scholarly journals Epigenetic control of cell fate in mouse blastocysts: The role of covalent histone modifications and chromatin remodeling

2013 ◽  
Vol 81 (2) ◽  
pp. 171-182 ◽  
Author(s):  
Soumen Paul ◽  
Jason G. Knott
Keyword(s):  
Cell Fate ◽  
Chromatin Remodeling ◽  
Histone Modifications ◽  
Epigenetic Control ◽  
Covalent Histone Modifications

scholarly journals Choose Your Own Adventure: The Role of Histone Modifications in Yeast Cell Fate

2017 ◽  
Vol 429 (13) ◽  
pp. 1946-1957 ◽  
Author(s):  
Deepika Jaiswal ◽  
Rashi Turniansky ◽  
Erin M. Green
Keyword(s):  
Yeast Cell ◽  
Cell Fate ◽  
Histone Modifications

Gata1 Regulates Erythroid Transcription by Cooperating with Chromatin Remodeling Protein Snf2h

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4759-4759
Author(s):  
Jarmila Podskocova ◽  
Pavel Burda ◽  
Karin Vargova ◽  
Juraj Kokavec ◽  
Nikola Curik ◽  
...  
Keyword(s):  
Binding Site ◽  
Chromatin Remodeling ◽  
Histone Modifications ◽  
Binding Sites ◽  
Direct Interaction ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Regular Array ◽  
H4k16 Acetylation

Abstract Gata1 is transcription factor that regulates erythropoiesis and its direct interaction with chromatin remodeling protein Snf2h may affect chromatin structure (Rodriguez 2005). Snf2h belongs to SWI/SNF2 superfamily of ATPases regulating structure of nuclear chromatin by nucleosome movement and assembly. Snf2h knockout in mice is embryonic lethal and heterozygotes display mild growth retardation (Stopka 2003). We studied nuclear localization of Snf2h and detected its presence in euchromatin and to a lesser extent in heterochromatin. Decreased Snf2h levels in Snf2h heterozygotes and Snf2h-null embryos exhibit significantly decreased heterochromatin size. In addition, histone modifications associated with transcription activation (histone H3K79 dimethylation and H4K16 acetylation) are globally decreased in Snf2h mutants. To test the involvement of Snf2h in hematopoiesis, ectopically expressed Snf2h mutants were tested in Gata1-mediated transcription assay in HeLa cells and demonstrated that Snf2h efficiently repressed Gata1 transactivation. Testing whether the ATPase domain is required for the repression mechanism we found the Snf2h dominant negative mutant (DN) can also repress Gata1-dependent transcription in both HeLa and Snf2h +/− fibroblasts. We next studied the effect of Snf2h DN mutant on histone modifications downstream the Gata1 binding site and found that Snf2h DN further increases H3K79 dimethylation induced by Gata1. In contrast, an occupancy of histone H3 downstream the Gata1 binding site was significantly reduced by Snf2h DN mutant indicated it caused a defect in chromatin remodeling. Collectively, our data demonstrate a cooperative role of Gata1 and Snf2h in erythroid transcription regulation and propose that Snf2h in both ATP-dependent and ATPindependent manner represses transcription by disrupting the regular array of nucleosomes near Gata1 binding sites.

How do histone modifications contribute to transgenerational epigenetic inheritance in C. elegans?

2020 ◽  
Vol 48 (3) ◽  
pp. 1019-1034 ◽  
Author(s):  
Rachel M. Woodhouse ◽  
Alyson Ashe
Keyword(s):  
Histone Modifications ◽  
Molecular Mechanisms ◽  
Epigenetic Inheritance ◽  
Nematode Caenorhabditis Elegans ◽  
Histone Methyltransferases ◽  
Transgenerational Epigenetic Inheritance ◽  
C Elegans ◽  
Recent Developments ◽  
Gene Regulatory

Gene regulatory information can be inherited between generations in a phenomenon termed transgenerational epigenetic inheritance (TEI). While examples of TEI in many animals accumulate, the nematode Caenorhabditis elegans has proven particularly useful in investigating the underlying molecular mechanisms of this phenomenon. In C. elegans and other animals, the modification of histone proteins has emerged as a potential carrier and effector of transgenerational epigenetic information. In this review, we explore the contribution of histone modifications to TEI in C. elegans. We describe the role of repressive histone marks, histone methyltransferases, and associated chromatin factors in heritable gene silencing, and discuss recent developments and unanswered questions in how these factors integrate with other known TEI mechanisms. We also review the transgenerational effects of the manipulation of histone modifications on germline health and longevity.

Centrosome Aurora A gradient ensures single polarity axis in C. elegans embryos

2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak
Keyword(s):  
Symmetry Breaking ◽  
Cell Fate ◽  
Cell Cortex ◽  
Axis Formation ◽  
Aurora A Kinase ◽  
Aurora A ◽  
C Elegans ◽  
Cell Embryo ◽  
Polarity Establishment

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.

Tumor suppressor role of chromatin-remodeling factor ARID1A

2013 ◽  
Vol 35 (3) ◽  
pp. 255-261 ◽  
Author(s):  
Xiao-Qiang GUO ◽  
Qiao-Xia ZHANG ◽  
Wei-Ren HUANG ◽  
Xiang-Lin DUAN ◽  
Zhi-Ming CAI
Keyword(s):  
Tumor Suppressor ◽  
Chromatin Remodeling
Sign in / Sign up

Export Citation Format

Share Document