scholarly journals The SWI/SNF ATP-Dependent Chromatin Remodeling Complex in Arabidopsis Responds to Environmental Changes in Temperature-Dependent Manner

2020 ◽  
Vol 21 (3) ◽  
pp. 762 ◽  
Author(s):  
Dominika M. Gratkowska-Zmuda ◽  
Szymon Kubala ◽  
Elzbieta Sarnowska ◽  
Pawel Cwiek ◽  
Paulina Oksinska ◽  
...  
Keyword(s):  
Plant Growth ◽  
Chromatin Remodeling ◽  
Target Genes ◽  
Environmental Changes ◽  
Fine Tuning ◽  
Regulation Of Transcription ◽  
Dependent Manner ◽  
Growth Responses ◽  
Nucleosome Remodeling ◽  
The Core

SWI/SNF ATP-dependent chromatin remodeling complexes (CRCs) play important roles in the regulation of transcription, cell cycle, DNA replication, repair, and hormone signaling in eukaryotes. The core of SWI/SNF CRCs composed of a SWI2/SNF2 type ATPase, a SNF5 and two of SWI3 subunits is sufficient for execution of nucleosome remodeling in vitro. The Arabidopsis genome encodes four SWI2/SNF2 ATPases, four SWI3, a single SNF5 and two SWP73 subunits. Genes of the core SWI/SNF components have critical but not fully overlapping roles during plant growth, embryogenesis, and sporophyte development. Here we show that the Arabidopsis swi3c mutant exhibits a phenotypic reversion when grown at lower temperature resulting in partial restoration of its embryo, root development and fertility defects. Our data indicates that the swi3c mutation alters the expression of several genes engaged in low temperature responses. The location of SWI3C-containing SWI/SNF CRCs on the ICE1, MYB15 and CBF1 target genes depends on the temperature conditions, and the swi3c mutation thus also influences the transcription of several cold-responsive (COR) genes. These findings, together with genetic analysis of swi3c/ice1 double mutant and enhanced freezing tolerance of swi3c plants illustrate that SWI/SNF CRCs contribute to fine-tuning of plant growth responses to different temperature regimes.

scholarly journals Transcriptional Suppression by Transient Recruitment of ARIP4 to Sumoylated Nuclear Receptor Ad4BP/SF-1

2009 ◽  
Vol 20 (19) ◽  
pp. 4235-4245 ◽  
Author(s):  
Hidesato Ogawa ◽  
Tomoko Komatsu ◽  
Yasushi Hiraoka ◽  
Ken-ichirou Morohashi
Keyword(s):  
Transcription Factors ◽  
Atpase Activity ◽  
Nuclear Receptors ◽  
Chromatin Remodeling ◽  
Target Genes ◽  
Fine Tuning ◽  
Binding Region ◽  
Interacting Protein ◽  
Double Stranded Dna ◽  
Transcriptional Suppression

The small ubiquitin-like modifier SUMO conjugates transcription factors and suppresses their respective activation of target genes. Although various SUMO-modified transcription factors have been isolated, mechanisms whereby sumoylated-substrates modulate transcription remain unknown. Here, we purified ARIP4 (AR interacting protein 4, a Rad54 family member and a SNF2 chromatin remodeling factor), which interacts with sumoylated Ad4BP/SF-1 through two SUMO-interacting motifs and one Ad4BP/SF-1–binding region. Remarkably, ARIP4 also interacts selectively with other sumoylated nuclear receptors including LRH-1, AR, and GR. Interestingly, the ATPase activity of ARIP4 was stimulated in the presence of sumoylated Ad4BP/SF-1 and the Ad4BP/SF-1–binding site containing double-stranded DNA. ChIP assays and siRNA studies strongly suggested that ARIP4 temporally suppresses Ad4BP/SF-1–mediated transcription through its transient recruitment to target genes. These findings suggest that ARIP4 may be a cofactor that modulates SUMO-mediated fine-tuning of transcriptional suppression.

scholarly journals Brassinosteroid Signaling Pathways Interplaying with Diverse Signaling Cues for Crop Enhancement

Agronomy ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 556
Author(s):  
Hyeona Hwang ◽  
Hojin Ryu ◽  
Hyunwoo Cho
Keyword(s):  
Plant Growth ◽  
Signaling Pathways ◽  
Stress Responses ◽  
Environmental Changes ◽  
Crop Yields ◽  
Crop Improvement ◽  
Fine Tuning ◽  
Model Organisms ◽  
Diverse Range ◽  
Recent Advances

The signaling pathways of brassinosteroids (BRs), a unique plant steroid hormone, are critically involved in a diverse range of plant growth and developmental processes as well as many important agronomic traits. Recent advances in the understanding of BR biosynthetic and signaling pathways in model organisms and crops have increased the feasibility of modulating BR responses in crop plants to enhance adaptation to various vulnerable environmental changes. In particular, the identification and functional analysis of BR signaling components in rice (Oryza sativa) present the possibility of their utilization to improve many agricultural traits involved in crop yields. In this review, we summarize recent advances and progress in the understanding of the BR signaling pathway and its interactions with diverse internal and external signaling cues. We also discuss how these physiological modulations of BR and the abundant signaling crosstalk can be applied to enhance rice productivity through the manipulation of plant architecture and fine-tuning of stress responses. Finally, we discuss how the complex regulation of BR signaling pathways could favor application in the molecular design of plant growth and development, precise breeding strategies, and cultivation methods for rice crop improvement.

Nucleosome organization and targeting of SWI/SNF chromatin-remodeling complexes: contributions of the DNA sequenceThis paper is one of a selection of papers published in this Special Issue, entitled 28th International West Coast Chromatin and Chromosomes Conference, and has undergone the Journal's usual peer review process.

2007 ◽  
Vol 85 (4) ◽  
pp. 419-425 ◽  
Author(s):  
Martin Montecino ◽  
Janet L. Stein ◽  
Gary S. Stein ◽  
Jane B. Lian ◽  
Andre J. van Wijnen ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Transcriptional Activation ◽  
Molecular Mechanisms ◽  
Protein Complexes ◽  
Peer Review Process ◽  
Gene Promoter ◽  
Limited Attention ◽  
Dependent Manner ◽  
Nucleosome Remodeling ◽  
Eukaryotic Genes

Chromatin organization within the nuclear compartment is a fundamental mechanism to regulate the expression of eukaryotic genes. During the last decade, a number of nuclear protein complexes with the ability to remodel chromatin and regulate gene transcription have been reported. Among these complexes is the SWI/SNF family, which alters chromatin structure in an ATP-dependent manner. A considerable effort has been made to understand the molecular mechanisms by which SWI/SNF catalyzes nucleosome remodeling. However, limited attention has been dedicated to studying the role of the DNA sequence in this remodeling process. Therefore, in this minireview, we discuss the contribution of nucleosome positioning and nucleosome excluding sequences to the targeting and activity of SWI/SNF complexes. This discussion includes results from our group using the rat osteocalcin gene promoter as a model. Based on these results, we postulate a model for chromatin remodeling and transcriptional activation of this gene in osteoblastic cells.

scholarly journals lncRNA transcription induces meiotic recombination through chromatin remodelling in fission yeast

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Satoshi Senmatsu ◽  
Ryuta Asada ◽  
Arisa Oda ◽  
Charles S. Hoffman ◽  
Kunihiro Ohta ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Chromatin Remodeling ◽  
Meiotic Recombination ◽  
Consensus Sequence ◽  
Metabolic Stress ◽  
Strand Break ◽  
Upstream Region ◽  
Yeast Genome ◽  
Regulation Of Transcription ◽  
Dependent Manner

AbstractNoncoding RNAs (ncRNAs) are involved in various biological processes, including gene expression, development, and disease. Here, we identify a novel consensus sequence of a cis-element involved in long ncRNA (lncRNA) transcription and demonstrate that lncRNA transcription from this cis-element activates meiotic recombination via chromatin remodeling. In the fission yeast fbp1 gene, glucose starvation induces a series of promoter-associated lncRNAs, referred to as metabolic-stress-induced lncRNAs (mlonRNAs), which contribute to chromatin remodeling and fbp1 activation. Translocation of the cis-element required for mlonRNA into a well-characterized meiotic recombination hotspot, ade6-M26, further stimulates transcription and meiotic recombination via local chromatin remodeling. The consensus sequence of this cis-element (mlon-box) overlaps with meiotic recombination sites in the fission yeast genome. At one such site, the SPBC24C6.09c upstream region, meiotic double-strand break (DSB) formation is induced in an mlon-box-dependent manner. Therefore, mlonRNA transcription plays a universal role in chromatin remodeling and the regulation of transcription and recombination.

scholarly journals Apigenin Inhibits the Growth of Hepatocellular Carcinoma Cells by Affecting the Expression of microRNA Transcriptome

2021 ◽  
Vol 11 ◽  
Author(s):  
Shou-Mei Wang ◽  
Pei-Wei Yang ◽  
Xiao-Jun Feng ◽  
Yi-Wei Zhu ◽  
Feng-Jun Qiu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Dependent Manner ◽  
Regulatory Pathways ◽  
The Core ◽  
Huh7 Cells

BackgroundApigenin, as a natural flavonoid, has low intrinsic toxicity and has potential pharmacological effects against hepatocellular carcinoma (HCC). However, the molecular mechanisms involving microRNAs (miRNAs) and their target genes regulated by apigenin in the treatment of HCC have not been addressed.ObjectiveIn this study, the molecular mechanisms of apigenin involved in the prevention and treatment of HCC were explored in vivo and in vitro using miRNA transcriptomic sequencing to determine the basis for the clinical applications of apigenin in the treatment of HCC.MethodsThe effects of apigenin on the proliferation, cell cycle progression, apoptosis, and invasion of human hepatoma cell line Huh7 and Hep3B were studied in vitro, and the effects on the tumorigenicity of Huh7 cells were assessed in vivo. Then, a differential expression analysis of miRNAs regulated by apigenin in Huh7 cells was performed using next-generation RNA sequencing and further validated by qRT-PCR. The potential genes targeted by the differentially expressed miRNAs were identified using a curated miRTarBase miRNA database and their molecular functions were predicted using Gene Ontology and KEGG signaling pathway analysis.ResultsCompared with the control treatment group, apigenin significantly inhibited Huh7 cell proliferation, cell cycle, colony formation, and cell invasion in a concentration-dependent manner. Moreover, apigenin reduced tumor growth, promoted tumor cell necrosis, reduced the expression of Ki67, and increased the expression of Bax and Bcl-2 in the xenograft tumors of Huh7 cells. Bioinformatics analysis of the miRNA transcriptome showed that hsa-miR-24, hsa-miR-6769b-3p, hsa-miR-6836-3p, hsa-miR-199a-3p, hsa-miR-663a, hsa-miR-4739, hsa-miR-6892-3p, hsa-miR-7107-5p, hsa-miR-1273g-3p, hsa-miR-1343, and hsa-miR-6089 were the most significantly up-regulated miRNAs, and their key gene targets were MAPK1, PIK3CD, HRAS, CCND1, CDKN1A, E2F2, etc. The core regulatory pathways of the up-regulated miRNAs were associated with the hepatocellular carcinoma pathway. The down-regulated miRNAs were hsa-miR-181a-5p and hsa-miR-148a-3p, and the key target genes were MAPK1, HRAS, STAT3, FOS, BCL2, SMAD2, PPP3CA, IFNG, MET, and VAV2, with the core regulatory pathways identified as proteoglycans in cancer pathway.ConclusionApigenin can inhibit the growth of HCC cells, which may be mediated by up-regulation or down-regulation of miRNA molecules and their related target genes.

scholarly journals Regulation of Transcription Factor SP1 by the β-Catenin Destruction Complex Modulates Wnt Response

2018 ◽  
Vol 38 (22) ◽  
Author(s):  
Rafeeq Mir ◽  
Ankita Sharma ◽  
Saurabh J. Pradhan ◽  
Sanjeev Galande
Keyword(s):  
Transcription Factor ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Target Genes ◽  
Glycogen Synthase ◽  
Wnt Signaling Pathway ◽  
Feedback Mechanism ◽  
Regulation Of Transcription ◽  
Dependent Manner ◽  
Factor Specificity

ABSTRACT The ubiquitous transcription factor specificity protein 1 (SP1) is heavily modified posttranslationally. These modifications are critical for switching its functions and modulation of its transcriptional activity and DNA binding and stability. However, the mechanism governing the stability of SP1 by cellular signaling pathways is not well understood. Here, we provide biochemical and functional evidence that SP1 is an integral part of the Wnt signaling pathway. We identified a phosphodegron motif in SP1 that is specific to mammals. In the absence of Wnt signaling, glycogen synthase kinase 3β (GSK3β)-mediated phosphorylation and β-TrCP E3 ubiquitin ligase-mediated ubiquitination are required to induce SP1 degradation. When Wnt signaling is on, SP1 is stabilized in a β-catenin-dependent manner. SP1 directly interacts with β-catenin, and Wnt signaling induces the stabilization of SP1 by impeding its interaction with β-TrCP and axin1, components of the destruction complex. Wnt signaling suppresses ubiquitination and subsequent proteosomal degradation of SP1. Furthermore, SP1 regulates Wnt-dependent stability of β-catenin and their mutual stabilization is critical for target gene expression, suggesting a feedback mechanism. Upon stabilization, SP1 and β-catenin cooccupy the promoters of TCFL2/β-catenin target genes. Collectively, this study uncovers a direct link between SP1 and β-catenin in the Wnt signaling pathway.

scholarly journals Regulation of transcription factor SP1 by β-catenin destruction complex modulates Wnt response

2018 ◽  
Author(s):  
Rafeeq Mir ◽  
Ankita Sharma ◽  
Saurabh J. Pradhan ◽  
Sanjeev Galande
Keyword(s):  
Transcription Factor ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Target Genes ◽  
Wnt Signaling Pathway ◽  
Feedback Mechanism ◽  
Regulation Of Transcription ◽  
Dependent Manner ◽  
Factor Specificity ◽  
The Stability

AbstractThe ubiquitous transcription factor Specificity protein 1 (SP1) is heavily modified post-translationally. These modifications are critical for switching its functions and modulation of its transcriptional activity, DNA-binding and stability. However the mechanism governing the stability of SP1 by cellular signaling pathways is not well understood. Here, we provide biochemical and functional evidences that SP1 is an integral part of the Wnt signaling pathway. We identified a phosphodegron motif in SP1 that is specific to mammals. In absence of Wnt signaling, GSK3β kinase mediated phosphorylation and β-TrCP E3 ubiquitin ligase mediated ubiquitination is required to induce SP1 degradation. When Wnt signaling is on, SP1 is stabilized in β-catenin-dependent manner. SP1 directly interacts with β-catenin and Wnt signaling induces the stabilization of SP1 by impeding its interaction with β-TrCP and AXIN1, components of the destruction complex. Wnt signaling suppresses ubiquitination and subsequent proteosomal degradation of SP1. Furthermore, SP1 regulates Wnt-dependent stability of β-catenin and their mutual stabilization is critical for target gene expression, suggesting a feedback mechanism. Upon stabilization SP1 and β-catenin co-occupy the promoters of TCFL2/β-catenin target genes. Collectively, this study uncovers a direct link between SP1 and β-catenin in Wnt signaling pathway.

scholarly journals GFI1 tethers the NuRD complex to open and transcriptionally active chromatin in myeloid progenitors

2021 ◽  
Author(s):  
Anne Helness ◽  
Jennifer Fraszczak ◽  
Charles Joly-Beauparlant ◽  
Halil Bagci ◽  
Christian Trahan ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Target Genes ◽  
Myeloid Differentiation ◽  
Open Chromatin ◽  
Nurd Complex ◽  
Active Chromatin ◽  
Nucleosome Remodeling ◽  
Nucleosome Organization ◽  
Active Transcription ◽  
Neutrophil Differentiation

Abstract GFI1 is a SNAG-domain, DNA binding transcriptional repressor which controls myeloid differentiation, in particular the formation of neutrophils. Here we show that GFI1 interacts with the chromodomain helicase CHD4 and other components of the “Nucleosome remodeling and deacetylase” (NuRD) complex. In granulo-monocytic precursors, GFI1, CHD4 or GFI1/CHD4 complexes occupy sites of open chromatin enriched for histone marks associated with active transcription suggesting that GFI1 recruits the NuRD complex to target genes that are regulated by active or bivalent promoters and active enhancers. Our data also show that GFI1 and GFI1/CHD4 complexes occupy promoters of different sets of genes that are either enriched for IRF1 or SPI-1 consensus sites, respectively. During neutrophil differentiation, overall chromatin closure and depletion of H3K4me2 occurs at different degrees depending on whether GFI1, CHD4 or both are present, indicating that GFI1 affects the chromatin remodeling activity of the NuRD complex. Moreover, GFI1/CHD4 complexes regulate chromatin openness and histone modifications differentially to enable regulation of target genes affecting the signaling pathways of the immune response or nucleosome organization or cellular metabolic processes.

scholarly journals The Roles of Hippo Signaling Transducers Yap and Taz in Chromatin Remodeling

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 502 ◽  
Author(s):  
Ryan E. Hillmer ◽  
Brian A. Link
Keyword(s):  
Chromatin Remodeling ◽  
Transcriptional Control ◽  
Target Genes ◽  
Hippo Signaling ◽  
Major Pathway ◽  
Nucleosome Remodeling ◽  
Cellular Processes ◽  
Disease States ◽  
Chromatin Remodeling Complexes ◽  
Dna Packing

Hippo signaling controls cellular processes that ultimately impact organogenesis and homeostasis. Consequently, disease states including cancer can emerge when signaling is deregulated. The major pathway transducers Yap and Taz require cofactors to impart transcriptional control over target genes. Research into Yap/Taz-mediated epigenetic modifications has revealed their association with chromatin-remodeling complex proteins as a means of altering chromatin structure, therefore affecting accessibility and activity of target genes. Specifically, Yap/Taz have been found to associate with factors of the GAGA, Ncoa6, Mediator, Switch/sucrose nonfermentable (SWI/SNF), and Nucleosome Remodeling and Deacetylase (NuRD) chromatin-remodeling complexes to alter the accessibility of target genes. This review highlights the different mechanisms by which Yap/Taz collaborate with other factors to modify DNA packing at specific loci to either activate or repress target gene transcription.

Transcription Factor Bach1 and Bach2 Operate Erythro-Myeloid Competitive Differentiation By Responding to Environmental Changes

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2649-2649
Author(s):  
Hiroki Kato ◽  
Ari Itoh-Nakadai ◽  
Mitsuyo Matsumoto ◽  
Risa Ebina-Shibuya ◽  
Yuki Sato ◽  
...  
Keyword(s):  
Target Genes ◽  
Environmental Changes ◽  
Bone Marrow Cells ◽  
Conflicts Of Interest ◽  
Lymphoid Cells ◽  
Myeloid Differentiation ◽  
Dependent Manner ◽  
Double Knockout ◽  
Hematopoietic Stem ◽  
Expression Levels

Abstract Hematopoietic system is maintained by the differentiation and proliferation of hematopoietic stem/progenitor cells (HSPCs) and their commitment to the mature blood cells should be tightly controlled by gene regulatory networks (GRNs) governed by transcription factors (TFs). To keep the homeostasis, GRNs should respond to the environmental changes, such as infection. However, the precise mechanism of such a system remains to be elucidated. TFs Bach1 and Bach2 belong to the basic region-leucine zipper family and recognize Maf-recognition elements containing AP-1 site (Oyake et al., 1996). We have previously shown that Bach1-/-Bach2-/-(DKO; double knockout) mice show erythropoiesis disorders with increased myelopoiesis from common myeloid progenitors (CMPs), which is an erythro-myeloid bifurcation point (ASH2015; Abstract ID# 81562) (Akashi et al., 2000). Since this phenotype is similar to that of LPS treated mice (O'Connell et al., 2008), we hypothesized that Bach factors work as sensors for infection. First, to evaluate the cell-intrinsic function of Bach factors, WT or DKO bone marrow cells were depleted of mature differentiated cells and transplanted to lethally irradiated WT mice. After 8 weeks, DKO donor cells showed greater myelopoiesis and lesser lymphogenesis compared to WT, suggesting Bach factors are necessary to suppress myelopoiesis to the appropriate level in regenerating hematopoiesis. To reveals the function of Bach factors in HSPCs from other aspect, LSKs (Lin-Sca1+c-kit+) were infected with retroviruses expressing Bach1-IRES-eGFP or Bach2-IRES-eGFP and transplanted to lethally irradiated WT mice. Cells derived from transgene induced LSKs were monitored by GFP fluorescence. After 2 weeks, Bach1 overexpressing LSKs did not show any difference in erythropoiesis and myelopoiesis. This might be explained by the high Bach1 expression levels in HSPCs according to the previous report (Lara-Astiaso et al., 2014). On the other hand, Bach2 overexpressing LSKs showed increased erythropoiesis and decreased myelopoiesis, suggesting that Bach2 regulates the erythro-myeloid lineage specification as expected by the observations of DKO mice. To assess the function of Bach factors under infection, we used M1 murine myeloid leukemia cells that differentiate to macrophage-like cells by LPS stimulation. LPS stimulation reduced expressions of Bach1, Bach2 and erythroid gene Gata1, and induced those of myeloid genes such as Cebpb and Csf1rin a dose-dependent manner. To determine if down-regulation of Bach factors is necessary for myeloid differentiation, Bach1 or Bach2 were transgenically overexpressed in M1 cells. Both of the M1 cells overexpressing Bach1 or Bach2 showed lower expression levels of myeloid marker CD11b compared to control under LPS stimulation. Thus, reductions of the expression of Bach factors in response to LPS were necessary for appropriate myeloid differentiation. To identify the direct target genes of Bach factors, Bach1 or Bach2 ChIP-seq data of M1 cells (Ebina-Shibuya et al., 2016) were merged with results of expression profile of WT and DKO CMPs. Several myeloid or inflammatory genes such as Cebpb, Fcgr1 and Tlr4 were identified as putative repressed target genes and several erythroid or lymphoid genes such as Klf1, Rag1 and Rag2 were identified as putative activated target genes. In addition, when Bach1 or Bach2 ChIP-seq data were merged by that of C/EBPb, which also possesses AP-1 site as its target motif, obtained from ENCODE database (ENCSR000AIB), we found that there were several co-localized regions of Bach and C/EBPb near the myeloid genes such as Cebpa, Il6 and Fcgr1. These observations suggest that Bach factors repress myeloid genes by competitively working with C/EBPb at same genomic regions. This is particularly interesting in the light of the latest findings showing the Bach2 function on AP-1 site in lymphoid cells (Sidwell et al., 2016). These results reveal a novel mechanism by which how the differentiation of erythro-myeloid bifurcation is controlled by responding to environmental changes. Bach factors regulate erythro-myeloid competitive differentiation by promoting and repressing erythroid and myeloid differentiation, respectively. We suggest that infection promote myelopoiesis at the expense of erythropoiesis by reducing the expression of Bach factors. Therefore, Bach factors may function as sensors for environmental changes. Disclosures No relevant conflicts of interest to declare.

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