Arabidopsis thaliana
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ABSTRACT:
PROVIDER: PRJNA175634 | ENA |
REPOSITORIES: ENA
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Project description:Leaf senescence is the final developmental process that includes the mobilization of nutrients from old leaves to newly growing tissues. The progression of leaf senescence requires dynamic but coordinated changes of gene expression. Although several transcription factors (TFs) are known to be involved in both negative and positive modes of regulation of leaf senescence, detailed mechanisms that underlie the progression of leaf senescence are largely unknown. We report here that the class II ERF transcriptional repressors are controlled by proteasome and regulate the progression of leaf senescence in Arabidopsis. Since we had previously demonstrated that NtERF3, a model of tobacco class II ERFs, specifically interacts with a ubiquitin-conjugating enzyme, we examined the stability of NtERF3 and found that bacterially produced NtERF3 was rapidly degraded by plant protein extracts in vitro. Whereas NtERF3 accumulation was low in plants, it was increased by treatment with a proteasome inhibitor. Arabidopsis class II ERFs, namely, AtERF4 and AtERF8, were also controlled by proteasome and stabilized by aging of plants. The transgenic plants in which NtERF3, AtERF4, and AtERF8 were individually expressed under the control of the 35S promoter exhibited the precocious leaf senescence. Our microarray and RT-PCR analyses revealed that AtERF4 regulated expression of genes involving in various stress responses and leaf senescence. In contrast, aterf4 aterf8 mutant exhibited delayed leaf senescence. Taken together, we present the important role of class II ERFs in the regulation of leaf senescence. Transcriptomes of 35S:AtERF4-HA and 35S:NLS-GFP-HA (control) Arabidopsis two-weeks seedling were compared.
2013-07-02 | E-GEOD-41053 | biostudies-arrayexpress
Project description:Leaf senescence is the final developmental process that includes the mobilization of nutrients from old leaves to newly growing tissues. The progression of leaf senescence requires dynamic but coordinated changes of gene expression. Although several transcription factors (TFs) are known to be involved in both negative and positive modes of regulation of leaf senescence, detailed mechanisms that underlie the progression of leaf senescence are largely unknown. We report here that the class II ERF transcriptional repressors are controlled by proteasome and regulate the progression of leaf senescence in Arabidopsis. Since we had previously demonstrated that NtERF3, a model of tobacco class II ERFs, specifically interacts with a ubiquitin-conjugating enzyme, we examined the stability of NtERF3 and found that bacterially produced NtERF3 was rapidly degraded by plant protein extracts in vitro. Whereas NtERF3 accumulation was low in plants, it was increased by treatment with a proteasome inhibitor. Arabidopsis class II ERFs, namely, AtERF4 and AtERF8, were also controlled by proteasome and stabilized by aging of plants. The transgenic plants in which NtERF3, AtERF4, and AtERF8 were individually expressed under the control of the 35S promoter exhibited the precocious leaf senescence. Our microarray and RT-PCR analyses revealed that AtERF4 regulated expression of genes involving in various stress responses and leaf senescence. In contrast, aterf4 aterf8 mutant exhibited delayed leaf senescence. Taken together, we present the important role of class II ERFs in the regulation of leaf senescence.
2013-07-02 | GSE41053 | GEO
Project description:Leaf senescence is a tightly controlled and complex developmental process that shares many similarities across species, yet our understanding of the underlying conserved molecular mechanisms is still lacking. Here, we observed functional conservation of leaf senescence underlying pathways in A. thaliana, O. sativa, and S. lycopersicum. From machine learning-based integration of data from nearly 10 000 samples to obtain a universal regulatory network of leaf senescence, it was found that mitostasis is the cross-species central biological hub. We measure and compare changes in the transcriptome and metabolome of A. thaliana, O. sativa, and S. lycopersicum leaves under mitostress/natural senescence. In data from different species, mitostasis-related transcription factors binding site enrichment and amino acids expression changes converge on putative senescence modulators. Our study provides a cross-species, multi-omics perspective for understanding the leaf senescence conserved mechanisms.
2022-05-03 | GSE201607 | GEO
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
Project description:Leaf senescence is governed by a complex regulatory network involving dynamic reprogramming of gene expression. Recent evidence indicates that trimethylation of histone H3 at lysine 4 (H3K4me3) alters gene expression during leaf senescence. However, it is largely unknown how histone modification is regulated in an age-dependent manner. We found that JMJ16, an Arabidopsis JmjC-domain containing protein, is a specific H3K4 demethylase that negatively regulates leaf senescence. The histone demethylase activity and the JmjN, JmjC, and FYR domains of JMJ16, but not the zf-C5HC2 domain, are essential for JMJ16 function in the regulation of leaf senescence. Genome-wide analysis revealed a widespread coordinated up-regulation of H3K4me3 and gene expression associated with leaf senescence in the loss-of-function jmj16 mutant compared with the wild type. Genetic analysis indicated that JMJ16 negatively regulates leaf senescence at least partly through repressing the expression of WRKY53 and SAG201, two known positive regulators of leaf senescence. Further analyses demonstrated that JMJ16 associates with WRKY53 and SAG201, and represses precocious expression of WRKY53 and SAG201 in mature leaves by reducing H3K4me3 levels at these loci. Moreover, association of JMJ16 on WRKY53 and SAG201 loci increased at mature stage but decreased at later stage, suggesting that the age-dependent dynamic chromatin association of JMJ16 is required for precise transcriptional activation of SAGs during leaf senescence. Thus, JMJ16 is an important regulator of leaf senescence that demethylates H3K4 at senescence-associated genes in an age-dependent manner.
2019-04-17 | GSE115362 | GEO
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
Project description:Immune tolerance to allografts has been pursued for decades as an important goal in transplantation. Administration of apoptotic donor splenocytes effectively induces antigen-specific tolerance to allografts in murine studies. Here we show that two peritransplant infusions of apoptotic donor leukocytes under short-term immunotherapy with antagonistic anti-CD40 antibody 2C10R4, rapamycin, soluble tumor necrosis factor receptor and anti-interleukin 6 receptor antibody induce long-term (≥1 year) tolerance to islet allografts in 5 of 5 nonsensitized, MHC class I-disparate, and 1 MHC class II DRB allele-matched rhesus macaques. Tolerance in our preclinical model is associated with a regulatory network, involving antigen-specific Tr1 cells exhibiting a distinct transcriptome and indirect specificity for matched MHC class II and mismatched class I peptides. Apoptotic donor leukocyte infusions warrant continued investigation as a cellular, nonchimeric and translatable method for inducing antigen- specific tolerance in transplantation.
2019-07-02 | GSE132496 | GEO
Project description:We report our results of RNA-seq analysis on flow sorted Tr1 cells Immune tolerance to allografts has been pursued as an important goal in transplantation for decades. Administration of apoptotic donor splenocytes effectively induced antigen-specific tolerance to allografts in murine studies. Here we show that two peritransplant infusions of apoptotic donor leukocytes under short-term immunotherapy with antagonistic anti-CD40 antibody 2C10R4, rapamycin, soluble tumor necrosis factor receptor, and anti-interleukin 6 receptor antibody induce long-term (≥1 year) tolerance to islet allografts in 5 of 5 nonsensitized, MHC class I-disparate, and 1 MHC class II DRB allele- matched rhesus macaques. Tolerance in our preclinical model is associated with a regulatory network, involving antigen-specific Tr1 cells exhibiting a distinct transcriptome and indirect specificity for matched MHC class II and mismatched class I peptides. Apoptotic donor leukocyte infusions warrant continued investigation as a cellular, nonchimeric, and translatable method for inducing antigen- specific tolerance in transplantation.
2019-07-03 | GSE132691 | GEO