Ontology highlight
ABSTRACT:
PROVIDER: PRJNA783896 | 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, the last step of leaf development, is a highly regulated process, modulated by a number of internal and external factors. During the senescence process resources like nitrogen (N) are remobilized from senescent tissues to sink tissues. This intrinsically depends on the accurate dispersion of resources according to sink strength of various organs competing with each other. Consequently, N deficiency accelerates barley leaf senescence and its resupply can delay the senescence progression. In order to identify genetic and metabolic factors that regulate leaf senescence in response to N supply, transcriptomic and global metabolic rearrangements were analyzed in barley primary at early and later stages of N deprivation, and after N resupply to N-deficient plants.
2018-04-09 | E-MTAB-6710 | biostudies-arrayexpress
Project description:Sensing environmental changes is important for survival of plants, as sessile organisms, in habi-tat. Recently, latitudinal clines in leaf senescence have been reported to be influenced by tem-perature and photoperiod. However, the relationship of light quality with latitudinal response of leaf senescence is still unclear. Here, we found that Arabidopsis accessions in far-red (FR) showed a strong negative correlation of leaf senescence with the latitude of their origin. phyto-chrome A (phyA) and B (phyB) mutants showed early and delayed senescence in FR, respec-tively, suggesting that PHYA and PHYB are involved in FR-dependent leaf senescence. Tran-scriptomic analysis identified genes oppositely regulated by PHYA and PHYB, and they were mainly associated with phytohormone, temperature, and defense, suggesting their associations with FR-dependent antagonistic effects of PHYA and PHYB on leaf senescence. Among these genes, the expression of WRKY6 in Arabidopsis accessions showed the highest correlation with latitude of their origin. Consistently, wrky6 mutant exhibited delayed senescence phenotype in FR. In conclusion, we propose that PHYs-regulated genes, including WRKY6, are involved in latitudinal leaf senescence in FR and this regulatory mode may contribute to latitudinal adapta-tion by responding FR, as a piece of geographical information.
2018-09-30 | GSE103946 | GEO
Project description:Our study identified long term salt stress treatment to induce symptoms similar to developmental senescence. In order to identify possible crosstalk components shared between developmental and salt-triggered senescence. We first obtained the expression profile of Arabidopsis leaves under the condition of salt-induced senescence (4 days) and then compared it with the transcriptome of developmental leaf senescence.
2014-06-01 | GSE53308 | GEO
Project description:Plants trigger leaf senescence to relocate energy and nutrients from aging leaves to developing tissues or storage organs to optimize the growth and reproduction under limited nutrients and energy conditions. Jasmonate signaling is one of the major endogenous hormone signals to induced leaf senescence in Arabidopsis. However, whether circadian clock will gate Jasmonate signaling to induce leaf senescence and the underlying precise mechanism is unclear. Here we find that the Evening Complex (EC) of core oscillator closely regulates leaf senescence. To identify the underlying mechanism of EC regulating leaf senescence, we conducted RNA-sequencing. Transcriptomic data reveals Evening complex extensively involves into JA signal transduction and responses. Moreover, the mutants of ELF3, ELF4 and LUX universly display the accelerated JA-induced leaf senescence phenotype, while their overexpression lines act reversely. In accordance with the transcript levels of JA immediate early induced JA-responsive gene MYC2 are up-regulated in lux mutants. Futhermore we demonstrated LUX can bind to to the promoter of MYC2 in vivo to represses its transcription. In addition, the accelerated JA-induced leaf senescence in mutants of evening complex can be overturned by myc2, myc3 and myc4 mutants redundantly. Collectively, our findings demonstrated the underlying molecular basis for circadian clock gating jasmonate signaling to induce leaf senescence through the module of evening complex to directly repressing MYC2 transcription. This novel established molecular module also refines complicated nodes between circadian clock and jasmonate signal in Arabidopsis.
2018-02-06 | GSE99290 | GEO
Project description:Our study identified long term salt stress treatment to induce symptoms similar to developmental senescence. In order to identify possible crosstalk components shared between developmental and salt-triggered senescence. We first obtained the expression profile of Arabidopsis leaves under the condition of salt-induced senescence (4 days) and then compared it with the transcriptome of developmental leaf senescence. Wild type Arabidopsis Col-0 plants were grown hydroponically and treated with or without 150mM NaCl and harvested after 4 days of treatment.
2014-06-01 | E-GEOD-53308 | biostudies-arrayexpress
Project description:Transcriptional profiling of Arabidopsis dark-induced senescence comparing wild type (Col-0) with pif quadruple (pif1/3/4/5) mutant. After synchronized germination, the plants were grown under continuous white light for 7 days and transferred to darkness for 2 days to induce senescence. Goal was to determine the effect of PIFs on transcriptomic regulation during dark-induced senescence.
2014-08-04 | GSE52646 | GEO
Project description:To find the miRNAs that may be involved in dark-induced leaf senescence, we identified miRNAs by microarray platform using Arabidopsis thaliana leaves from both whole darkened plants (DPs) and individually darkened leaves (IDLs). Control, IDLs and DPs were treated for 2, 4 or 6 d in the same climate chambers (16 h light/8 h dark, 250 mmol m-2 s-1).
2016-09-19 | GSE74376 | GEO
Project description:Abscisic acid (ABA) is a phytohormone that promotes leaf senescence in response to environmental stress. We previously identified methyl CpG-binding domain 10 (MBD10) as a phosphoprotein that becomes differentially phosphorylated after ABA treatment in Arabidopsis. ABA-induced leaf senescence was delayed in mbd10 knockout plants but accelerated in MBD10-overexpressing plants, suggesting that MBD10 positively regulates ABA-induced leaf senescence. ABA-induced phosphorylation of MBD10 occurs in planta on Thr-89, and our results demonstrated that Thr-89 phosphorylation is essential for MBD10’s function in leaf senescence. The in vivo phosphorylation of Thr-89 in MBD10 was significantly downregulated in a quadruple mutant of group C MAPKs (mpk1/2/7/14), and group C MAPKs directly phosphorylated MBD10 in vitro.
2023-09-30 | PXD045815 | JPOST Repository