scholarly journals Dynamic histone acetylation in floral volatile synthesis and emission in petunia flowers

2021 ◽  
Author(s):  
Ryan M. Patrick ◽  
Xing-Qi Huang ◽  
Natalia Dudareva ◽  
Ying Li
Keyword(s):  
Transcriptional Activation ◽  
Metabolic Pathways ◽  
Transcriptional Repression ◽  
Metabolic Networks ◽  
Floral Scent ◽  
Underlying Mechanism ◽  
Expression Of Genes ◽  
Genome Wide ◽  
Chemical Inhibitors ◽  
Floral Volatile

ABSTRACTBiosynthesis of secondary metabolites relies on primary metabolic pathways to provide precursors, energy, and cofactors, thus requiring coordinated regulation of primary and secondary metabolic networks. However, to date it remains largely unknown how this coordination is achieved. Using Petunia hybrida flowers, which emit high levels of phenylpropanoid/benzenoid volatile organic compounds (VOCs), we uncovered genome-wide dynamic deposition of histone H3 lysine 9 acetylation (H3K9ac) during anthesis as an underlying mechanism to coordinate primary and secondary metabolic networks. The observed epigenome reprogramming is accompanied by transcriptional activation, at gene loci involved in primary metabolic pathways that provide precursor phenylalanine, as well as secondary metabolic pathways to produce volatile compounds. We also observed transcriptional repression among genes involved in alternative phenylpropanoid branches that compete for metabolic precursors. We show that GNAT family histone acetyltransferase(s) (HATs) are required for the expression of genes involved in VOC biosynthesis and emission, by using chemical inhibitors of HATs, and by knocking down a specific HAT, ELP3, through transient RNAi. Together, our study supports that chromatin level regulatory mechanisms may play an essential role in activating primary and secondary metabolic pathways to regulate VOC synthesis in petunia flowers.HIGHLIGHTOur study shows that posttranslational modification of histones is essential for regulating the biosynthesis and emission of floral scent compounds, thus providing insights into chromatin level regulation of secondary metabolism.

scholarly journals Dynamic histone acetylation in floral volatile synthesis and emission in petunia flowers

2021 ◽  
Author(s):  
Ryan M Patrick ◽  
Xing-Qi Huang ◽  
Natalia Dudareva ◽  
Ying Li
Keyword(s):  
Transcriptional Activation ◽  
Metabolic Pathways ◽  
Transcriptional Repression ◽  
Metabolic Networks ◽  
Underlying Mechanism ◽  
Expression Of Genes ◽  
Genome Wide ◽  
Chemical Inhibitors ◽  
Volatile Organic ◽  
Floral Volatile

Abstract Biosynthesis of secondary metabolites relies on primary metabolic pathways to provide precursors, energy, and cofactors, thus requiring coordinated regulation of primary and secondary metabolic networks. However, to date, it remains largely unknown how this coordination is achieved. Using Petunia hybrida flowers, which emit high levels of phenylpropanoid/benzenoid volatile organic compounds (VOCs), we uncovered genome-wide dynamic deposition of histone H3 lysine 9 acetylation (H3K9ac) during anthesis as an underlying mechanism to coordinate primary and secondary metabolic networks. The observed epigenome reprogramming is accompanied by transcriptional activation at gene loci involved in primary metabolic pathways that provide precursor phenylalanine, as well as secondary metabolic pathways to produce volatile compounds. We also observed transcriptional repression among genes involved in alternative phenylpropanoid branches that compete for metabolic precursors. We show that GNAT family histone acetyltransferase(s) (HATs) are required for the expression of genes involved in VOC biosynthesis and emission, by using chemical inhibitors of HATs, and by knocking down a specific HAT gene, ELP3, through transient RNAi. Together, our study supports that regulatory mechanisms at chromatin level may play an essential role in activating primary and secondary metabolic pathways to regulate VOC synthesis in petunia flowers.

scholarly journals Evolution of a novel and adaptive floral scent in wild tobacco

2019 ◽  
Author(s):  
Han Guo ◽  
Nathalie D. Lackus ◽  
Tobias G. Köllner ◽  
Ran Li ◽  
Julia Bing ◽  
...  
Keyword(s):  
Metabolic Pathways ◽  
Phenylalanine Ammonia Lyase ◽  
Floral Scent ◽  
Nicotiana Attenuata ◽  
Plant Environment ◽  
Intraspecific Variations ◽  
In The Wild ◽  
Isoflavone Reductase ◽  
Floral Volatile ◽  
Species Specific

AbstractMany plants emit diverse floral scents that mediate plant-environment interactions and attain reproductive success. However, how plants evolve novel adaptive floral volatiles remains unclear. Here, we show that in the wild tobacco, Nicotiana attenuata, a dominant species-specific floral volatile (benzyl acetone, BA) that attracts pollinators and deters florivore is synthesized by phenylalanine ammonia-lyase 4 (NaPAL4), isoflavone reductase 3 (NaIFR3), and chalcone synthase 3 (NaCHAL3). Transient expression of NaFIR3 alone in N. attenuata leaves is sufficient and necessary for ectopic foliar BA emissions, and the BA emission level is increased by co-expressing NaIFR3 with NaPAL4 and NaCHAL3. Independent changes in transcription in all three genes contributed to intraspecific variations of floral BA emission. However, among species, the gain-of-expression in NaIFR3 resulted in the biosynthesis of BA that was only found in N. attenuata. This study suggests that novel metabolic pathways associated with adaptation can arise via re-configurations of gene expression.

Regulation of subtelomeric fungal secondary metabolite genes by H3K4me3 regulators CclA and KdmB

2020 ◽  
Author(s):  
Yonathan Lukito ◽  
T Chujo ◽  
TK Hale ◽  
W Mace ◽  
LJ Johnson ◽  
...  
Keyword(s):  
Secondary Metabolite ◽  
Transcriptional Activation ◽  
Transcriptional Repression ◽  
Target Genes ◽  
H3k4 Methylation ◽  
Genome Wide ◽  
H3k4me3 Mark ◽  
Transcriptional Changes ◽  
Histone H3k4 ◽  
A Site

© 2019 John Wiley & Sons Ltd Studies on the regulation of fungal secondary metabolism highlight the importance of histone H3K4 methylation regulators Set1, CclA (Ash2) and KdmB (KDM5), but it remains unclear whether these proteins act by direct modulation of H3K4me3 at the target genes. In filamentous fungi, secondary metabolite genes are frequently located near telomeres, a site where H3K4 methylation is thought to have a repressive role. Here we analyzed the role of CclA, KdmB and H3K4me3 in regulating the subtelomeric EAS and LTM cluster genes in Epichloë festucae. Depletion of H3K4me3 correlated with transcriptional activation of these genes in ΔcclA, similarly enrichment of H3K4me3 correlated with transcriptional repression of the genes in ΔkdmB which was accompanied by significant reduction in the levels of the agriculturally undesirable lolitrems. These transcriptional changes could only be explained by the alterations in H3K4me3 and not in the subtelomerically-important marks H3K9me3/K27me3. However, H3K4me3 changes in both mutants were not confined to these regions but occurred genome-wide, and at other subtelomeric loci there were inconsistent correlations between H3K4me3 enrichment and gene repression. Our study suggests that CclA and KdmB are crucial regulators of secondary metabolite genes, but these proteins likely act via means independent to, or in conjunction with the H3K4me3 mark.

scholarly journals mSin3A/Histone Deacetylase 2- and PRMT5-Containing Brg1 Complex Is Involved in Transcriptional Repression of the Myc Target Gene cad

2003 ◽  
Vol 23 (21) ◽  
pp. 7475-7487 ◽  
Author(s):  
Sharmistha Pal ◽  
Romy Yun ◽  
Antara Datta ◽  
Lynne Lacomis ◽  
Hediye Erdjument-Bromage ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Transcriptional Activation ◽  
Transcriptional Repression ◽  
Target Genes ◽  
Carbamoyl Phosphate ◽  
Histone Deacetylase 2 ◽  
Protein Protein Interaction ◽  
Corepressor Complex ◽  
Expression Of Genes ◽  
In Cells

ABSTRACT The role of hSWI/SNF complexes in transcriptional activation is well characterized; however, little is known about their function in transcriptional repression. We have previously shown that subunits of the mSin3A/histone deacetylase 2 (HDAC2) corepressor complex copurify with hSWI/SNF complexes. Here we show that the type II arginine-specific methyltransferase PRMT5, which is involved in cyclin E repression, can be found in association with Brg1 and hBrm-based hSWI/SNF complexes. We also show that hSWI/SNF-associated PRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. Protein-protein interaction studies indicate that PRMT5 and mSin3A interact with the same hSWI/SNF subunits as those targeted by c-Myc. These observations prompted us to examine the expression profile of the c-Myc target genes, carbamoyl-phosphate synthase-aspartate carbamoyltransferase-dihydroorotase (cad) and nucleolin (nuc). We found that cad repression is altered in cells that express inactive Brg1 and in cells treated with the HDAC inhibitor depsipeptide. Using chromatin immunoprecipitation assays, we found that Brg1, mSin3A, HDAC2, and PRMT5 are directly recruited to the cad promoter. These results suggest that hSWI/SNF complexes, through their ability to interact with activator and repressor proteins, control expression of genes involved in cell growth and proliferation.

scholarly journals Evolution of a Novel and Adaptive Floral Scent in Wild Tobacco

2019 ◽  
Vol 37 (4) ◽  
pp. 1090-1099 ◽  
Author(s):  
Han Guo ◽  
Nathalie D Lackus ◽  
Tobias G Köllner ◽  
Ran Li ◽  
Julia Bing ◽  
...  
Keyword(s):  
Metabolic Pathways ◽  
Phenylalanine Ammonia Lyase ◽  
Floral Scent ◽  
Nicotiana Attenuata ◽  
Plant Environment ◽  
Intraspecific Variations ◽  
In The Wild ◽  
Isoflavone Reductase ◽  
Floral Volatile ◽  
Species Specific

Abstract Many plants emit diverse floral scents that mediate plant–environment interactions and attain reproductive success. However, how plants evolve novel and adaptive biosynthetic pathways for floral volatiles remains unclear. Here, we show that in the wild tobacco, Nicotiana attenuata, a dominant species-specific floral volatile (benzyl acetone, BA) that attracts pollinators and deters florivore is synthesized by phenylalanine ammonia-lyase 4 (NaPAL4), isoflavone reductase 3 (NaIFR3), and chalcone synthase 3 (NaCHAL3). Transient expression of NaFIR3 alone in N. attenuata leaves is sufficient and necessary for ectopic foliar BA emissions, and coexpressing NaIFR3 with NaPAL4 and NaCHAL3 increased the BA emission levels. Independent changes in transcription of NaPAL4 and NaCHAL3 contributed to intraspecific variations of floral BA emission. However, among species, the gain of expression of NaIFR3 resulted in the biosynthesis of BA, which was only found in N. attenuata. This study suggests that novel metabolic pathways associated with adaptation can arise via reconfigurations of gene expression.

scholarly journals RPA1 binding to NRF2 switches ARE-dependent transcriptional activation to ARE-NRE–dependent repression

2018 ◽  
Vol 115 (44) ◽  
pp. E10352-E10361 ◽  
Author(s):  
Pengfei Liu ◽  
Montserrat Rojo de la Vega ◽  
Saad Sammani ◽  
Joseph B. Mascarenhas ◽  
Michael Kerins ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Transcriptional Repression ◽  
Target Genes ◽  
Redox Homeostasis ◽  
Antioxidant Response ◽  
Rna Seq ◽  
Vascular Integrity ◽  
Genome Wide ◽  
Antioxidant Response Elements ◽  
Injury Models

NRF2 regulates cellular redox homeostasis, metabolic balance, and proteostasis by forming a dimer with small musculoaponeurotic fibrosarcoma proteins (sMAFs) and binding to antioxidant response elements (AREs) to activate target gene transcription. In contrast, NRF2-ARE–dependent transcriptional repression is unreported. Here, we describe NRF2-mediated gene repression via a specific seven-nucleotide sequence flanking the ARE, which we term the NRF2-replication protein A1 (RPA1) element (NRE). Mechanistically, RPA1 competes with sMAF for NRF2 binding, followed by interaction of NRF2-RPA1 with the ARE-NRE and eduction of promoter activity. Genome-wide in silico and RNA-seq analyses revealed this NRF2-RPA1-ARE-NRE complex mediates negative regulation of many genes with diverse functions, indicating that this mechanism is a fundamental cellular process. Notably, repression ofMYLK, which encodes the nonmuscle myosin light chain kinase, by the NRF2-RPA1-ARE-NRE complex disrupts vascular integrity in preclinical inflammatory lung injury models, illustrating the translational significance of NRF2-mediated transcriptional repression. Our findings reveal a gene-suppressive function of NRF2 and a subset of negatively regulated NRF2 target genes, underscoring the broad impact of NRF2 in physiological and pathological settings.

scholarly journals Locus of Enterocyte Effacement: A Pathogenicity Island Involved in the Virulence of Enteropathogenic and EnterohemorragicEscherichia coliSubjected to a Complex Network of Gene Regulation

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Fernanda M. Franzin ◽  
Marcelo P. Sircili
Keyword(s):  
Complex Network ◽  
Transcriptional Activation ◽  
Transcriptional Repression ◽  
Feedback Inhibition ◽  
Pathogenicity Island ◽  
Open Reading Frames ◽  
Severe Diarrhea ◽  
Expression Of Genes ◽  
Enterocyte Effacement ◽  
Reading Frames

The locus of enterocyte effacement (LEE) is a 35.6 kb pathogenicity island inserted in the genome of some bacteria such as enteropathogenicEscherichia coli, enterohemorrhagicE.coli,Citrobacter rodentium, andEscherichia albertii. LEE comprises the genes responsible for causing attaching and effacing lesions, a characteristic lesion that involves intimate adherence of bacteria to enterocytes, a signaling cascade leading to brush border and microvilli destruction, and loss of ions, causing severe diarrhea. It is composed of 41 open reading frames and five major operons encoding a type three system apparatus, secreted proteins, an adhesin, called intimin, and its receptor called translocated intimin receptor (Tir). LEE is subjected to various levels of regulation, including transcriptional and posttranscriptional regulators located both inside and outside of the pathogenicity island. Several molecules were described being related to feedback inhibition, transcriptional activation, and transcriptional repression. These molecules are involved in a complex network of regulation, including mechanisms such as quorum sensing and temporal control of LEE genes transcription and translation. In this mini review we have detailed the complex network that regulates transcription and expression of genes involved in this kind of lesion.

Regulation of subtelomeric fungal secondary metabolite genes by H3K4me3 regulators CclA and KdmB

2020 ◽  
Author(s):  
Yonathan Lukito ◽  
T Chujo ◽  
TK Hale ◽  
W Mace ◽  
LJ Johnson ◽  
...  
Keyword(s):  
Secondary Metabolite ◽  
Transcriptional Activation ◽  
Transcriptional Repression ◽  
Target Genes ◽  
H3k4 Methylation ◽  
Genome Wide ◽  
H3k4me3 Mark ◽  
Transcriptional Changes ◽  
Histone H3k4 ◽  
A Site

© 2019 John Wiley & Sons Ltd Studies on the regulation of fungal secondary metabolism highlight the importance of histone H3K4 methylation regulators Set1, CclA (Ash2) and KdmB (KDM5), but it remains unclear whether these proteins act by direct modulation of H3K4me3 at the target genes. In filamentous fungi, secondary metabolite genes are frequently located near telomeres, a site where H3K4 methylation is thought to have a repressive role. Here we analyzed the role of CclA, KdmB and H3K4me3 in regulating the subtelomeric EAS and LTM cluster genes in Epichloë festucae. Depletion of H3K4me3 correlated with transcriptional activation of these genes in ΔcclA, similarly enrichment of H3K4me3 correlated with transcriptional repression of the genes in ΔkdmB which was accompanied by significant reduction in the levels of the agriculturally undesirable lolitrems. These transcriptional changes could only be explained by the alterations in H3K4me3 and not in the subtelomerically-important marks H3K9me3/K27me3. However, H3K4me3 changes in both mutants were not confined to these regions but occurred genome-wide, and at other subtelomeric loci there were inconsistent correlations between H3K4me3 enrichment and gene repression. Our study suggests that CclA and KdmB are crucial regulators of secondary metabolite genes, but these proteins likely act via means independent to, or in conjunction with the H3K4me3 mark.

scholarly journals SET1B facilitates activation of the hypoxia response through site-specific histone methylation

2020 ◽  
Author(s):  
Brian Ortmann ◽  
Natalie Burrows ◽  
Peter Bailey ◽  
Ian Lobb ◽  
Ana Peñalver ◽  
...  
Keyword(s):  
Histone Methylation ◽  
Transcriptional Activation ◽  
Target Genes ◽  
Human Cancer ◽  
Selective Reduction ◽  
Low Oxygen ◽  
Site Specific ◽  
Human Cancer Cells ◽  
Expression Of Genes ◽  
Genome Wide

Abstract Hypoxia-inducible transcription factors (HIFs) are fundamental to the cellular adaptation to low oxygen levels but how they interact with chromatin and efficiently activate their target genes is unclear. Using genome-wide mutagenesis in human cancer cells, we define genes required for HIF transcriptional activation, and identify a requirement for the Histone 3 lysine 4 (H3K4) methyltransferase SET1B. Loss of SET1B leads to a selective reduction in HIF transcriptional activity in hypoxia, with SET1B driving expression of genes involved in angiogenesis rather than glycolysis, resulting in impaired tumour establishment in SET1B deficient xenografts. Mechanistically, we show that SET1B is itself oxygen regulated, accumulates on chromatin in hypoxia, and is recruited to HIF target genes through HIF-1α. Accordingly, we show that the hypoxic induction of H3K4me3 at specific HIF targets is both HIF and SET1B dependent, and when impaired, decreases promoter acetylation and gene expression. Together, these findings reveal SET1B as a determinant of site-specific histone methylation and provide insight into how HIF target genes are differentially regulated.

scholarly journals Deciphering the Roles of the Histone H2B N-Terminal Domain in Genome-Wide Transcription

2006 ◽  
Vol 26 (10) ◽  
pp. 3842-3852 ◽  
Author(s):  
Michael A. Parra ◽  
David Kerr ◽  
Deirdre Fahy ◽  
Derek J. Pouchnik ◽  
John J. Wyrick
Keyword(s):  
Posttranslational Modifications ◽  
Transcriptional Activation ◽  
Transcriptional Repression ◽  
Yeast Genome ◽  
Lysine Acetylation ◽  
Histone H2b ◽  
Terminal Domain ◽  
Genome Wide ◽  
Lysine Residues ◽  
Terminal Domains

ABSTRACT Histone N-terminal domains are frequent targets of posttranslational modifications. Multiple acetylated lysine residues have been identified in the N-terminal domain of H2B (K6, K11, K16, K17, K21, and K22), but little is known about how these modifications regulate transcription. We systematically mutated the N-terminal domain of histone H2B, both at known sites of lysine acetylation and elsewhere, and characterized the resulting changes in genome-wide expression in each mutant strain. Our results indicate that known sites of lysine acetylation in this domain are required for gene-specific transcriptional activation. However, the entire H2B N-terminal domain is principally required for the transcriptional repression of a large subset of the yeast genome. We find that the histone H2B repression (HBR) domain, comprised of residues 30 to 37, is necessary and sufficient for this repression. Many of the genes repressed by the HBR domain are located adjacent to telomeres or function in vitamin and carbohydrate metabolism. Deletion of the HBR domain also confers an increased sensitivity to DNA damage by UV irradiation. We mapped the critical residues in the HBR domain required for its repression function. Finally, comparisons of these data with previous studies reveal that a surprising number of genes are coregulated by the N-terminal domains of histone H2B, H3, and H4.

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