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Stress-related transcriptomic changes associated with GFP transgene overexpression and active transgene silencing in plants

ABSTRACT: We performed gene expression analysis using RNA-seq data of four plant samples for each of the following groups: Wild Type (WT) plants and transgenic GFP6.4 Non-Silenced (NS), Ongoing Spreading (OS) post-transcriptional gene silencing, and Systemically Spread (SS) post-transcriptional gene silencing.

ORGANISM(S): Nicotiana benthamiana

PROVIDER: GSE230128 | GEO | 2023/08/25

REPOSITORIES: GEO

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Whole transcriptome analysis in nicotiana benthamiana WT and transgenic lines presenting spontaneous systemic posttranscriptional silencing (PTGS) of a GFP transgene (line GFP6.4 described in Kalantidis Plant J 2006). Change in gene expression was analysed in WT versus GFP6.4 before initiation, during spreading and maintenance of GFP-PTGS.

Project description:Detect the global transcriptional changes occuring during spreading and maintenance of systemic post transcriptional silencing . Test the hypothesis that activation of systemic PTGS induces parallel antiviral defense pathways. Gene expression was analysed by MACE method (Massive Analysis of cDNA Ends) on total RNA extracted from leaf tissues of WT plants (WT), and GFP6.4 presenting no-silencing (NS sample), ongoing spreading of silencing (OS) and maintenance of silencing (SS). Plants were grown in parallel, and silencing state was monitored under UV. After 3 weeks of growth, total RNAs were extracted using the Trizol method from leaf tissues of 2-3 leaf stage plants. A total of 4 plants were sampled per variable (WT/NS/OS/SS). RNA from 4 plants were pooled and sequenced.

2019-04-19 | E-MTAB-7851 | biostudies-arrayexpress

Functional dissection of hematopoietic stem cell population by a stemness-monitoring system with NS-GFP transgene

Project description:Hematopoietic stem cells (HSCs) in a steady state are efficiently purified by the combination of several cell surface markers, however, such markers do not consistently reflect HSC activity. In this study, we successfully isolated functional HSCs by a unique stemness monitoring system using a transgenic mouse, in which green florescence protein (GFP) is driven by promoter/enhancer region of nucleostemin (NS) gene. We found that phenotypically defined long-term (LT)-HSC population exhibited the highest level of the NS-GFP intensity, whereas it was remarkably down-regulated during differentiation in vitro and in vivo. Importantly, among the LT-HSC population, the NS-GFPhigh cells significantly exhibited higher repopulating capacity than NS-GFPlow cells. Gene expression analysis revealed that 9 genes, including Vwf and Cdkn1c (p57), are highly expressed in NS-GFPhigh cells, which may represent signature of functional HSCs, i.e., stemness signature. When LT-HSCs suffered from remarkable stresses, such as transplantation or irradiation, NS-GFP intensity was downregulated, suggesting that NS-GFP accurately reflects HSC function. Finally, we found that functional HSCs were identified as NS-GFPhigh cells in CD34+ LSK cells, which has been recognized as progenitor cells without long-term reconstitution ability. Thus, high NS-GFP intensity represents stem cell characteristics in hematopoiesis and this system is useful for identification of uncharacterized HSCs.

2017-12-20 | GSE98500 | GEO

Epigenetic differences between transgenes and endogenous genes promote transgene silencing in plants

Project description:Transgene loci that spontaneously undergo RNA silencing have been instrumental to decipher RNA silencing pathways in plants. In contrast, transgene loci that are stably expressed have been poorly characterized. Here we show that stably expressed transgene loci epigenetically differ from endogenous genes. Impairing the histone H3K4me3 demethylase JMJ14 increases DNA methylation at stably expressed transgene loci but not at endogenous genes, whereas impairing the histone H3K9me2 demethylase IBM1 increases DNA methylation at endogenous genes, but decreases DNA methylation at stably expressed transgene loci. Moreover, impairing IBM1 promotes post-transcriptional gene silencing (PTGS) at stably expressed transgene loci, whereas impairing JMJ14 prevents PTGS induced systemically by grafting onto silenced rootstocks. Given that impairing DNA methylation suppresses the effect of impairing JMJ14 and restores transgene capacity to undergo graft-induced PTGS, we propose that transgene DNA methylation prevents PTGS, likely by limiting the transcription of aberrant RNA by-products that are transformed into dsRNA by cellular RNA-dependent RNA polymerases to activate PTGS.

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Gene expression analysis of host spleen responses to Marek's disease virus infection in susceptible and resistant chickens

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Project description:In eukaryotes, heterochromatin is characterized by numerous epigenetic marks, including DNA methylation. Spreading of these marks into nearby active genes must be avoided in order to maintain appropriate gene expression. Here, we uncover Arabidopsis Methyl-CpG-Binding Domain 7 (MBD7) and Increased DNA Methylation 3 (IDM3) as anti-silencing factors that prevent transgene repression and genome-wide DNA hypermethylation. MBD7 preferentially binds to highly methylated, CG-dense regions associated with non-CG methylation and physically associates with other anti-silencing factors, including the histone acetyltransferase IDM1, IDM2, and IDM3. IDM1 and IDM2 were previously shown to facilitate active DNA demethylation by the 5-methylcytosine DNA glycosylase/lyase ROS1. Thus, MBD7 tethers the IDM proteins to methylated DNA, which enables the function of DNA demethylases that in turn establish chromatin boundaries and limit DNA methylation Using ChIP-seq to study the genomic targeting principle of MBD7 protein Examination of MBD7 protein binding principle using ChIP-Seq. WT and proMBD7::gMBD7::4xMYC transgenic plants were used for ChIP-seq.

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Expression data from GFP- or GFP Satellite alpha-transfected human retinal pigment epithelia cell line ARPE19

Project description:Oxidative stress (OS) and inflammation play pivotal roles in retinal pigment epithelium (RPE) degeneration and age-related macular degeneration (AMD) pathogenesis. Interleukin 17 (IL17) signaling is a founding pathway regulating inflammatory response, the IL17 ligand has been shown to induce RPE degeneration and is emerging as a potential target for AMD treatment. However, the regulation and function of IL17 receptors are largely unexplored in RPE cells under OS. Here, we identified that IL17RA was significantly upregulated in the presence of OS both in human and mouse RPE cells. We found that OS upregulates expression of reprogramming factor Kruppel-like factor 4 (KLF4), which directly binds to the IL17RA promoter and activates IL17RA transcription, therefore inducing RPE proinflammatory response. Furthermore, our results reveal that KLF4 isoform 2, but not the canonical KLF4 isoform1, is the major isoform in RPE cells that activates IL17RA transcription. Finally, we demonstrate that mRNA level of IL17RA was positively correlated with that of KLF4 isoform2 in AMD patients. Together, our data demonstrates a new regulatory mechanism of IL17RA by KLF4 upon OS exposure, which is likely to play a role in AMD pathogenesis.

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ChIP-seq of WT(with 35S-SUC2 transgene) and proMBD7::gMBD7:4xMYC transgenic plants

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Wnt inhibitory factor 1 (WIF1) is a marker of osteoblastic differentiation stage and is not silenced by DNA methylation in osteosarcoma (methylation)

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