scholarly journals Condensins, Chromatin Remodeling and Gene Transcription

10.5772/55732 ◽  
2013 ◽  
Author(s):  
Laurence O. W. Wilson ◽  
Aude M.
Keyword(s):  
Chromatin Remodeling ◽  
Gene Transcription

scholarly journals CHD8 Is an ATP-Dependent Chromatin Remodeling Factor That Regulates β-Catenin Target Genes

2008 ◽  
Vol 28 (12) ◽  
pp. 3894-3904 ◽  
Author(s):  
Brandi A. Thompson ◽  
Véronique Tremblay ◽  
Grace Lin ◽  
Daniel A. Bochar
Keyword(s):  
Gene Expression ◽  
Rna Interference ◽  
Chromatin Remodeling ◽  
Gene Transcription ◽  
Chromatin Structure ◽  
Target Genes ◽  
Promoter Regions ◽  
Hairpin Rna ◽  
Short Hairpin ◽  
Targeted Gene Expression

ABSTRACT ATP-dependent chromatin remodeling by the CHD family of proteins plays an important role in the regulation of gene transcription. Here we report that full-length CHD8 interacts directly with β-catenin and that CHD8 is also recruited specifically to the promoter regions of several β-catenin-responsive genes. Our results indicate that CHD8 negatively regulates β-catenin-targeted gene expression, since short hairpin RNA against CHD8 results in the activation of several β-catenin target genes. This regulation is also conserved through evolution; RNA interference against kismet, the apparent Drosophila ortholog of CHD8, results in a similar activation of β-catenin target genes. We also report the first demonstration of chromatin remodeling activity for a member of the CHD6-9 family of proteins, suggesting that CHD8 functions in transcription through the ATP-dependent modulation of chromatin structure.

scholarly journals LincRNA-Cox2 Promotes Late Inflammatory Gene Transcription in Macrophages through Modulating SWI/SNF-Mediated Chromatin Remodeling

2016 ◽  
Vol 196 (6) ◽  
pp. 2799-2808 ◽  
Author(s):  
Guoku Hu ◽  
Ai-Yu Gong ◽  
Yang Wang ◽  
Shibin Ma ◽  
Xiqiang Chen ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Gene Transcription ◽  
Inflammatory Gene

scholarly journals Cooperation between the INO80 Complex and Histone Chaperones Determines Adaptation of Stress Gene Transcription in the Yeast Saccharomyces cerevisiae

2009 ◽  
Vol 29 (18) ◽  
pp. 4994-5007 ◽  
Author(s):  
Eva Klopf ◽  
Ludmila Paskova ◽  
Carme Solé ◽  
Gloria Mas ◽  
Andriy Petryshyn ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Gene Transcription ◽  
Acute Stress ◽  
Histone Chaperones ◽  
Yeast Saccharomyces Cerevisiae ◽  
Direct Function ◽  
Stress Genes ◽  
Active Transcription ◽  
Stress Gene ◽  
Dependent Mechanism

ABSTRACT In yeast, environmental stresses provoke sudden and dramatic increases in gene expression at stress-inducible loci. Stress gene transcription is accompanied by the transient eviction of histones from the promoter and the transcribed regions of these genes. We found that mutants defective in subunits of the INO80 complex, as well as in several histone chaperone systems, exhibit extended expression windows that can be correlated with a distinct delay in histone redeposition during adaptation. Surprisingly, Ino80 became associated with the ORFs of stress genes in a stress-specific way, suggesting a direct function in the repression during adaptation. This recruitment required elongation by RNA polymerase (Pol) II but none of the histone modifications that are usually associated with active transcription, such as H3 K4/K36 methylation. A mutant lacking the Asf1-associated H3K56 acetyltransferase Rtt109 or Asf1 itself also showed enhanced stress-induced transcript levels. Genetic data, however, suggest that Asf1 and Rtt109 function in parallel with INO80 to restore histone homeostasis, whereas Spt6 seems to have a function that overlaps that of the chromatin remodeler. Thus, chromatin remodeling by INO80 in cooperation with Spt6 determines the shape of the expression profile under acute stress conditions, possibly by an elongation-dependent mechanism.

Runx2/Cbfa1 Functions: Diverse Regulation of Gene Transcription by Chromatin Remodeling and Co-Regulatory Protein Interactions

2003 ◽  
Vol 44 (1) ◽  
pp. 141-148 ◽  
Author(s):  
Jane B. Lian ◽  
Janet L. Stein ◽  
Gary S. Stein ◽  
André J. van Wijnen ◽  
Martin Montecino ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Gene Transcription ◽  
Protein Interactions ◽  
Regulatory Protein

Altered Erythroid and Megakaryocytic Differentiation in Mice Expressing a Unique Chromatin Remodeling Domain of Erythroid Krüppel-Like Factor (EKLF)

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 132-132
Author(s):  
Valerie M. Jansen ◽  
Tatiana Abramova ◽  
Eun-Hee Shim ◽  
Shaji Ramachandran ◽  
Aurelie Desgardin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Zinc Finger ◽  
Chromatin Remodeling ◽  
Gene Transcription ◽  
Globin Gene ◽  
Megakaryocytic Differentiation ◽  
Amino Terminal ◽  
Chromatin Architecture

Abstract The zinc finger-encoding transacting factor EKLF binds key regulatory elements of many erythroid-specific genes, and is essential for definitive erythropoiesis. Mice lacking this factor (EKLF−/−) die of anemia by E15.5 of gestation, failing to activate β-globin gene transcription, and demonstrating a block in the erythroid differentiation program at the primitive erythroblast stage. In contrast, megakaryocytic progenitors are amplified in EKLFnull embryos, with increased Fli-1 gene expression (a marker of early megakaryocytic differentiation), consistent with the idea that EKLF modulates the megakaryocyticerythroid (M-E) differentiation switch. We have demonstrated that an amino terminal mutant of EKLF (Δ221EKLF), is required to induce chromatin remodeling at the β-globin promoter in an EKLF-null erythroid cell line, but additional amino terminal sequences are required for initiation of β-globin gene transcription (Brown et al., 2002). To evaluate the role of this chromatin remodeling (CR) domain in erythroid and megakaryocytic differentiation in vivo, we have generated a knock-in allele of EKLFCR allele. Similar to EKLF-null embryos, mice homozygous for this mutant allele die of anemia by E15.5 of gestation. In contrast to erythroid cells lacking EKLF, EKLFCR/CR progenitors demonstrate appropriate binding of the CR encoding domain to all EKLF-regulatory sequences; a block in erythropoiesis at a more a mature stage in differentiation a chromatin architecture and histone modification pattern at erythroid-specific genes that recapitulates the events observed in EKLF+/+ erythroblasts at a similar stage of erythroid ontogeny; a failure of terminal erythroid gene transcription. Examining the role of EKLFCR in megakaryopoiesis, we observed inhibition of megakaryocytic progenitor amplification in EKLFCR/CR fetal hematopoietic cell populations when compared to EKLF-null embryos; loss of Fli-1 gene expression in EKLFCR expressing cells; binding of the EKLFCR mutant protein to the Fli-1 promoter with inhibition of gene transcription; a repressed chromatin architecture at megakaryocytic gene loci. In contrast to these results, mice homozygous for a knockin allele encoding the zinc finger DNA binding domain alone (Δ253EKLF), a region shown previously to be sufficient for chromatin remodeling in vitro, demonstrate erythroid and megakaryocytic phenotypes that resemble those observed in EKLF-null hematopoietic progenitors. Taken together, our results suggest strongly that the unique EKLFCR domain is necessary and sufficient to modulate the chromatin-specific roles of EKLF at erythroid- and megakaryocytic-specific loci in definitive hematopoietic cells in vivo.

Context-Specific KLF-1 Mediated Transcriptional Activation at the Alpha Hemoglobin-Stabilizing Protein and Dematin Promoters in Erythroid Cells.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 461-461
Author(s):  
Aurelie Desgardin ◽  
Valerie M. Jansen ◽  
Eun-Hee Shim ◽  
Tatiana Abramova ◽  
Shaji Ramachandran ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Gene Transcription ◽  
Transcriptional Activation ◽  
Molecular Mechanisms ◽  
Globin Gene ◽  
Erythroid Cell ◽  
Specific Gene ◽  
Gene Promoters ◽  
Post Induction ◽  
Kinetics Of

Abstract Abstract 461 Krüppel-like factor 1 (KLF1) is essential for erythroid gene expression. Key molecular mechanisms modulated by this transacting factor have been elucidated at the b-globin locus. KLF1 has been associated with recruitment of SWI/SNF and RNA polymerase (PolII) complexes necessary for chromatin remodeling and gene transcription respectively, and for facilitating the apposition of the promoter with the far-upstream locus control region. More recently, KLF1 has been implicated in the regulation of an erythroid-specific gene program unlinked to the b-globin locus. Coordinated expression of these genes, including Alpha Hemoglobin-Stabilizing Protein (AHSP), a factor required for globin tetramer stability, and the red cell membrane protein Dematin, are critical for erythroid ontogeny. To compare the role(s) of KLF1 at these loci, we have used a unique 4-OH-Tamoxifen (4-OHT) inducible erythroid cell line, which facilitates the characterization of the temporal kinetics of KLF1-dependent erythroid gene activation. In preliminary experiments, we observed that KLF1 binding was maximal at the three loci within 60 minutes of 4-OHT induction. AHSP and dematin primary RNA transcripts followed similar kinetics, being maximal at 60-90 minutes post-induction. In contrast, b-globin gene transcription reached a plateau 4-6 hours post-induction. From these observations, we hypothesized that transcriptional activation at AHSP and dematin differs from that observed at the b-globin cluster. Consistent with this hypothesis, we observed significant differences in chromatin remodeling at the three loci. At the b-globin promoter, we observed a small but statistically significant increase in DNaseI sensitivity, a measure of chromatin remodeling, with KLF1 binding. In contrast, we observed a complete loss of DNaseI resistance after KLF1 binding at the AHSP and dematin promoters. Consistent with these findings, we observed a five-fold reduction in histone H3 occupancy at the AHSP and dematin promoters, contrasting with no significant change in occupancy at the b-promoter. Importantly, these differences were not observed in regions 1-5 kb upstream of the promoters. These observations, coupled with similar differences in DNaseI hypersensitivity and histone occupancy in fetal liver erythroblasts from wild type and KLF1-null mice, suggest a profound difference in the mechanisms of chromatin remodeling at KLF1-dependent erythroid gene loci. To explore the potential mechanisms underlying these differences in chromatin accessibility, we examined the kinetics of recruitment of other transacting factors and co-activators to the three loci. We observed similar increases in binding of serine-5 phosphorylated PolII, GATA-1, and p45NF-E2 at the promoters. In contrast, binding of BRG1, the core ATPase component of the SWI/SNF complex differed between the b–promoter and the other erythroid genes. Although BRG1 binding was co-incident with KLF1 binding to the b-gene, we observed significant albeit weak binding of this complex to the AHSP and Dematin promoters only after maximal gene transcription had occurred. Our results suggest that different KLF1 multiprotein complexes are recruited to remodel target gene promoters in vivo. Furthermore, we propose that KLF1's chromatin remodeling capabilities are not limited to the recruitment of the SWI/SNF complexes Disclosures: No relevant conflicts of interest to declare.

scholarly journals Estradiol-Induced Epigenetically Mediated Mechanisms and Regulation of Gene Expression

2020 ◽  
Vol 21 (9) ◽  
pp. 3177 ◽  
Author(s):  
Tamás Kovács ◽  
Edina Szabó-Meleg ◽  
István M. Ábrahám
Keyword(s):  
Dna Methylation ◽  
Chromatin Remodeling ◽  
Gene Transcription ◽  
Regulation Of Gene Expression ◽  
Dna Demethylation ◽  
Gonadal Hormone ◽  
Active Dna Demethylation ◽  
Physiological Processes ◽  
Chromatin Remodeling Complexes ◽  
17Β Estradiol

Gonadal hormone 17β-estradiol (E2) and its receptors are key regulators of gene transcription by binding to estrogen responsive elements in the genome. Besides the classical genomic action, E2 regulates gene transcription via the modification of epigenetic marks on DNA and histone proteins. Depending on the reaction partner, liganded estrogen receptor (ER) promotes DNA methylation at the promoter or enhancer regions. In addition, ERs are important regulators of passive and active DNA demethylation. Furthermore, ERs cooperating with different histone modifying enzymes and chromatin remodeling complexes alter gene transcription. In this review, we survey the basic mechanisms and interactions between estrogen receptors and DNA methylation, demethylation and histone modification processes as well as chromatin remodeling complexes. The particular relevance of these mechanisms to physiological processes in memory formation, embryonic development, spermatogenesis and aging as well as in pathophysiological changes in carcinogenesis is also discussed.

scholarly journals Eda-activated RelB recruits an SWI/SNF (BAF) chromatin-remodeling complex and initiates gene transcription in skin appendage formation

2018 ◽  
Vol 115 (32) ◽  
pp. 8173-8178 ◽  
Author(s):  
Jian Sima ◽  
Zhijiang Yan ◽  
Yaohui Chen ◽  
Elin Lehrmann ◽  
Yongqing Zhang ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Gene Transcription ◽  
Target Genes ◽  
Specific Gene ◽  
Open Chromatin ◽  
Transcription Profiling ◽  
Baf Complex ◽  
Skin Appendage ◽  
Chromatin Remodeling Complex ◽  
Appendage Formation

Ectodysplasin A (Eda) signaling activates NF-κB during skin appendage formation, but how Eda controls specific gene transcription remains unclear. Here, we find that Eda triggers the formation of an NF-κB–associated SWI/SNF (BAF) complex in which p50/RelB recruits a linker protein, Tfg, that interacts with BAF45d in the BAF complex. We further reveal that Tfg is initially induced by Eda-mediated RelB activation and then bridges RelB and BAF for subsequent gene regulation. The BAF component BAF250a is particularly up-regulated in skin appendages, and epidermal knockout of BAF250a impairs skin appendage development, resulting in phenotypes similar to those of Eda-deficient mouse models. Transcription profiling identifies several target genes regulated by Eda, RelB, and BAF. Notably, RelB and the BAF complex are indispensable for transcription of Eda target genes, and both BAF complex and Eda signaling are required to open chromatin of Eda targets. Our studies thus suggest that Eda initiates a signaling cascade and recruits a BAF complex to specific gene loci to facilitate transcription during organogenesis.

Sign in / Sign up

Export Citation Format

Share Document