ENAP1 retrains seed germination via H3K9 acetylation mediated positive feedback regulation of ABI5

Histone acetylation is involved in the regulation of seed germination. The transcription factor ABI5 plays an essential role in ABA- inhibited seed germination. However, the molecular mechanism of how ABI5 and histone acetylation coordinate to regulate gene expression during seed germination is still ambiguous. Here, we show that ENAP1 interacts with ABI5 and they co-bind to ABA responsive genes including ABI5 itself. The hypersensitivity to ABA of ENAP1ox seeds germination is recovered by the abi5 null mutation. ABA enhances H3K9Ac enrichment in the promoter regions as well as the transcription of target genes co-bound by ENAP1 and ABI5, which requires both ENAP1 and ABI5. ABI5 gene is directly regulated by ENAP1 and ABI5. In the enap1 deficient mutant, H3K9Ac enrichment and the binding activity of ABI5 in its own promoter region, along with ABI5 transcription and protein levels are all reduced; while in the abi5-1 mutant, the H3K9Ac enrichment and ENAP1 binding activity in ABI5 promoter are decreased, suggesting that ENAP1 and ABI5 function together to regulate ABI5- mediated positive feedback regulation. Overall, our research reveals a new molecular mechanism by which ENAP1 regulates H3K9 acetylation and mediates the positive feedback regulation of ABI5 to inhibit seed germination.

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ABA-induced cytoplasmic translocation of COP1 enhances ROS accumulation through the HY5-ABI5 pathway to modulate seed germination

10.22541/au.163257697.75025095/v1 ◽

2021 ◽

Author(s):

Qing-Bin Chen ◽

Wenjing Wang ◽

Yue Zhang ◽

Qidi Zhan ◽

Kang Liu ◽

...

Keyword(s):

Seed Germination ◽

Target Genes ◽

Seedling Survival ◽

Signal Transduction Pathway ◽

Negative Regulator ◽

Protein Levels ◽

Aba Signal Transduction ◽

Ros Accumulation ◽

Light Signals ◽

Cytoplasmic Translocation

Seed germination is a physiological process regulated by multiple factors. Abscisic acid (ABA) can inhibit seed germination to improve seedling survival under conditions of abiotic stress, and this process is often regulated by light signals. Constitutive Photomorphogenic 1 (COP1) is an upstream core repressor of light signals, and is involved in several ABA responses. Here, we demonstrate that COP1 is a negative regulator of the ABA-mediated inhibition of seed germination. Disruption of COP1 enhanced Arabidopsis seed sensitivity to ABA and increased ROS levels. In seeds, ABA induced the translocation of COP1 to the cytoplasm, resulting in enhanced ABA-induced ROS levels. Genetic evidence indicated that HY5 and ABI5 act downstream of COP1 in the ABA-mediated inhibition of seed germination. ABA-induced COP1 cytoplasmic localization increased HY5 and ABI5 protein levels in the nucleus, leading to increased expression of ABI5 target genes and ROS levels in seeds. Together, our results reveal that ABA-induced cytoplasmic translocation of COP1 activates the HY5-ABI5 pathway to promote the expression of ABA-responsive genes and the accumulation of ROS during ABA-mediated inhibition of seed germination. These findings enhance the role of COP1 in the ABA signal transduction pathway.

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Ethylene promotes ethylene biosynthesis during pea seed germination by positive feedback regulation of 1-aminocyclo-propane-1-carboxylic acid oxidase

Planta ◽

10.1007/s004250000274 ◽

2000 ◽

Vol 211 (1) ◽

pp. 144-149 ◽

Cited By ~ 90

Author(s):

Luciana Petruzzelli ◽

Immacolata Coraggio ◽

Gerhard Leubner-Metzger

Keyword(s):

Carboxylic Acid ◽

Seed Germination ◽

Positive Feedback ◽

Feedback Regulation ◽

Ethylene Biosynthesis ◽

Acid Oxidase ◽

Pea Seed

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A long hypoxia-inducible factor 3 isoform 2 is a transcription activator that regulates erythropoietin

Cellular and Molecular Life Sciences ◽

10.1007/s00018-019-03387-9 ◽

2019 ◽

Vol 77 (18) ◽

pp. 3627-3642 ◽

Cited By ~ 3

Author(s):

Jussi-Pekka Tolonen ◽

Minna Heikkilä ◽

Marjo Malinen ◽

Hang-Mao Lee ◽

Jorma J. Palvimo ◽

...

Keyword(s):

Target Genes ◽

Hypoxia Inducible Factor ◽

Negative Regulator ◽

Luciferase Reporter ◽

Transcription Activator ◽

Promoter Regions ◽

Α Subunit ◽

Hypoxia Response ◽

Protein Levels ◽

Oxygen Homeostasis

AbstractHypoxia-inducible factor (HIF), an αβ dimer, is the master regulator of oxygen homeostasis with hundreds of hypoxia-inducible target genes. Three HIF isoforms differing in the oxygen-sensitive α subunit exist in vertebrates. While HIF-1 and HIF-2 are known transcription activators, HIF-3 has been considered a negative regulator of the hypoxia response pathway. However, the human HIF3A mRNA is subject to complex alternative splicing. It was recently shown that the long HIF-3α variants can form αβ dimers that possess transactivation capacity. Here, we show that overexpression of the long HIF-3α2 variant induces the expression of a subset of genes, including the erythropoietin (EPO) gene, while simultaneous downregulation of all HIF-3α variants by siRNA targeting a shared HIF3A region leads to downregulation of EPO and additional genes. EPO mRNA and protein levels correlated with HIF3A silencing and HIF-3α2 overexpression. Chromatin immunoprecipitation analyses showed that HIF-3α2 binding associated with canonical hypoxia response elements in the promoter regions of EPO. Luciferase reporter assays showed that the identified HIF-3α2 chromatin-binding regions were sufficient to promote transcription by all three HIF-α isoforms. Based on these data, HIF-3α2 is a transcription activator that directly regulates EPO expression.

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Abscisic acid (ABA)-mediated inhibition of seed germination involves a positive feedback regulation of ABA biosynthesis in Arachis hypogaea L.

AFRICAN JOURNAL OF BIOTECHNOLOGY ◽

10.5897/ajb10.1819 ◽

2010 ◽

Vol 9 (11) ◽

pp. 1578-1586 ◽

Cited By ~ 9

Author(s):

Hu Bo ◽

Wan Xiao rong ◽

Liu Xiao hui ◽

Guo Dong liang ◽

Li Ling

Keyword(s):

Abscisic Acid ◽

Seed Germination ◽

Arachis Hypogaea ◽

Positive Feedback ◽

Feedback Regulation ◽

Arachis Hypogaea L ◽

Aba Biosynthesis

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Postrepression Activation of NF-κB Requires the Amino-Terminal Nuclear Export Signal Specific to IκBα

Molecular and Cellular Biology ◽

10.1128/mcb.21.14.4737-4747.2001 ◽

2001 ◽

Vol 21 (14) ◽

pp. 4737-4747 ◽

Cited By ~ 67

Author(s):

Tony T. Huang ◽

Shigeki Miyamoto

Keyword(s):

Nuclear Export ◽

Mammalian Cells ◽

Target Genes ◽

Nuclear Export Signal ◽

Feedback Regulation ◽

Mechanistic Explanation ◽

Binding Activity ◽

Critical Event ◽

Specific Function ◽

Amino Terminal

ABSTRACT One of the most prominent NF-κB target genes in mammalian cells is the gene encoding one of its inhibitor proteins, IκBα. The increased synthesis of IκBα leads to postinduction repression of nuclear NF-κB activity. However, it is unknown why IκBα, among multiple IκB family members, is involved in this process and what significance this feedback regulation has beyond terminating NF-κB activity. Herein, we report an important IκBα-specific function dictated by its amino-terminal nuclear export sequence (N-NES). The IκBα N-NES is necessary for the postinduction export of nuclear NF-κB, which is a critical event in reestablishing a permissive condition for NF-κB to be rapidly reactivated. We show that although IκBα and another IκB member, IκBβ, can enter the nucleus and repress NF-κB DNA-binding activity during the postinduction phase, only IκBα allows the efficient export of nuclear NF-κB. Moreover, swapping the N-terminal region of IκBβ for the corresponding IκBα sequence is sufficient for the IκB chimera protein to export NF-κB similarly to IκBα during the postinduction state. Our findings provide a mechanistic explanation of why IκBα but not other IκB members is crucial for postrepression activation of NF-κB. We propose that this IκBα-specific function is important for certain physiological and pathological conditions where NF-κB needs to be rapidly reactivated.

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Preparation of a miR-155-activating Nucleic Acid Nanoflower to Study the Molecular Mechanism of miR-155 in Inflammation

10.21203/rs.3.rs-1133989/v1 ◽

2021 ◽

Author(s):

Wenxin Wang ◽

Jie Geng ◽

Xiaohan Wu ◽

Jianguang Zhang ◽

Chenna Zheng ◽

...

Keyword(s):

Nucleic Acid ◽

Inflammatory Response ◽

Molecular Mechanism ◽

Molecular Mechanisms ◽

Target Genes ◽

Umbilical Vein ◽

Inflammatory Factors ◽

Related Factors ◽

Protein Levels ◽

Gene And Protein Expression

Abstract BackgroundAt present, the molecular mechanisms underlying inflammation remain unclear. In recent years, research on inflammation has focused on stimulating cell inflammation by using external pathogens such as LPS or inflammatory factors. To investigate the molecular mechanism of inflammation from a new perspective, we designed a nucleic acid nanoflowers (NFs) complex to directly activate inflammatory genes to study the inflammatory response without the need for external microbial factors to trigger an inflammatory response. ResultsAn RNAa-type target gene-activated NF was designed. Human umbilical vein endothelial cells (HUVECs) were transfected with NFs carrying saRNAs to directly co-activate microRNA (miR)-155 and SHIP1 genes. Inflammatory gene and protein expression in the HUVECs were evaluated to assess whether miR-155 overexpression can trigger inflammation. After RNAa-type NFs were transferred into HUVECs, the expression of miR-155 and pro-inflammatory and cancer-related factors increased, anti-inflammatory factors were reduced, cell proliferation increased, and cell migration was promoted. IL-1β protein levels were decreased and SHIP1 expression was downregulated. When miR-155 and its target SHIP1 were both activated, the expression of both was unaltered, maintaining cell homeostasis. ConclusionMiR-155 and its target genes act as a molecular switch role in the development of inflammation.

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Evidence That Regulation of Pri-miRNA/miRNA Expression Is Not a General Rule of miPEPs Function in Humans

International Journal of Molecular Sciences ◽

10.3390/ijms22073432 ◽

2021 ◽

Vol 22 (7) ◽

pp. 3432

Author(s):

Anne Prel ◽

Christine Dozier ◽

Jean-Philippe Combier ◽

Serge Plaza ◽

Arnaud Besson

Keyword(s):

Mirna Expression ◽

Positive Feedback ◽

Target Genes ◽

Feedback Regulation ◽

General Rule ◽

Ribosome Profiling ◽

Open Reading Frames ◽

Expression Activity ◽

Reading Frames

Some miRNAs are located in RNA precursors (pri-miRNAs) annotated as long non-coding (lncRNAs) due to absence of long open reading frames (ORFs). However, recent studies have shown that some lnc pri-miRNAs encode peptides called miPEPs (miRNA-encoded peptides). Initially discovered in plants, three miPEPs have also been identified in humans. Herein, we found that a dozen human pri-miRNAs potentially encode miPEPs, as revealed by ribosome profiling and proteomic databases survey. So far, the only known function of plant miPEPs is to enhance the transcription of their own pri-miRNAs, thereby increasing the level and activity of their associated miRNAs and downregulating the expression of their target genes. To date, in humans, only miPEP133 was shown to promote a positive autoregulatory loop. We investigated whether other human miPEPs are also involved in regulating the expression of their miRNAs by studying miPEP155, encoded by the lnc MIR155HG, miPEP497, a sORF-encoded peptide within lnc MIR497HG, and miPEP200a, encoded by the pri-miRNA of miR-200a/miR-200b. We show that overexpression of these miPEPs is unable to impact the expression/activity of their own pri-miRNA/miRNAs in humans, indicating that the positive feedback regulation observed with plant miPEPs and human miPEP133 is not a general rule of human miPEP function.

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ZFARED: A Database of the Antioxidant Response Elements in Zebrafish

Current Bioinformatics ◽

10.2174/1574893614666191018172213 ◽

2020 ◽

Vol 15 (5) ◽

pp. 415-419

Author(s):

Azhwar Raghunath ◽

Raju Nagarajan ◽

Ekambaram Perumal

Keyword(s):

Target Genes ◽

Antioxidant Response ◽

Zebrafish Genome ◽

Promoter Regions ◽

Protein Coding ◽

Response Elements ◽

Toxic Agents ◽

Upstream Promoter ◽

Its Gene ◽

Antioxidant Response Elements

Background: Antioxidant Response Elements (ARE) play a key role in the expression of Nrf2 target genes by regulating the Keap1-Nrf2-ARE pathway, which offers protection against toxic agents and oxidative stress-induced diseases. Objective: To develop a database of putative AREs for all the genes in the zebrafish genome. This database will be helpful for researchers to investigate Nrf2 regulatory mechanisms in detail. Methods: To facilitate researchers functionally characterize zebrafish AREs, we have developed a database of AREs, Zebrafish Antioxidant Response Element Database (ZFARED), for all the protein-coding genes including antioxidant and mitochondrial genes in the zebrafish genome. The front end of the database was developed using HTML, JavaScript, and CSS and tested in different browsers. The back end of the database was developed using Perl scripts and Perl-CGI and Perl- DBI modules. Results: ZFARED is the first database on the AREs in zebrafish, which facilitates fast and efficient searching of AREs. AREs were identified using the in-house developed Perl algorithms and the database was developed using HTML, JavaScript, and Perl-CGI scripts. From this database, researchers can access the AREs based on chromosome number (1 to 25 and M for mitochondria), strand (positive or negative), ARE pattern and keywords. Users can also specify the size of the upstream/promoter regions (5 to 30 kb) from transcription start site to access the AREs located in those specific regions. Conclusion: ZFARED will be useful in the investigation of the Keap1-Nrf2-ARE pathway and its gene regulation. ZFARED is freely available at http://zfared.buc.edu.in/.

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