Stress Induced Calcium Signaling Facilitates ABA Mediated Transcriptional Adaptation
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PROVIDER: PRJEB20510 | ENA |
REPOSITORIES: ENA
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Project description:ABA and calcium both function as central signals in developmental programs and environmental responses. Little is known about the way how both messengers functionally interact. Here we report that stress induced calcium signatures are essential and likely sufficient for inducing ABA accumulation in roots. Moreover, we show that calcium activated calcium sensor/kinase complexes directly phosphorylate and activate ABA responsive transcription factors. Our results reveal a molecular mechanism that allows for integrating, fine tuning and termination of hormonal and calcium signaling on the level of gene transcription.
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Project description:Chloroplast-nuclear retrograde signaling is viewed as a mechanism for inter-organelle communication. Here we show the SAL1-PAP (3′-phosphoadenosine 5′- phosphate) retrograde pathway functions more broadly in guard cells, interacting with abscisic acid (ABA) signaling at least in part via exoribonucleases. Unexpectedly, PAP bypasses the canonical signaling components ABA Insensitive 1 (ABI1) and Open Stomata 1 (OST1) by priming an alternative pathway that restores ABA-responsive gene expression, ROS bursts, ion channel function and stomatal closure in ost1-2. This alternative pathway up-regulates lowly expressed Calcium Dependent Protein Kinases (CDPKs) which have the capacity to activate the key slow anion channel SLAC1 in response to ABA-mediated and ost1-2 independent calcium release. The role of PAP in priming an alternative pathway to bypass components previously considered essential for stomatal closure demonstrates how a chloroplast signal can have broader roles as a secondary messenger to directly intersect with and tune hormone signaling.
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Project description:Abscisic acid (ABA) plays a key role in plant development and responses to abiotic stress. A wide number of regulatory mechanisms on ABA perception and signaling are known, including transcriptional regulation and post-translational regulations; however, less to know about the post-transcriptional regulations. In this work, we have found that SKIP, a splicing factor in spliceosome, positively regulates ABA signal transduction. Mutation of SKIP, skip-1, confers ABA insensitive phenotype in seed germination, root growth, and ABA-responsive gene expression. Transformation of SKIP genomic DNA to skip-1 is able to recover its defects. SKIP binds to the pre-mRNA of genes in ABA signaling, such as PYL8, to regulate their splicing. The alternative splicing of PYL7, PYL8, ABF2, and ABI5 in ABA pathway is disrupted by skip-1, reducing the mRNA levels of them. The abnormal splicing of PP2Cs activates their transcription by skip-1, suggesting there is a feedback regulation for PP2Cs caused by skip-1. The down-regulation of PYL ABA receptors, ABF2 and ABI5 ABA response transcription factors, and the up-regulation of PP2Cs through alternative splicing reduce the plant responses to ABA in skip-1. SKIP is required for ABA-mediated genome-wide alternative splicing. ABA treatment enhances the novel splicing events in WT genome-widely. The novel alternative splicing events are increased by skip-1 in the absence and present of ABA. Our results first reveal a principle on how a splicing factor affects the ABA signaling.
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Project description:In this study, we have identified genes that are respectively activated and repressed by the low concentration of ABA and show that ROP10 gates a specific subset of genes that are responsive only to a low ABA concentration. Keywords: Whole seedlings of wild-type (Ws) and the mutant (rop10-1) treated with or without ABA
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Project description:Coordinated regulation of protection mechanisms against environmental abiotic stress and pathogen attack is essential for plant adaptation and survival. Initial abiotic stress can interfere with disease resistance signaling. Conversely, initial plant immune signaling may interrupt subsequent ABA signal transduction. However, the processes involved in cross talk between these signaling networks have not been determined. By screening a 9,600 compound chemical library, we identified a small molecule [5-(3,4-Dichlorophenyl)Furan-2-yl]-Piperidin-1-ylMethanethione that rapidly down-regulates ABA-dependent gene expression and also inhibits ABA-induced stomatal closure. Transcriptome analyses show that DFPM also stimulates expression of plant defense-related genes. Plate grown 12-day-old seedlings were transferred into 6 well plates with 1:5000 (V/V) DMSO in water as a control, 30uM DFPM, and 10uM ABA in water as a treatment for 6 hours. DFPM was added 30 min prior to ABA treatment. RNA was extracted using Trizol (Invitrogen, Carlsbad, CA, USA) and further purified using RNeasy Plant RNA purification kit (QIAgen, Valencia, CA, USA). Three biological replicates of ATH1 oligonucleotide arrays were hybridized with labeled samples from 1) wild-type Columbia (WT) untreated, 2) WT with 30uM DFPM treatment, 3) WT with 10uM ABA treatment, 4) WT with 30uM DFPM and 10uM ABA treatment. Each biological replicate was prepared by combining 7 independently-treated samples.
2011-12-31 | GSE28800 | GEO
Project description:Coordinated regulation of protection mechanisms against environmental abiotic stress and pathogen attack is essential for plant adaptation and survival. Initial abiotic stress can interfere with disease resistance signaling. Conversely, initial plant immune signaling may interrupt subsequent ABA signal transduction. However, the processes involved in cross talk between these signaling networks have not been determined. By screening a 9,600 compound chemical library, we identified a small molecule [5-(3,4-Dichlorophenyl)Furan-2-yl]-Piperidin-1-ylMethanethione that rapidly down-regulates ABA-dependent gene expression and also inhibits ABA-induced stomatal closure. Transcriptome analyses show that DFPM also stimulates expression of plant defense-related genes. Plate grown 12-day-old seedlings were transferred into 6 well plates with 1:5000 (V/V) DMSO in water as a control, 30uM DFPM, and 10uM ABA in water as a treatment for 6 hours. DFPM was added 30 min prior to ABA treatment. RNA was extracted using Trizol (Invitrogen, Carlsbad, CA, USA) and further purified using RNeasy Plant RNA purification kit (QIAgen, Valencia, CA, USA). Three biological replicates of ATH1 oligonucleotide arrays were hybridized with labeled samples from 1) wild-type Columbia (WT) untreated, 2) WT with 30uM DFPM treatment, 3) WT with 10uM ABA treatment, 4) WT with 30uM DFPM and 10uM ABA treatment. Each biological replicate was prepared by combining 7 independently-treated samples. Seedling treatments, 4 agent, 1 genotype/variation sets.
2011-12-31 | E-GEOD-28800 | biostudies-arrayexpress