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Glycosyltransferase-like RSE1 negatively regulates leaf senescence by modulating salicylic acid signaling in Arabidopsis

ABSTRACT: Glycosyltransferase-like RSE1 negatively regulates leaf senescence by modulating salicylic acid signaling in Arabidopsis

PROVIDER: PRJNA548877 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9302510_1.fastq.gz	Fastqsanger.gz
	SRR9302510_2.fastq.gz	Fastqsanger.gz
	SRR9302511_1.fastq.gz	Fastqsanger.gz
	SRR9302511_2.fastq.gz	Fastqsanger.gz
	SRR9302512_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Glycosyltransferase-like RSE1 negatively regulates leaf senescence by modulating salicylic acid signaling in Arabidopsis

Project description:Leaf senescence is a developmental process designed for nutrient recycling and relocation to maximize growth competence and reproductive capacity of plants. Thus, plants integrate developmental and environmental signals to precisely control senescence. However, it remains largely elusive as to how plants coordinate genetic, epigenetic, and metabolic pathways for the regulation of senescence. To genetically dissect the complex regulatory mechanism underlying leaf senescence, we identified an early leaf senescence mutant, rse1. RSE1 encodes a putative glycosyltranferase. Loss-of-function mutations in RSE1 resulted in precocious leaf yellowing and up-regulation of senescence maker genes, indicating enhanced leaf senescence. Transcriptome analysis revealed that salicylic acid (SA) and defense signaling cascades were activated in rse1 prior to the onset of leaf senescence. In agreement with the phenotypes, we found that SA accumulation was significantly increased in rse1. We also discovered that the rse1 phenotypes are dependent on SA-INDUCTION DEFICIENT 2 (SID2), indicating a role of SA in accelerated leaf senescence in rse1. Furthermore, RSE1 protein was localized to the cell walls, and rse1 displayed increased glucose contents in the cell walls, implying a possible link between the cell walls and RSE1 function. Together, we show that RSE1 negatively modulate leaf senescence through an SID2-dependent SA signaling pathway.

2019-10-18 | GSE132740 | GEO

Glycosyltransferase-Like RSE1 Negatively Regulates Leaf Senescence Through Salicylic Acid Signaling in Arabidopsis.

Project description:Leaf senescence is a developmental process designed for nutrient recycling and relocation to maximize growth competence and reproductive capacity of plants. Thus, plants integrate developmental and environmental signals to precisely control senescence. To genetically dissect the complex regulatory mechanism underlying leaf senescence, we identified an early leaf senescence mutant, rse1. RSE1 encodes a putative glycosyltransferase. Loss-of-function mutations in RSE1 resulted in precocious leaf yellowing and up-regulation of senescence marker genes, indicating enhanced leaf senescence. Transcriptome analysis revealed that salicylic acid (SA) and defense signaling cascades were up-regulated in rse1 prior to the onset of leaf senescence. We found that SA accumulation was significantly increased in rse1. The rse1 phenotypes are dependent on SA-INDUCTION DEFICIENT 2 (SID2), supporting a role of SA in accelerated leaf senescence in rse1. Furthermore, RSE1 protein was localized to the cell wall, implying a possible link between the cell wall and RSE1 function. Together, we show that RSE1 negatively modulates leaf senescence through an SID2-dependent SA signaling pathway.

| S-EPMC7242760 | biostudies-literature

A Tripartite Amplification Loop Involving WRKY75, Salicylic Acid and ROS Accelerates Leaf Senescence in Arabidopsis

Project description:Leaf senescence is a highly coordinated and complicated process with the integration of numerous internal and environmental signals. Salicylic acid (SA) and reactive oxygen species (ROS) are two well-defined inducers of leaf senescence, whose contents progressively and inter-dependently increase during leaf senescence via a yet unknown mechanism. Here, we have characterized a newly identified positive regulator of leaf senescence, WRKY75, and demonstrated that knock-down or knock-out of WRKY75 delays, while over-expression of WRKY75 accelerates age-dependent leaf senescence. The WRKY75 transcription is induced by age, SA, H2O2, as well as multiple plant hormones. Meanwhile, WRKY75 is able to promote SA production by inducing the transcription of SA INDUCTION-DEFICIENT 2 (SID2), and suppress H2O2 scavenging partly by repressing the transcription of CATALASE 2 (CAT2). Genetic analysis reveals that the SID2 mutation or an increase of catalase activity rescues the precocious leaf senescence phenotype evoked by WRKY75 over-expression. Based on these results, we propose a “tripartite amplification loop” model in which WRKY75, SA and ROS undergo a gradual but self-sustained rise driven by three interlinked positive feedback regulations. This tripartite amplification loop provides a molecular framework connecting the upstream signals, such as age, ethylene, JA and ABA, to the downstream regulatory network executed by those SA-responsive and H2O2-responsive transcription factors during leaf senescence.

2017-11-07 | GSE102302 | GEO

Endothelial senescence mediates hypoxia-induced vascular remodeling by modulating PDGFB expression

Project description:Endothelial senescence mediates hypoxia-induced vascular remodeling by modulating PDGFB expression

| PRJNA795518 | ENA

Quercetin attenuates atherosclerosis via modulating oxidized LDL-induced endothelial cellular senescence

Project description:Quercetin attenuates atherosclerosis via modulating oxidized LDL-induced endothelial cellular senescence

| PRJNA579159 | ENA

Ethylene Responsive Factor 34 (ERF34) negatively mediates salt stress-induced leaf senescence by regulating the expression of salt stress-responsive genes in Arabidopsis

Project description:Leaf senescence, the last step of leaf development which is important for plant’s fitness, proceeds with age but is modulated by various environmental stresses and hormones. Salt stress is one of the well-known environmental stresses that accelerate leaf senescence. However, the molecular mechanisms how the signal of salt stress is integrated into leaf senescence programs are still elusive. In this study, we characterized the function of an Arabidopsis APETALA 2/ETHYLENE RESPONSIVE FACTOR (AP2/ERF) family transcription factor, ERF34, in salt stress-induced leaf senescence. ERF34 was differentially expressed under leaf senescence-inducing conditions including age, dark, and high salt. ERF34 negatively regulated salt stress-induced leaf senescence as well as promoted salt stress tolerance at diverse developmental stages. Analysis of genome-wide targets of ERF34 revealed that the overexpression of ERF34 could alter salt-responsive gene expression. Moreover, ERF34 directly bound to the promoters of EARLY RESPONSIVE TO DEHYDRATION 10 and RESPONSE TO DESICCATION 29A and activated their expression. Our findings imply that ERF34 is a key regulator in the convergence of salt stress response with the regulatory programs of leaf senescence and is a potential candidate for crop improvement, particularly by enhancing salt stress tolerance.

2024-07-01 | GSE180096 | GEO

hnRNP R negatively regulates transcription by modulating the association of P-TEFb with 7SK and BRD4

Project description:hnRNP R negatively regulates transcription by modulating the association of P-TEFb with 7SK and BRD4

| PRJNA837107 | ENA

Endothelial senescence mediates hypoxia-induced vascular remodeling by modulating PDGFB expression

Project description:Uncontrolled accumulation of pulmonary artery smooth muscle cells (PASMC) to the distal pulmonary arterioles (PAs) is one of the major characteristics of pulmonary hypertension (PH). Cellular senescence contributes to aging and lung diseases associated with PH and links to PH progression. However, the mechanism by which cellular senescence controls vascular remodeling in PH is not fully understood. The levels of senescence marker, p16INK4A and senescence-associated β-galactosidase (SA-β-gal) activity are higher in PA endothelial cells (ECs) isolated from idiopathic pulmonary arterial hypertension (IPAH) patients compared to those from healthy individuals. Hypoxia-induced accumulation of α-smooth muscle actin (αSMA)-positive cells to the PAs is attenuated in p16fl/fl-Cdh5(PAC)-CreERT2 (p16iΔEC) mice after tamoxifen induction. We have reported that endothelial TWIST1 mediates hypoxia-induced vascular remodeling by increasing platelet-derived growth factor (PDGFB) expression. Transcriptomic analyses of IPAH patient or hypoxia-induced mouse lung ECs reveal the alteration of senescence-related gene expression and their interaction with TWIST1. Knockdown of p16INK4A attenuates the expression of PDGFB and TWIST1 in IPAH patient PAECs or hypoxia-treated mouse lungs and suppresses accumulation of αSMA–positive cells to the supplemented ECs in the gel implanted on the mouse lungs. Hypoxia-treated mouse lung EC-derived exosomes stimulate DNA synthesis and migration of PASMCs in vitro and in the gel implanted on the mouse lungs, while p16iΔEC mouse lung EC-derived exosomes inhibit the effects. These results suggest that endothelial senescence controls αSMA–positive cell proliferation and migration in PH through TWIST1-PDGFB signaling.

2022-10-15 | PXD033549 | Pride

Glycosyltransferase Extl1 promotes CCR7-mediated dendritic cell migration to restrain infection and autoimmunity

Project description:Purpose: mRNAs sequencing of the gene expression differences in LPS-stimulated Extl1-dificient mDC and wild-type mDC. The goals of this study are to investigate the biological effect of glycosyltransferase Extl1 in regulating dendritic cell function.

2023-01-19 | GSE184976 | GEO

Glycosyltransferase enzyme GCNT3 overexpression effect on SW620 colon cancer cells

Project description:In order to investigate glycosyltransferase enzyme GCNT3 function and to identify putative GCNT3 partners, regulators and/or downstream targets, we performed genomic analysis of GCNT3 overexpression in colon cancer cells. Data from three independent experiments were assayed in a whole genome microarray analysis. We compared patterns of global expression between GCNT3 and No ORF SW620 cells.

2017-06-12 | GSE88792 | GEO

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