scholarly journals Catalytic inhibition of H3K9me2 writers disturbs epigenetic marks during bovine nuclear reprogramming

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Rafael Vilar Sampaio ◽  
Juliano Rodrigues Sangalli ◽  
Tiago Henrique Camara De Bem ◽  
Dewison Ricardo Ambrizi ◽  
Maite del Collado ◽  
...  
Keyword(s):  
Nuclear Reprogramming ◽  
Epigenetic Marks

scholarly journals Catalytic inhibition of H3K9me2 writers disturbs epigenetic marks during bovine nuclear reprogramming

2019 ◽  
Author(s):  
RV Sampaio ◽  
JR Sangalli ◽  
THC De Bem ◽  
DR Ambrizi ◽  
M del Collado ◽  
...  
Keyword(s):  
Donor Cell ◽  
Early Embryo ◽  
Nuclear Reprogramming ◽  
Toxic Chemical ◽  
Somatic Nucleus ◽  
Epigenetic Marks ◽  
Early Embryos ◽  
Donor Cells ◽  
Reprogramming Efficiency ◽  
Developmental Rates

AbstractOrchestrated events, including extensive changes in epigenetic marks, allow a somatic nucleus to become totipotent after transfer into an oocyte, a process termed nuclear reprogramming. Recently, several strategies have been applied in order to improve reprogramming efficiency, mainly focused on removing repressive epigenetic marks such as histone methylation from the somatic nucleus. Herein we used the specific and non-toxic chemical probe UNC0638 to inhibit the catalytic activity of the histone metyltransferases EHMT1 and EHMT2. Either the donor cell (before reconstruction) or the early embryo was exposed to the probe to assess its effect on developmental rates and epigenetic marks. First, we showed that the treatment of bovine fibroblasts with UNC0638 did mitigate the levels of H3K9me2. Moreover, H3K9me2 levels were decreased in cloned embryos regardless of treating either donor cells or early embryos with UNC0638. Additional epigenetic marks such as H3K9me3, 5mC, and 5hmC were also affected by the UNC0638 treatment. Therefore, the use of UNC0638 did diminish the levels of H3K9me2 and H3K9me3 in SCNT-derived blastocysts, but this was unable to improve their preimplantation development. These results indicate that the specific reduction of H3K9me2 by inhibiting EHMT1/2 causes diverse modifications to the chromatin during early development, suggesting an intense epigenetic crosstalk during nuclear reprogramming.

321-LB: The Link between Obesity and Changes in Epigenetic Marks in Adipose Tissue—In Vivo Study

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 321-LB
Author(s):  
ANETA ALAMA ◽  
DOROTA PAWE?KA ◽  
ANETA MYSZCZYSZYN ◽  
MALGORZATA MALODOBRA-MAZUR
Keyword(s):  
Adipose Tissue ◽  
In Vivo Study ◽  
Epigenetic Marks

scholarly journals Changes Induced by Mind–Body Intervention Including Epigenetic Marks and Its Effects on Diabetes

2021 ◽  
Vol 22 (3) ◽  
pp. 1317
Author(s):  
Hyun-Jeong Yang ◽  
Eugene Koh ◽  
Min-Kyu Sung ◽  
Hojung Kang
Keyword(s):  
Risk Factors ◽  
Well Being ◽  
Epigenetic Modifications ◽  
Cortisol Secretion ◽  
Physiological Changes ◽  
Epigenetic Marks ◽  
Reduce Blood Glucose ◽  
Early Life Events ◽  
Mental Well Being

Studies have evidenced that epigenetic marks associated with type 2 diabetes (T2D) can be inherited from parents or acquired through fetal and early-life events, as well as through lifelong environments or lifestyles, which can increase the risk of diabetes in adulthood. However, epigenetic modifications are reversible, and can be altered through proper intervention, thus mitigating the risk factors of T2D. Mind–body intervention (MBI) refers to interventions like meditation, yoga, and qigong, which deal with both physical and mental well-being. MBI not only induces psychological changes, such as alleviation of depression, anxiety, and stress, but also physiological changes like parasympathetic activation, lower cortisol secretion, reduced inflammation, and aging rate delay, which are all risk factors for T2D. Notably, MBI has been reported to reduce blood glucose in patients with T2D. Herein, based on recent findings, we review the effects of MBI on diabetes and the mechanisms involved, including epigenetic modifications.

scholarly journals Chromatin Manipulation and Editing: Challenges, New Technologies and Their Use in Plants

2021 ◽  
Vol 22 (2) ◽  
pp. 512
Author(s):  
Kateryna Fal ◽  
Denisa Tomkova ◽  
Gilles Vachon ◽  
Marie-Edith Chabouté ◽  
Alexandre Berr ◽  
...  
Keyword(s):  
Cell Fate ◽  
Dna Sequence ◽  
Zinc Finger ◽  
Chromatin Structure ◽  
New Technologies ◽  
Dna Interaction ◽  
The Other ◽  
Proof Of Concept ◽  
Epigenetic Marks ◽  
Molecular Events

An ongoing challenge in functional epigenomics is to develop tools for precise manipulation of epigenetic marks. These tools would allow moving from correlation-based to causal-based findings, a necessary step to reach conclusions on mechanistic principles. In this review, we describe and discuss the advantages and limits of tools and technologies developed to impact epigenetic marks, and which could be employed to study their direct effect on nuclear and chromatin structure, on transcription, and their further genuine role in plant cell fate and development. On one hand, epigenome-wide approaches include drug inhibitors for chromatin modifiers or readers, nanobodies against histone marks or lines expressing modified histones or mutant chromatin effectors. On the other hand, locus-specific approaches consist in targeting precise regions on the chromatin, with engineered proteins able to modify epigenetic marks. Early systems use effectors in fusion with protein domains that recognize a specific DNA sequence (Zinc Finger or TALEs), while the more recent dCas9 approach operates through RNA-DNA interaction, thereby providing more flexibility and modularity for tool designs. Current developments of “second generation”, chimeric dCas9 systems, aiming at better targeting efficiency and modifier capacity have recently been tested in plants and provided promising results. Finally, recent proof-of-concept studies forecast even finer tools, such as inducible/switchable systems, that will allow temporal analyses of the molecular events that follow a change in a specific chromatin mark.

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