scholarly journals PU.1 inhibits the erythroid program by binding to GATA-1 on DNA and creating a repressive chromatin structure

2005 ◽  
Vol 24 (21) ◽  
pp. 3712-3723 ◽  
Author(s):  
Tomas Stopka ◽  
Derek F Amanatullah ◽  
Michael Papetti ◽  
Arthur I Skoultchi
Keyword(s):  
Chromatin Structure ◽  
Repressive Chromatin

scholarly journals Interplay between Chromatin and trans-Acting Factors on the IME2 Promoter upon Induction of the Gene at the Onset of Meiosis

2006 ◽  
Vol 27 (4) ◽  
pp. 1254-1263 ◽  
Author(s):  
Tomomi Inai ◽  
Masashi Yukawa ◽  
Eiko Tsuchiya
Keyword(s):  
Histone Deacetylase ◽  
Chromatin Structure ◽  
Molecular Basis ◽  
Histone Acetyltransferase ◽  
Histone H3 ◽  
Repressive Chromatin ◽  
Tata Element ◽  
Histone H3 Acetylation ◽  
Low Levels ◽  
H3 Acetylation

ABSTRACT The IME2 gene is one of the key regulators of the initiation of meiosis in budding yeast. This gene is repressed during mitosis through the repressive chromatin structure at the promoter, which is maintained by the Rpd3-Sin3 histone deacetylase (HDAC) complex. IME2 expression in meiosis requires Gcn5/histone acetyltransferase, the transcriptional activator Ime1, and the chromatin remodeler RSC; however, the molecular basis of IME2 activation had not been previously defined. We found that, during mitotic growth, a nucleosome masked the TATA element of IME2, and this positioning depended on HDAC. This chromatin structure was remodeled at meiosis by RSC that was recruited to TATA by Ime1. Stable tethering of Ime1 to the promoter required the presence of Gcn5. Interestingly, Ime1 binding to the promoter was kept at low levels during the very early stages in meiosis, even when the levels of Ime1 and histone H3 acetylation at the promoter were at their highest, making a 4- to 6-h delay of the IME2 expression from that of IME1. HDAC was continuously present at the promoter regardless of the transcriptional condition of IME2, and deletion of RPD3 allowed the IME2 expression shortly after the expression of IME1, suggesting that HDAC plays a role in regulating the timing of IME2 expression.

scholarly journals Distinct Chromatin Modulators Regulate the Formation of Accessible and Repressive Chromatin at the Fission Yeast Recombination Hotspot ade6-M26

2008 ◽  
Vol 19 (3) ◽  
pp. 1162-1173 ◽  
Author(s):  
Kouji Hirota ◽  
Ken-ichi Mizuno ◽  
Takehiko Shibata ◽  
Kunihiro Ohta
Keyword(s):  
Chromatin Remodeling ◽  
Chromatin Structure ◽  
Meiotic Recombination ◽  
Initiation Site ◽  
Regulation Of Transcription ◽  
Transcriptional Initiation ◽  
Recombination Hotspot ◽  
Repressive Chromatin ◽  
Chromatin Configuration ◽  
Responsive Element

Histone acetyltransferases (HATs) and ATP-dependent chromatin remodeling factors (ADCRs) regulate transcription and recombination via alteration of local chromatin configuration. The ade6-M26 allele of Schizosaccharomyces pombe creates a meiotic recombination hotspot that requires a cAMP-responsive element (CRE)-like sequence M26, the Atf1/Pcr1 heterodimeric ATF/CREB transcription factor, the Gcn5 HAT, and the Snf22 SWI2/SNF2 family ADCR. Chromatin alteration occurs meiotically around M26, leading to the activation of meiotic recombination. We newly report the roles of other chromatin remodeling factors that function positively and negatively in chromatin alteration at M26: two CHD-1 family ADCRs (Hrp1 and Hrp3), a Spt-Ada-Gcn5 acetyltransferase component (Ada2), and a member of Moz-Ybf2/Sas3-Sas2-Tip60 family (Mst2). Ada2, Mst2, and Hrp3 are required for the full activation of chromatin changes around M26 and meiotic recombination. Acetylation of histone H3 around M26 is remarkably reduced in gcn5Δ, ada2Δ and snf22Δ, suggesting cooperative functions of these HAT complexes and Snf22. Conversely, Hrp1, another CHD-1 family ADCR, maintains repressive chromatin configuration at ade6-M26. Interestingly, transcriptional initiation site is shifted to a site around M26 from the original initiation sites, in couple with the histone acetylation and meiotic chromatin alteration induced around 3′ region of M26, suggesting a collaboration between these chromatin modulators and the transcriptional machinery to form accessible chromatin. These HATs and ADCRs are also required for the regulation of transcription and chromatin structure around M26 in response to osmotic stress. Thus, we propose that multiple chromatin modulators regulate chromatin structure reversibly and participate in the regulation of both meiotic recombination and stress-induced transcription around CRE-like sequences.

scholarly journals L3MBTL2 Protein Acts in Concert with PcG Protein-Mediated Monoubiquitination of H2A to Establish a Repressive Chromatin Structure

2011 ◽  
Vol 42 (4) ◽  
pp. 438-450 ◽  
Author(s):  
Patrick Trojer ◽  
Alina R. Cao ◽  
Zhonghua Gao ◽  
Yan Li ◽  
Jin Zhang ◽  
...  
Keyword(s):  
Chromatin Structure ◽  
Repressive Chromatin

scholarly journals An epigenetic gene silencing pathway selectively acting on transgenic DNA in the green alga Chlamydomonas

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Juliane Neupert ◽  
Sean D. Gallaher ◽  
Yinghong Lu ◽  
Daniela Strenkert ◽  
Na’ama Segal ◽  
...  
Keyword(s):  
Chromatin Structure ◽  
Transgene Expression ◽  
Environmental Dna ◽  
Genetic Screens ◽  
Exogenous Dna ◽  
Endogenous Gene ◽  
Repressive Chromatin ◽  
Epigenetic Gene Silencing ◽  
Unknown Gene ◽  
Foreign Genes

AbstractSilencing of exogenous DNA can make transgene expression very inefficient. Genetic screens in the model alga Chlamydomonas have demonstrated that transgene silencing can be overcome by mutations in unknown gene(s), thus producing algal strains that stably express foreign genes to high levels. Here, we show that the silencing mechanism specifically acts on transgenic DNA. Once a permissive chromatin structure has assembled, transgene expression can persist even in the absence of mutations disrupting the silencing pathway. We have identified the gene conferring the silencing and show it to encode a sirtuin-type histone deacetylase. Loss of gene function does not appreciably affect endogenous gene expression. Our data suggest that transgenic DNA is recognized and then quickly inactivated by the assembly of a repressive chromatin structure composed of deacetylated histones. We propose that this mechanism may have evolved to provide protection from potentially harmful types of environmental DNA.

scholarly journals Histone Chaperone Asf1 Is Required for the Establishment of Repressive Chromatin in Schizosaccharomyces pombe fbp1 Gene Repression

2018 ◽  
Vol 38 (18) ◽  
Author(s):  
Miki Umeda ◽  
Chiaki Tsunekawa ◽  
Satoshi Senmatsu ◽  
Ryuta Asada ◽  
Takuya Abe ◽  
...  
Keyword(s):  
Schizosaccharomyces Pombe ◽  
Fission Yeast ◽  
Rna Polymerase Ii ◽  
Chromatin Structure ◽  
Glucose Repression ◽  
Gene Activation ◽  
Histone Chaperone ◽  
Glucose Starvation ◽  
Content Type ◽  
Repressive Chromatin

ABSTRACT The arrangement of nucleosomes in chromatin plays a role in transcriptional regulation by restricting the accessibility of transcription factors and RNA polymerase II to cis-acting elements and promoters. For gene activation, the chromatin structure is altered to an open configuration. The mechanism for this process has been extensively analyzed. However, the mechanism by which repressive chromatin is reconstituted to terminate transcription has not been fully elucidated. Here, we investigated the mechanisms by which chromatin is reconstituted in the fission yeast Schizosaccharomyces pombe fbp1 gene, which is robustly induced upon glucose starvation but tightly repressed under glucose-rich conditions. We found that the chromatin structure in the region upstream from fbp1 is closed by a two-step process. When cells are returned to glucose-rich medium following glucose starvation, changes in the nucleosome pattern alter the chromatin configuration at the transcription factor binding site to an inaccessible state, after which the nucleosome density upstream from fbp1 gradually increases via histone loading. Interestingly, this histone loading was observed in the absence of the Tup family corepressors Tup11 and Tup12. Analysis of strains carrying either gene disruptions or mutations affecting nine fission yeast histone chaperone genes demonstrated that the histone chaperone Asf1 induces nucleosome loading during glucose repression. These data establish a previously unappreciated chromatin reconstitution mechanism in fbp1 repression.

scholarly journals SAS4 and SAS5 Are Locus-Specific Regulators of Silencing in Saccharomyces cerevisiae

Genetics ◽  
1999 ◽  
Vol 153 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Eugenia Y Xu ◽  
Susan Kim ◽  
David H Rivier
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Chromatin Structure ◽  
Null Alleles ◽  
Negative Regulators ◽  
The Core ◽  
Repressive Chromatin ◽  
Core Histones ◽  
Positive Regulators

Abstract Sir2p, Sir3p, Sir4p, and the core histones form a repressive chromatin structure that silences transcription in the regions near telomeres and at the HML and HMR cryptic mating-type loci in Saccharomyces cerevisiae. Null alleles of SAS4 and SAS5 suppress silencing defects at HMR; therefore, SAS4 and SAS5 are negative regulators of silencing at HMR. This study revealed that SAS4 and SAS5 contribute to silencing at HML and the telomeres, indicating that SAS4 and SAS5 are positive regulators of silencing at these loci. These paradoxical locus-specific phenotypes are shared with null alleles of SAS2 and are unique among phenotypes of mutations in other known regulators of silencing. This work also determined that these SAS genes play roles that are redundant with SIR1 at HML, yet distinct from SIR1 at HMR. Furthermore, these SAS genes are not redundant with each other in silencing HML. Collectively, these data suggest that SAS2, SAS4, and SAS5 constitute a novel class of regulators of silencing and reveal fundamental differences in the regulation of silencing at HML and HMR. We provide evidence for a model that accounts for the observation that these SAS genes are both positive and negative regulators of silencing.

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