSCs during mouse sepsis. A major unanswered question is what molecular processes control Hotairm1 expression. In this study, we found by a genetic deletion that a specific PU.1-binding site is indispensable in controlling Hotairm1 transcription. We then identified H3K4me3 and H3K27me3 at the PU.1 site on the Hotairm1 promoter. Controlling an epigenetic switch of Hotairm1 transcription by PU.1 was histone KDM6A demethylase for H3K27me3 that derepressed its transcription with possible contributions from Ezh2 methyltransferase for H3K27me3. KDM6A knockdown in MDSCs increased H3K27me3, decreased H3K4me3, and inhibited Hotairm1 transcription activation by PU.1. These results enlighten clinical translation research of PU.1 epigenetic regulation as a potential sepsis immune-checkpoint treatment site.

scholarly journals A Long ncRNA Links Copy Number Variation to a Polycomb/Trithorax Epigenetic Switch in FSHD Muscular Dystrophy

Cell ◽  
2012 ◽  
Vol 149 (4) ◽  
pp. 819-831 ◽  
Author(s):  
Daphne S. Cabianca ◽  
Valentina Casa ◽  
Beatrice Bodega ◽  
Alexandros Xynos ◽  
Enrico Ginelli ◽  
...  
Keyword(s):  
Muscular Dystrophy ◽  
Copy Number Variation ◽  
Copy Number ◽  
Epigenetic Switch ◽  
Number Variation

scholarly journals An epigenetic switch repressingTet1in gonadotropes activates the reproductive axis

2017 ◽  
Vol 114 (38) ◽  
pp. 10131-10136 ◽  
Author(s):  
Yahav Yosefzon ◽  
Cfir David ◽  
Anna Tsukerman ◽  
Lilach Pnueli ◽  
Sen Qiao ◽  
...  
Keyword(s):  
Ovarian Function ◽  
Ovarian Follicle ◽  
Gene Promoter ◽  
Follicle Development ◽  
Mrna Levels ◽  
Epigenetic Switch ◽  
Ovarian Follicle Development ◽  
Reproductive Axis ◽  
Poorly Differentiated ◽  
Tet Enzymes

The TET enzymes catalyze conversion of 5-methyl cytosine (5mC) to 5-hydroxymethyl cytosine (5hmC) and play important roles during development. TET1 has been particularly well-studied in pluripotent stem cells, butTet1-KO mice are viable, and the most marked defect is abnormal ovarian follicle development, resulting in impaired fertility. We hypothesized that TET1 might play a role in the central control of reproduction by regulating expression of the gonadotropin hormones, which are responsible for follicle development and maturation and ovarian function. We find that all three TET enzymes are expressed in gonadotrope-precursor cells, butTet1mRNA levels decrease markedly with completion of cell differentiation, corresponding with an increase in expression of the luteinizing hormone gene,Lhb. We demonstrate that poorly differentiated gonadotropes express a TET1 isoform lacking the N-terminal CXXC-domain, which repressesLhbgene expression directly and does not catalyze 5hmC at the gene promoter. We show that this isoform is also expressed in other differentiated tissues, and that it is regulated by an alternative promoter whose activity is repressed by the liganded estrogen and androgen receptors, and by the hypothalamic gonadotropin-releasing hormone through activation of PKA. Its expression is also regulated by DNA methylation, including at an upstream enhancer that is protected by TET2, to allowTet1expression. The down-regulation of TET1 relieves its repression of the methylatedLhbgene promoter, which is then hydroxymethylated and activated by TET2 for full reproductive competence.

scholarly journals An Epigenetic Switch Involving Overlapping Fur and DNA Methylation Optimizes Expression of a Type VI Secretion Gene Cluster

PLoS Genetics ◽  
2011 ◽  
Vol 7 (7) ◽  
pp. e1002205 ◽  
Author(s):  
Yannick R. Brunet ◽  
Christophe S. Bernard ◽  
Marthe Gavioli ◽  
Roland Lloubès ◽  
Eric Cascales
Keyword(s):  
Dna Methylation ◽  
Gene Cluster ◽  
Epigenetic Switch ◽  
Type Vi Secretion

scholarly journals Exploring the role of SlrR and SlrA in the SinR epigenetic switch

2013 ◽  
Vol 6 (6) ◽  
pp. e25658 ◽  
Author(s):  
Joseph Newman ◽  
Richard J. Lewis
Keyword(s):  
Epigenetic Switch

scholarly journals An epigenetic switch induced by Shh signalling regulates gene activation during development and medulloblastoma growth

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Xuanming Shi ◽  
Zilai Zhang ◽  
Xiaoming Zhan ◽  
Mou Cao ◽  
Takashi Satoh ◽  
...  
Keyword(s):  
Gene Activation ◽  
Epigenetic Switch
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