Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA397381 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5905045_1.fastq.gz | Fastqsanger.gz | |||
| SRR5905045_2.fastq.gz | Fastqsanger.gz | |||
| SRR5905046_1.fastq.gz | Fastqsanger.gz | |||
| SRR5905046_2.fastq.gz | Fastqsanger.gz |
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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:The downstream events and target genes of p53 in senescence responses are not fully understood. Here, we report a novel function of the forkhead transcription factor Foxp3, a key player in mediating T cell inhibitory function, in p53-mediated cellular senescence. Overexpression of Foxp3 in mouse embryonic fibroblasts (MEFs) accelerates senescence, whereas Foxp3 knockdown leads to escape from p53-mediated senescence in p53-expressing MEFs. Consistently, Foxp3 expression resulted in the induction of senescence in epithelial cancer cells, including MCF7 and HCT116. Foxp3 overexpression also increased the intracellular levels of reactive oxygen species (ROS). The ROS inhibitor N-acetyl-L-cysteine rescued Foxp3 expression-induced senescence. Furthermore, the elevated ROS levels that accompanied Foxp3 overexpression were paralleled by an increase in p21 expression. Knockdown of p21 in Foxp3-expressing MEFs abrogated the Foxp3-dependent increase in ROS levels, indicating that Foxp3 acts through p21 induction and subsequent ROS elevation to trigger senescence. Collectively, these results suggest that Foxp3 is a downstream target of p53 that is sufficient to induce p21 expression and ROS production and is necessary for p53-mediated senescence. control and treated samples (human), young passage (p3) or old passage (p7) samples (mouse)
2015-08-13 | E-GEOD-71980 | biostudies-arrayexpress
Project description:Analysis of leaves from 3-week old transgenic plants overexpressing AAF, which is a senescence-associated gene. Overexpression of AAF promoted leaf senescence and accumulation of reactive oxygen species (ROS) in transgenic plants. Results provide insight in the role of AAF in ROS homeostasis and the function in leaf senescence.
2010-09-30 | GSE18336 | 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:In order to dissect the roles of sequence-specific transcription factors WRKY25, WRKY33 and WRKY75 in apoplastic ROS signaling, a transcriptome profiling of ozone response was done using two arabidopsis mutants: a double mutant wrky25 wrky33 and a single mutant wrky75. The single mutant lines used for transcriptomic analyses were obtained from NASC: wrky25 (SAIL_529_B11) and wrky33 (SALK_006603) were crossed to generate double mutant wrky25 wrky33. T-DNA insertion mutant wrky75-25 (N121525) was obtained from NASC.
2016-04-03 | GSE79855 | GEO
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
Project description:Analysis of leaves from 3-week old transgenic plants overexpressing AAF, which is a senescence-associated gene. Overexpression of AAF promoted leaf senescence and accumulation of reactive oxygen species (ROS) in transgenic plants. Results provide insight in the role of AAF in ROS homeostasis and the function in leaf senescence. 3-week-old plants of Col-0 (wild type, as control) and AAF-OX (overexpression line) were grown in long day condition (16hr light/8hr dark). Rosette leaves of Col-0 and AAF-OX were used for total RNA extraction and cDNA synthesis. cDNA labeling, array hybridization, and scanning followed standard Affymetrix expression array protocol. Two independent sets of microarray analyses were performed in this study.
2010-09-30 | E-GEOD-18336 | biostudies-arrayexpress
Project description:In order to dissect the roles of sequence-specific transcription factors WRKY25, WRKY33 and WRKY75 in apoplastic ROS signaling, a transcriptome profiling of ozone response was done using two arabidopsis mutants: a double mutant wrky25 wrky33 and a single mutant wrky75. The single mutant lines used for transcriptomic analyses were obtained from NASC: wrky25 (SAIL_529_B11) and wrky33 (SALK_006603) were crossed to generate double mutant wrky25 wrky33. T-DNA insertion mutant wrky75-25 (N121525) was obtained from NASC. Three biological replicates, five plants per replicate, treated with 350 ppb ozone for 2 hours, were used for RNA-seq analysis. For each genotype, also non-ozone-treated samples were collected. For the Col-0 control line, an additional fourth replicate with/without ozone was done.
2016-04-03 | E-GEOD-79855 | biostudies-arrayexpress
Project description:The downstream events and target genes of p53 in the process of senescence are not fully understood. Here, we report a novel function of the forkhead transcription factor Foxp3, which is a key player in mediating T cell inhibitory functions, in p53-mediated cellular senescence. The overexpression of Foxp3 in mouse embryonic fibroblasts (MEFs) accelerates senescence, whereas Foxp3 knockdown leads to escape from p53-mediated senescence in p53-expressing MEFs. Consistent with these results, Foxp3 expression resulted in the induction of senescence in epithelial cancer cells, including MCF7 and HCT116 cells. Foxp3 overexpression also increased the intracellular levels of reactive oxygen species (ROS). The ROS inhibitor N-acetyl-L-cysteine rescued cells from Foxp3-expression-induced senescence. Furthermore, the elevated ROS levels that accompanied Foxp3 overexpression were paralleled by an increase in p21 expression. Knockdown of p21 in Foxp3-expressing MEFs abrogated the Foxp3-dependent increase in ROS levels, indicating that Foxp3 acts through the induction of p21 and the subsequent ROS elevation to trigger senescence. Collectively, these results suggest that Foxp3 is a downstream target of p53 that is sufficient to induce p21 expression and ROS production and is necessary for p53-mediated senescence.
2015-08-13 | GSE71980 | GEO
Project description:Plants constantly and precisely control their growth by inducing distinct developmental programs to survive and produce high-quality offspring in the changing environment. The fine-tuning of the development according to endogenous and environmental signals requires exact intercellular signaling and a balanced response. Kinases of the Sucrose non-fermenting-1-Related protein Kinases type 2 (SnRK2s) family primarily take part in the response and adaptation to environmental stress factors. Notably, here we show that two ABA-non-activated SnRK2s, SnRK2.4 and SnRK2.10, are also activated in non-stress conditions in developmentally senescing leaves of Arabidopsis thaliana. Phenotypic, biochemical, and molecular analyses performed on single snrk2.4 or snrk2.10, and double snrk2.4/2.10 kinase mutants showed that SnRK2.4 and SnRK2.10, acting redundantly, promote developmental leaf senescence. Further, SnRK2.4 and SnRK2.10 enhance ABA accumulation in senescing leaves by inducing NCED2, one of key ABA biosynthesis-related genes. The two kinases induce developmental leaf senescence by modulating the expression of multiple ABA-responsive, osmotic stress, and senescence-related genes, such as the senescence master regulators ORE1, ORS1, WRKY33, WRKY75, and ANAC087. Furthermore, we show that SnRK2.4 and SnRK2.10 act upstream of MAPK signaling by enhancing the expression and activity of MAPKKK18, a senescence-inducing kinase. These results document a new regulatory function of SnRK2.4 and SnRK2.10: they are activated in Arabidopsis leaves in response to endogenous signals and redundantly induce developmental leaf senescence by stimulating ABA production and sustaining major ABA-dependent and –independent signaling pathways.
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