scholarly journals The Drosophila SWI/SNF chromatin-remodeling complexes BAP and PBAP play separate roles in regulating growth and cell fate during regeneration

2018 ◽  
Author(s):  
Yuan Tian ◽  
Rachel K. Smith-Bolton
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Chromatin Remodeling ◽  
Tissue Regeneration ◽  
Wing Disc ◽  
Epithelial Tissue ◽  
Growth Promoter ◽  
Jnk Signaling ◽  
Regenerative Growth ◽  
Chromatin Remodeling Complexes

AbstractTo regenerate, damaged tissue must heal the wound, regrow to the proper size, replace the correct cell types, and return to the normal gene-expression program. However, the mechanisms that temporally and spatially control the activation or repression of important genes during regeneration are not fully understood. To determine the role that chromatin modifiers play in regulating gene expression after tissue damage, we induced ablation in Drosophila imaginal wing discs, and screened for chromatin regulators that are required for epithelial tissue regeneration. Here we show that many of these genes are indeed important for promoting or constraining regeneration. Specifically, the two SWI/SNF chromatin-remodeling complexes play distinct roles in regulating different aspects of regeneration. The PBAP complex regulates regenerative growth and developmental timing, and is required for the expression of JNK signaling targets and the growth promoter Myc. By contrast, the BAP complex ensures correct patterning and cell fate by stabilizing expression of the posterior gene engrailed. Thus, both SWI/SNF complexes are essential for proper gene expression during tissue regeneration, but they play distinct roles in regulating growth and cell fate.Summary statementDuring regeneration of the Drosophila wing disc, the SWI/SNF PBAP complex is required for regenerative growth and expression of JNK signaling targets, while the BAP complex maintains posterior cell fate.

scholarly journals Regulation of growth and cell fate during tissue regeneration by the two SWI/SNF chromatin-remodeling complexes of Drosophila

Genetics ◽  
2020 ◽  
Vol 217 (1) ◽  
Author(s):  
Yuan Tian ◽  
Rachel K Smith-Bolton
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Chromatin Remodeling ◽  
Tissue Regeneration ◽  
Cell Types ◽  
Epithelial Tissue ◽  
Growth Promoter ◽  
Chromatin Regulators ◽  
Proper Size ◽  
Chromatin Remodeling Complexes

Abstract To regenerate, damaged tissue must heal the wound, regrow to the proper size, replace the correct cell types, and return to the normal gene-expression program. However, the mechanisms that temporally and spatially control the activation or repression of important genes during regeneration are not fully understood. To determine the role that chromatin modifiers play in regulating gene expression after tissue damage, we induced ablation in Drosophila melanogaster imaginal wing discs, and screened for chromatin regulators that are required for epithelial tissue regeneration. Here, we show that many of these genes are indeed important for promoting or constraining regeneration. Specifically, the two SWI/SNF chromatin-remodeling complexes play distinct roles in regulating different aspects of regeneration. The PBAP complex regulates regenerative growth and developmental timing, and is required for the expression of JNK signaling targets and the growth promoter Myc. By contrast, the BAP complex ensures correct patterning and cell fate by stabilizing the expression of the posterior gene engrailed. Thus, both SWI/SNF complexes are essential for proper gene expression during tissue regeneration, but they play distinct roles in regulating growth and cell fate.

scholarly journals Mammalian SWI/SNF Chromatin Remodeling Complexes in Embryonic Stem Cells: Regulating the Balance Between Pluripotency and Differentiation

2021 ◽  
Vol 8 ◽  
Author(s):  
Ying Ye ◽  
Xi Chen ◽  
Wensheng Zhang
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Cell Fate ◽  
Chromatin Remodeling ◽  
Molecular Mechanisms ◽  
Embryonic Stem ◽  
Self Renewal ◽  
Baf Complex ◽  
Chromatin Remodeling Complexes

The unique capability of embryonic stem cells (ESCs) to maintain and adjust the equilibrium between self-renewal and multi-lineage cellular differentiation contributes indispensably to the integrity of all developmental processes, leading to the advent of an organism in its adult form. The ESC fate decision to favor self-renewal or differentiation into specific cellular lineages largely depends on transcriptome modulations through gene expression regulations. Chromatin remodeling complexes play instrumental roles to promote chromatin structural changes resulting in gene expression changes that are key to the ESC fate choices governing the equilibrium between pluripotency and differentiation. BAF (Brg/Brahma-associated factors) or mammalian SWI/SNF complexes employ energy generated by ATP hydrolysis to change chromatin states, thereby governing the accessibility of transcriptional regulators that ultimately affect transcriptome and cell fate. Interestingly, the requirement of BAF complex in self-renewal and differentiation of ESCs has been recently shown by genetic studies through gene expression modulations of various BAF components in ESCs, although the precise molecular mechanisms by which BAF complex influences ESC fate choice remain largely underexplored. This review surveys these recent progresses of BAF complex on ESC functions, with a focus on its role of conditioning the pluripotency and differentiation balance of ESCs. A discussion of the mechanistic bases underlying the genetic requirements for BAF in ESC biology as well as the outcomes of its interplays with key transcription factors or other chromatin remodelers in ESCs will be highlighted.

scholarly journals The Circadian NAD+Metabolism: Impact on Chromatin Remodeling and Aging

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Yasukazu Nakahata ◽  
Yasumasa Bessho
Keyword(s):  
Gene Expression ◽  
Circadian Clock ◽  
Cell Fate ◽  
Chromatin Remodeling ◽  
Expression Patterns ◽  
Fine Tuning ◽  
Cellular Functions ◽  
Nad Metabolism ◽  
Structure Changes ◽  
Age Related

Gene expression is known to be a stochastic phenomenon. The stochastic gene expression rate is thought to be altered by topological change of chromosome and/or by chromatin modifications such as acetylation and methylation. Changes in mechanical properties of chromosome/chromatin by soluble factors, mechanical stresses from the environment, or metabolites determine cell fate, regulate cellular functions, or maintain cellular homeostasis. Circadian clock, which drives the expression of thousands of genes with 24-hour rhythmicity, has been known to be indispensable for maintaining cellular functions/homeostasis. During the last decade, it has been demonstrated that chromatin also undergoes modifications with 24-hour rhythmicity and facilitates the fine-tuning of circadian gene expression patterns. In this review, we cover data which suggests that chromatin structure changes in a circadian manner and that NAD+is the key metabolite for circadian chromatin remodeling. Furthermore, we discuss the relationship among circadian clock, NAD+metabolism, and aging/age-related diseases. In addition, the interventions of NAD+metabolism for the prevention and treatment of aging and age-related diseases are also discussed.

scholarly journals BRG1-Mediated Chromatin Remodeling Regulates Differentiation and Gene Expression of T Helper Cells

2008 ◽  
Vol 28 (24) ◽  
pp. 7274-7285 ◽  
Author(s):  
Andrea L. Wurster ◽  
Michael J. Pazin
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Chromatin Remodeling ◽  
Chromatin Structure ◽  
Target Genes ◽  
T Helper Cell ◽  
T Helper ◽  
T Helper 2 ◽  
Th2 Cytokine ◽  
Th2 Differentiation

ABSTRACT During T helper cell differentiation, distinct programs of gene expression play a key role in defining the immune response to an environmental challenge. How chromatin remodeling events at the associated cytokine loci control differentiation is not known. We found that the ATP-dependent remodeling enzyme subunit BRG1 was required for T helper 2 (Th2) differentiation and Th2 cytokine transcription. BRG1 binding to cytokine genes was regulated by the extent of differentiation, the extent of activation, and cell fate. BRG1 was required for some features of the chromatin structure in target genes (DNase I hypersensitivity and histone acetylation), suggesting that BRG1 remodeling activity was directly responsible for changes in gene expression. NFAT and STAT6 activity were required for BRG1 recruitment to the Th2 locus control region, and STAT6 associated with BRG1 in a differentiation-inducible manner, suggesting direct recruitment of BRG1 to the bound loci. Together, these findings suggest BRG1 interprets differentiation signals and plays a causal role in gene regulation, chromatin structure, and cell fate.

scholarly journals Hippo signaling promotes Ets21c-dependent apical cell extrusion in the Drosophila wing disc

2020 ◽  
Author(s):  
Xianlong Ai ◽  
Dan Wang ◽  
Junzheng Zhang ◽  
Jie Shen
Keyword(s):  
Basal Cell ◽  
Molecular Mechanisms ◽  
Apical Cell ◽  
Wing Disc ◽  
Epithelial Tissue ◽  
Hippo Signaling ◽  
Developmental Defects ◽  
Jnk Signaling ◽  
Signaling Activation ◽  
Cell Extrusion

ABSTRACTCell extrusion is a crucial regulator of epithelial tissue development and homeostasis. Epithelial cells undergoing apoptosis, bearing pathological mutations, and possessing developmental defects are actively extruded toward elimination. However, the molecular mechanisms of Drosophila epithelial cell extrusion are not fully understood. Here, we report that activation of the conserved Hippo (Hpo) signaling pathway induces both apical and basal cell extrusion in the Drosophila wing disc epithelia. We show that canonical Yorki targets Diap1, and that dMyc and Cyclin E are not required for either apical or basal cell extrusion induced by activation of this pathway. Another target gene, bantam, is only involved in basal cell extrusion, suggesting novel Hpo-regulated apical cell extrusion mechanisms. Using RNA-Seq analysis, we found that JNK signaling is activated in the extruding cells. We provide genetic evidence that JNK signaling activation is both sufficient and necessary for Hpo-regulated cell extrusion. Furthermore, we demonstrate that the ETS-domain transcription factor Ets21c, an ortholog of proto-oncogenes FLI1 and ERG, acts downstream of JNK signaling to mediate apical cell extrusion. Our findings reveal a novel molecular link between Hpo signaling and cell extrusion.SUMMARY STATEMENTActivation of Hippo signaling induces cell extrusion in the Drosophila wing epithelia, in which bantam mediates basal cell extrusion and Ets21c mediates apical cell extrusion.

scholarly journals Epigenetic Induction of Definitive and Pancreatic Endoderm Cell Fate in Human Fibroblasts

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Rangarajan Sambathkumar ◽  
Eric Kalo ◽  
Rob Van Rossom ◽  
Marijke M. Faas ◽  
Paul de Vos ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Chromatin Remodeling ◽  
Dna Methyltransferase ◽  
Epigenetic Modification ◽  
Trichostatin A ◽  
Human Fibroblasts ◽  
Marker Genes ◽  
Deacetylase Inhibitor ◽  
Affect Gene Expression

Reprogramming can occur by the introduction of key transcription factors (TFs) as well as by epigenetic changes. We demonstrated that histone deacetylase inhibitor (HDACi) Trichostatin A (TSA) combined with a chromatin remodeling medium (CRM) induced expression of a number of definitive endoderm and early and late pancreatic marker genes. When CRM was omitted, endoderm/pancreatic marker genes were not induced. Furthermore, treatment with DNA methyltransferase inhibitor (DNMTi) 5-azacytidine (5AZA) CRM did not affect gene expression changes, and when 5AZA was combined with TSA, no further increase in gene expression of endoderm, pancreatic endoderm, and endocrine markers was seen over levels induced with TSA alone. Interestingly, TSA-CRM did not affect expression of pluripotency and hepatocyte genes but induced some mesoderm transcripts. Upon removal of TSA-CRM, the endoderm/pancreatic gene expression profile returned to baseline. Our findings underscore the role epigenetic modification in transdifferentiation of one somatic cell into another. However, full reprogramming of fibroblasts to β-cells will require combination of this approach with TF overexpression and/or culture of the partially reprogrammed cells under β-cell specific conditions.

scholarly journals A Novel Mechanism of Antagonism between ATP-Dependent Chromatin Remodeling Complexes Regulates RNR3 Expression

2009 ◽  
Vol 29 (12) ◽  
pp. 3255-3265 ◽  
Author(s):  
Raghuvir S. Tomar ◽  
James N. Psathas ◽  
Hesheng Zhang ◽  
Zhengjian Zhang ◽  
Joseph C. Reese
Keyword(s):  
Gene Expression ◽  
Chromatin Remodeling ◽  
Chromatin Structure ◽  
Large Subunit ◽  
Nucleosome Positioning ◽  
Gene Encoding ◽  
Control Of Gene Expression ◽  
Dna Binding Factors ◽  
Chromatin Remodeling Complexes

ABSTRACT Gene expression depends upon the antagonistic actions of chromatin remodeling complexes. While this has been studied extensively for the enzymes that covalently modify the tails of histones, the mechanism of how ATP-dependent remodeling complexes antagonize each other to maintain the proper level of gene activity is not known. The gene encoding a large subunit of ribonucleotide reductase, RNR3, is regulated by ISW2 and SWI/SNF, complexes that repress and activate transcription, respectively. Here, we studied the functional interactions of these two complexes at RNR3. Deletion of ISW2 causes constitutive recruitment of SWI/SNF, and conditional reexpression of ISW2 causes the repositioning of nucleosomes and reduced SWI/SNF occupancy at RNR3. Thus, ISW2 is required for restriction of access of SWI/SNF to the RNR3 promoter under the uninduced condition. Interestingly, the binding of sequence-specific DNA binding factors and the general transcription machinery are unaffected by the status of ISW2, suggesting that disruption of nucleosome positioning does not cause a nonspecific increase in cross-linking of all factors to RNR3. We provide evidence that ISW2 does not act on SWI/SNF directly but excludes its occupancy by positioning nucleosomes over the promoter. Genetic disruption of nucleosome positioning by other means led to a similar phenotype, linking repressed chromatin structure to SWI/SNF exclusion. Thus, incorporation of promoters into a repressive chromatin structure is essential for prevention of the opportunistic actions of nucleosome-disrupting activities in vivo, providing a novel mechanism for maintaining tight control of gene expression.

scholarly journals Hippo signaling promotes Ets21c-dependent apical cell extrusion in the Drosophila wing disc

Development ◽  
2020 ◽  
Vol 147 (22) ◽  
pp. dev190124
Author(s):  
Xianlong Ai ◽  
Dan Wang ◽  
Junzheng Zhang ◽  
Jie Shen
Keyword(s):  
Basal Cell ◽  
Molecular Mechanisms ◽  
Apical Cell ◽  
Wing Disc ◽  
Epithelial Tissue ◽  
Hippo Signaling ◽  
Developmental Defects ◽  
Jnk Signaling ◽  
Signaling Activation ◽  
Cell Extrusion

ABSTRACTCell extrusion is a crucial regulator of epithelial tissue development and homeostasis. Epithelial cells undergoing apoptosis, bearing pathological mutations or possessing developmental defects are actively extruded toward elimination. However, the molecular mechanisms of Drosophila epithelial cell extrusion are not fully understood. Here, we report that activation of the conserved Hippo (Hpo) signaling pathway induces both apical and basal cell extrusion in the Drosophila wing disc epithelia. We show that canonical Yorkie targets Diap1, Myc and Cyclin E are not required for either apical or basal cell extrusion induced by activation of this pathway. Another target gene, bantam, is only involved in basal cell extrusion, suggesting novel Hpo-regulated apical cell extrusion mechanisms. Using RNA-seq analysis, we found that JNK signaling is activated in the extruding cells. We provide genetic evidence that JNK signaling activation is both sufficient and necessary for Hpo-regulated cell extrusion. Furthermore, we demonstrate that the ETS-domain transcription factor Ets21c, an ortholog of proto-oncogenes FLI1 and ERG, acts downstream of JNK signaling to mediate apical cell extrusion. Our findings reveal a novel molecular link between Hpo signaling and cell extrusion.

scholarly journals Transcriptional Coactivators Are Not Required for Herpes Simplex Virus Type 1 Immediate-Early Gene Expression In Vitro

2009 ◽  
Vol 83 (8) ◽  
pp. 3436-3449 ◽  
Author(s):  
Sebla B. Kutluay ◽  
Sarah L. DeVos ◽  
Jennifer E. Klomp ◽  
Steven J. Triezenberg
Keyword(s):  
Gene Expression ◽  
Chromatin Remodeling ◽  
Cultured Cells ◽  
Histone Acetyltransferases ◽  
Gene Promoters ◽  
Transcriptional Coactivators ◽  
Chromatin Remodeling Complexes ◽  
Simplex Virus

ABSTRACT Virion protein 16 (VP16) of herpes simplex virus type 1 (HSV-1) is a potent transcriptional activator of viral immediate-early (IE) genes. The VP16 activation domain can recruit various transcriptional coactivators to target gene promoters. However, the role of transcriptional coactivators in HSV-1 IE gene expression during lytic infection had not been fully defined. We showed previously that transcriptional coactivators such as the p300 and CBP histone acetyltransferases and the BRM and Brg-1 chromatin remodeling complexes are recruited to viral IE gene promoters in a manner dependent mostly on the presence of the activation domain of VP16. In this study, we tested the hypothesis that these transcriptional coactivators are required for viral IE gene expression during infection of cultured cells. The disrupted expression of the histone acetyltransferases p300, CBP, PCAF, and GCN5 or the BRM and Brg-1 chromatin remodeling complexes did not diminish IE gene expression. Furthermore, IE gene expression was not impaired in cell lines that lack functional p300, or BRM and Brg-1. We also tested whether these coactivators are required for the VP16-dependent induction of IE gene expression from transcriptionally inactive viral genomes associated with high levels of histones in cultured cells. We found that the disruption of coactivators also did not affect IE gene expression in this context. Thus, we conclude that the transcriptional coactivators that can be recruited by VP16 do not contribute significantly to IE gene expression during lytic infection or the induction of IE gene expression from nucleosomal templates in vitro.

scholarly journals Roles of the INO80 and SWR1 Chromatin Remodeling Complexes in Plants

2019 ◽  
Vol 20 (18) ◽  
pp. 4591 ◽  
Author(s):  
Jianhao Wang ◽  
Sujuan Gao ◽  
Xiuling Peng ◽  
Keqiang Wu ◽  
Songguang Yang
Keyword(s):  
Gene Expression ◽  
Arabidopsis Thaliana ◽  
Gene Regulation ◽  
Dna Replication ◽  
Chromatin Remodeling ◽  
Eukaryotic Genes ◽  
Eukaryotic Gene ◽  
Chromatin Remodeling Complexes ◽  
Eukaryotic Gene Regulation ◽  
Environmental Responses

Eukaryotic genes are packed into a dynamic but stable nucleoprotein structure called chromatin. Chromatin-remodeling and modifying complexes generate a dynamic chromatin environment that ensures appropriate DNA processing and metabolism in various processes such as gene expression, as well as DNA replication, repair, and recombination. The INO80 and SWR1 chromatin remodeling complexes (INO80-c and SWR1-c) are ATP-dependent complexes that modulate the incorporation of the histone variant H2A.Z into nucleosomes, which is a critical step in eukaryotic gene regulation. Although SWR1-c has been identified in plants, plant INO80-c has not been successfully isolated and characterized. In this review, we will focus on the functions of the SWR1-c and putative INO80-c (SWR1/INO80-c) multi-subunits and multifunctional complexes in Arabidopsis thaliana. We will describe the subunit compositions of the SWR1/INO80-c and the recent findings from the standpoint of each subunit and discuss their involvement in regulating development and environmental responses in Arabidopsis.

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