Browse
Submit Data
Databases
API
Help

Dataset Information

34 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SlJAZ10 and SlJAZ11 mediate dark-induced leaf senescence and regeneration.

ABSTRACT: During evolutionary adaptation, the mechanisms for self-regulation are established between the normal growth and development of plants and environmental stress. The phytohormone jasmonate (JA) is a key tie of plant defence and development, and JASMONATE-ZIM DOMAIN (JAZ) repressor proteins are key components in JA signalling pathways. Here, we show that JAZ expression was affected by leaf senescence from the transcriptomic data. Further investigation revealed that SlJAZ10 and SlJAZ11 positively regulate leaf senescence and that SlJAZ11 can also promote plant regeneration. Moreover, we reveal that the SlJAV1-SlWRKY51 (JW) complex could suppress JA biosynthesis under normal growth conditions. Immediately after injury, SlJAZ10 and SlJAZ11 can regulate the activity of the JW complex through the effects of electrical signals and Ca2+ waves, which in turn affect JA biosynthesis, causing a difference in the regeneration phenotype between SlJAZ10-OE and SlJAZ11-OE transgenic plants. In addition, SlRbcs-3B could maintain the protein stability of SlJAZ11 to protect it from degradation. Together, SlJAZ10 and SlJAZ11 not only act as repressors of JA signalling to leaf senescence, but also regulate plant regeneration through coordinated electrical signals, Ca2+ waves, hormones and transcriptional regulation. Our study provides critical insights into the mechanisms by which SlJAZ11 can induce regeneration.

SUBMITTER: Tang B

PROVIDER: S-EPMC9278786 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Barley leaf dark-induced senescence

2014-10-22 | GSE62539 | GEO

Barely leaf dark-induced senescence

Project description:Time-course transcriptional profiling of senescing barley leaves. In this model, the senescence process was induced by continued incubation of the seedlings in darkness. Plant samples for the expression analysis were collected before senescence induction (Day 0) and after 3,7 and 10 days of incubation in the dark. The goal was to find the genes differentially expressed during the senescence process . Additionally, a list of the genes with the invariant expression was generated as a resource for selecting references suitable for qPCR or ddPCR experiments. Time-course experiment, two-color, common reference design. All of the data were obtained from material collected in three independent, time-separated leaf senescing experiments (biological replicates). In each replicate, samples from senescing leaves (3 Days, 7 Days, 10 Days) were compared to samples collected before the senescence induction (Day 0). 3 biological replicates.Cy5-labeled samples of interest (Day 0, Day 3, Day 7 and Day 10 from each biological replicate) were each hybridized against a Cy3-labeled common reference (RNA pool of all samples) on a total of 12 microarrays.

2014-10-22 | E-GEOD-62539 | biostudies-arrayexpress

JAZ7 negatively regulates dark-induced leaf senescence in Arabidopsis.

Project description:JASMONATE ZIM-domain (JAZ) proteins play important roles in plant defence and growth by regulating jasmonate signalling. Through data mining, we discovered that the JAZ7 gene was up-regulated in darkness. In the dark, the jaz7 mutant displayed more severe leaf yellowing, quicker chlorophyll degradation, and higher hydrogen peroxide accumulation compared with wild-type (WT) plants. The mutant phenotype of dark-induced leaf senescence could be rescued in the JAZ7-complemented and -overexpression lines. Moreover, the double mutants of jaz7 myc2 and jaz7 coi1 exhibited delayed leaf senescence. We further employed GeneChip analysis to study the molecular mechanism. Some key genes down-regulated in the triple mutant myc2 myc3 myc4 were up-regulated in the jaz7 mutant under darkness. The Gene Ontology terms 'leaf senescence' and 'cell death' were significantly enriched in the differentially expressed genes. Combining the genetic and transcriptomic analyses together, we proposed a model whereby darkness can induce JAZ7, which might further block MYC2 to suppress dark-induced leaf senescence. In darkness, the mutation of JAZ7 might partially liberate MYC2/MYC3/MYC4 from suppression, leading the MYC proteins to bind to the G-box/G-box-like motifs in the promoters, resulting in the up-regulation of the downstream genes related to indole-glucosinolate biosynthesis, sulphate metabolism, callose deposition, and JA-mediated signalling pathways. In summary, our genetic and transcriptomic studies established the JAZ7 protein as an important regulator in dark-induced leaf senescence.

| S-EPMC4737072 | biostudies-literature

WRKY22 transcription factor mediates dark-induced leaf senescence in Arabidopsis.

Project description:Arabidopsis WRKY proteins are plant-specific transcription factors, encoded by a large gene family, which contain the highly conserved amino acid sequence WRKYGQK and the zinc-finger-like motifs, Cys(2)His(2) or Cys(2)HisCys. They can recognize and bind the TTGAC(C/T) W-box ciselements found in the promoters of target genes, and are involved in the regulation of gene expression during pathogen defense, wounding, trichome development, and senescence. Here we investigated the physiological function of the Arabidopsis WRKY22 transcription factor during dark-induced senescence. WRKY22 transcription was suppressed by light and promoted by darkness. In addition, AtWRKY22 expression was markedly induced by H(2)O(2). These results indicated that AtWRKY22 was involved in signal pathways in response to abiotic stress. Dark-treated AtWRKY22 over-expression and knockout lines showed accelerated and delayed senescence phenotypes, respectively, and senescence-associated genes exhibited increased and decreased expression levels. Mutual regulation existed between AtWRKY22 and AtWRKY6, AtWRKY53, and AtWRKY70, respectively. Moreover, AtWRKY22 could influence their relative expression levels by feedback regulation or by other, as yet unknown mechanisms in response to dark. These results prove that AtWRKY22 participates in the dark-induced senescence signal transduction pathway.

| S-EPMC3933965 | biostudies-literature

Arabidopsis Phototropins Participate in the Regulation of Dark-Induced Leaf Senescence.

Project description:Senescence is the final stage of plant development, affecting individual organs or the whole organism, and it can be induced by several environmental factors, including shading or darkness. Although inevitable, senescence is a complex and tightly regulated process, ensuring optimal remobilization of nutrients and cellular components from senescing organs. Photoreceptors such as phytochromes and cryptochromes are known to participate in the process of senescence, but the involvement of phototropins has not been studied to date. We investigated the role of these blue light photoreceptors in the senescence of individually darkened Arabidopsis thaliana leaves. We compared several physiological and molecular senescence markers in darkened leaves of wild-type plants and phototropin mutants (phot1, phot2, and phot1phot2). In general, all the symptoms of senescence (lower photochemical activity of photosystem II, photosynthetic pigment degradation, down-regulation of photosynthetic genes, and up-regulation of senescence-associated genes) were less pronounced in phot1phot2, as compared to the wild type, and some also in one of the single mutants, indicating delayed senescence. This points to different mechanisms of phototropin operation in the regulation of senescence-associated processes, either with both photoreceptors acting redundantly, or only one of them, phot1, playing a dominant role.

| S-EPMC7918785 | biostudies-literature

Rice Phytochrome B (OsPhyB) Negatively Regulates Dark- and Starvation-Induced Leaf Senescence.

Project description:Light regulates leaf senescence and light deprivation causes large-scale transcriptional reprogramming to dismantle cellular components and remobilize nutrients to sink organs, such as seeds and storage tissue. We recently reported that in Arabidopsis (Arabidopsis thaliana), Phytochrome-Interacting Factor4 (PIF4) and PIF5 promote dark-induced senescence and natural senescence by directly activating the expression of typical senescence-associated genes (SAGs), including ORESARA1 (ORE1) and ETHYLENE INSENSITIVE3 (EIN3). In contrast, phytochrome B (PhyB) inhibits leaf senescence by repressing PIF4 and PIF5 at the post-translational level. Although we found how red light signaling represses leaf senescence in Arabidopsis, it remains unknown whether PhyB and/or PhyA are involved in leaf senescence in rice (Oryza sativa). Here we show that rice phyB knockout mutants (osphyB-1, -2, and -3) exhibited an early senescence phenotype during dark-induced senescence, but an osphyA knockout mutant (osphyA-3) senesced normally. The RT-qPCR analysis revealed that several senescence-associated genes, including OsORE1 and OsEIN3, were significantly up-regulated in osphyB-2 mutants, indicating that OsPhyB also inhibits leaf senescence, like Arabidopsis PhyB. We also found that leaf segments of osphyB-2 senesced faster even under light conditions. Supplementation with nitrogen compounds, such as KNO? and NH?NO?, rescued the early senescence phenotype of osphyB-2, indicating that starvation is one of the major signaling factors in the OsPhyB-dependent leaf senescence pathway.

| S-EPMC4844404 | biostudies-literature

Proline oxidation fuels mitochondrial respiration during dark-induced leaf senescence in Arabidopsis thaliana.

Project description:Leaf senescence is a form of developmentally programmed cell death that allows the remobilization of nutrients and cellular materials from leaves to sink tissues and organs. Among the catabolic reactions that occur upon senescence, little is known about the role of proline catabolism. In this study, the involvement in dark-induced senescence of proline dehydrogenases (ProDHs), which catalyse the first and rate-limiting step of proline oxidation in mitochondria, was investigated using prodh single- and double-mutants with the help of biochemical, proteomic, and metabolomic approaches. The presence of ProDH2 in mitochondria was confirmed by mass spectrometry and immunogold labelling in dark-induced leaves of Arabidopsis. The prodh1 prodh2 mutant exhibited enhanced levels of most tricarboxylic acid cycle intermediates and free amino acids, demonstrating a role of ProDH in mitochondrial metabolism. We also found evidence of the involvement and the importance of ProDH in respiration, with proline as an alternative substrate, and in remobilization of proline during senescence to generate glutamate and energy that can then be exported to sink tissues and organs.

| S-EPMC6859731 | biostudies-literature

Ameliorative effects of melatonin on dark-induced leaf senescence in gardenia (Gardenia jasminoides Ellis): leaf morphology, anatomy, physiology and transcriptome.

Project description:Cut gardenia (Gardenia jasminoides Ellis) foliage is widely used as a vase material or flower bouquet indoors; however, insufficient indoor light accelerates its senescence, which shortens its viewing time. In this study, applying melatonin to delay gardenia leaf senescence when exposed to extremely low light condition (darkness), and the results showed that 1.0?mM was the effective concentration. At this concentration, chlorophyll contents and chlorophyll fluorescence parameters (Fv/Fm, Fv/F0 and Y(II)) increased, while the carotenoid and flavonoid contents decreased. Meanwhile, stress physiological indices decreased in response to exogenous melatonin application, whereas an increase in glutamine synthetase activity, water and soluble protein contents was observed. Moreover, exogenous melatonin application also reduced leaf programmed cell death under darkness, increased the endogenous melatonin level, expression levels of tryptophan decarboxylase gene, superoxide dismutase and catalase activities and the ascorbate-glutathione cycle, and maintained more intact anatomical structures. Furthermore, transcriptome sequencing revealed that various biological processes responded to exogenous melatonin application, including carbohydrate metabolism, amino acid metabolism, lipid metabolism, plant hormone signal transduction and pigment biosynthesis. Consequently, dark-induced leaf senescence in gardenia was significantly delayed. These results provided a better understanding for improving the ornamental value of cut gardenia foliage using melatonin.

| S-EPMC5585368 | biostudies-literature

Comparative transcriptome analysis in Arabidopsis ein2/ore3 and ahk3/ore12 mutants during dark-induced leaf senescence.

Project description:Leaf senescence involves degenerative but active biological processes that require balanced regulation of pro- and anti-senescing activities. Ethylene and cytokinin are major antagonistic regulatory hormones that control the timing and progression rate of leaf senescence. To identify the roles of these hormones in the regulation of leaf senescence in Arabidopsis, global gene expression profiles in detached leaves of the wild type, an ethylene-insensitive mutant (ein2/ore3), and a constitutive cytokinin response mutant (ahk3/ore12) were investigated during dark-induced leaf senescence. Comparative transcriptome analyses revealed that genes involved in oxidative or salt stress response were preferentially altered in the ein2/ore3 mutant, whereas genes involved in ribosome biogenesis were affected in the ahk3/ore12 mutant during dark-induced leaf senescence. Similar results were also obtained for developmental senescence. Through extensive molecular and physiological analyses in ein2/ore3 and ahk3/ore12 during dark-induced leaf senescence, together with responses when treated with cytokinin and ethylene inhibitor, we conclude that ethylene acts as a senescence-promoting factor via the transcriptional regulation of stress-related responses, whereas cytokinin acts as an anti-senescing agent by maintaining cellular activities and preserving the translational machinery. These findings provide new insights into how plants utilize two antagonistic hormones, ethylene and cytokinin, to regulate the molecular programming of leaf senescence.

| S-EPMC5972659 | biostudies-literature

Age-triggered and dark-induced leaf senescence require the bHLH transcription factors PIF3, 4, and 5.

Project description:Leaf senescence can be triggered and promoted by a large number of developmental and environmental factors. Numerous lines of evidence have suggested an involvement of phytochromes in the regulation of leaf senescence, but the related signaling pathways and physiological mechanisms are poorly understood. In this study, we initially identified phytochrome-interacting factors (PIFs) 3, 4, and 5 as putative mediators of leaf senescence. Mutations of the PIF genes resulted in a significantly enhanced leaf longevity in age-triggered and dark-induced senescence, whereas overexpressions of these genes accelerated age-triggered and dark-induced senescence in Arabidopsis. Consistently, loss-of-function of PIF4 attenuated dark-induced transcriptional changes associated with chloroplast deterioration and reactive oxygen species (ROS) generation. ChIP-PCR and Dual-Luciferase assays demonstrated that PIF4 can activate chlorophyll degradation regulatory gene NYE1 and repress chloroplast activity maintainer gene GLK2 by binding to their promoter regions. Finally, dark-induced ethylene biosynthesis and ethylene-induced senescence were both dampened in pif4, suggesting the involvement of PIF4 in both ethylene biosynthesis and signaling pathway. Our study provides evidence that PIF3, 4, and 5 are novel positive senescence mediators and gains an insight into the mechanism of light signaling involved in the regulation of leaf senescence.

| S-EPMC4261840 | biostudies-other

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data