Identifying phosphate deficiency responsive genes depend on SlNSP1 and SlNSP2 in tomato
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ABSTRACT:
PROVIDER: PRJNA1198054 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31710175_1.fastq.gz | Fastqsanger.gz | |||
| SRR31710175_2.fastq.gz | Fastqsanger.gz | |||
| SRR31710176_1.fastq.gz | Fastqsanger.gz | |||
| SRR31710176_2.fastq.gz | Fastqsanger.gz | |||
| SRR31710177_1.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study is to idetify phosphate deficiency induced genes depedent on SlNSP1 and SlNSP2 in tomato, by treating seedlings cultured in half-strength Hoagland solution with or without phosphate.
2025-02-07 | GSE284240 | GEO
Project description:Phosphate (Pi) deficiency triggers the differential expression of a large set of genes, which communally adapt the plant to low Pi bioavailability. To infer functional modules in early transcriptional responses to Pi deficiency, we conducted time-course microarray experiments and subsequent coexpression-based clustering of Pi-responsive genes by pairwise comparison of a large number of genes against a customized data base.
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Project description:Transcriptomic analysis of the phosphate-starvation response of tomato plants
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Project description:Mycobacterium tuberculosis persists in the lungs of mammalian hosts despite inducing an immune response dominated by the macrophage-activating cytokine interferon-gamma (IFN-gamma). We identified the M. tuberculosis phosphate uptake system component PstA1 as a factor required to resist IFN-gamma dependent immunity. A ∆pstA1 mutant was fully virulent in IFN-gamma-/- mice but was attenuated in mice lacking the IFN-gamma-inducible nitric oxide synthase (NOS2). This phenotype suggests that ∆pstA1 bacteria are hypersensitive to an IFN-gamma-dependent immune mechanism(s) other than NOS2. In other species, the Pst system participates in phosphate-responsive gene regulation by interacting with a two-component signal transduction system. We identified genes that exhibited dysregulated expression in the ∆pstA1 mutant and showed that aberrant gene expression was dependent on the two-component system response regulator RegX3. Deletion of regX3 suppressed the replication and virulence defects of ∆pstA1 bacteria in NOS2-/- mice, suggesting that the ∆pstA1 mutant is attenuated, in part, due to aberrant RegX3-dependent gene expression. Our data imply that phosphate is an important signal controlling M. tuberculosis gene expression during replication in the lung.
2013-01-01 | GSE36998 | GEO
Project description:Mycobacterium tuberculosis persists in the lungs of mammalian hosts despite inducing an immune response dominated by the macrophage-activating cytokine interferon-gamma (IFN-gamma). We identified the M. tuberculosis phosphate uptake system component PstA1 as a factor required to resist IFN-gamma dependent immunity. A ∆pstA1 mutant was fully virulent in IFN-gamma-/- mice but was attenuated in mice lacking the IFN-gamma-inducible nitric oxide synthase (NOS2). This phenotype suggests that ∆pstA1 bacteria are hypersensitive to an IFN-gamma-dependent immune mechanism(s) other than NOS2. In other species, the Pst system participates in phosphate-responsive gene regulation by interacting with a two-component signal transduction system. We identified genes that exhibited dysregulated expression in the ∆pstA1 mutant and showed that aberrant gene expression was dependent on the two-component system response regulator RegX3. Deletion of regX3 suppressed the replication and virulence defects of ∆pstA1 bacteria in NOS2-/- mice, suggesting that the ∆pstA1 mutant is attenuated, in part, due to aberrant RegX3-dependent gene expression. Our data imply that phosphate is an important signal controlling M. tuberculosis gene expression during replication in the lung. Aerobically growing logarithmic phase Wt or pstA1/regX3/pstA1regX3 mutant strains were grown in phosphate replete media and analyzed after several hours. Experiments were repeated in triplicate (pstA1 mutant) or quadruplicate (regX3/pstA1regX3 mutant).
2013-01-01 | E-GEOD-36998 | biostudies-arrayexpress
Project description:In bacteria, the availability of environmental inorganic phosphate is typically sensed by the conserved PhoRB two-component signaling pathway, which uses the flux through the Pst phosphate transporter as a readout of the extracellular phosphate level to control a variety of phosphate-responsive genes. While the sensing of environmental phosphate is well-established, the regulatory effects of cytoplasmic phosphate are still unclear. Here, we disentangle the physiological and transcriptional responses of Caulobacter crescentus to changes in the environmental and cytoplasmic phosphate levels. To this end, we are uncoupling phosphate uptake from the activity of the Pst system by producing an additional, heterologous phosphate transporter. This approach reveals a bi-pronged response of C.crescentus to phosphate limitation, in which the PhoRB signaling mostly facilitates the utilization of alternative phosphate sources, whereas the cytoplasmic phosphate level controls the morphological and physiological adaptation of cells to growth in conditions of global phosphate limitation. These findings open the door to a more comprehensive understanding of phosphate signaling in bacteria.
2023-10-20 | GSE244776 | GEO
Project description:cold-responsive genes in tomato Raw sequence reads
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Project description:Deep sequencing of Arabidopsis thaliana small RNAs was conducted to reveal microRNAs (miRNAs) and other small RNAs that were differentially expressed in response to phosphate (Pi) deficiency. About 3.5 million sequence reads corresponding to 0.6-1.2 million unique sequence tags from each Pi-sufficient or -deficient root or shoot sample were mapped to the Arabidopsis genome. We showed that upon Pi deprivation, the expression of miR156, miR399, miR778 and miR827 was induced, whereas the expression of miR169, miR395 and miR398 was repressed. We found crosstalks coordinated by these miRNAs under different nutrient deficiencies. Moreover, we found a new miRNA family upregulated specifically by Pi deficiency. In addition to miRNAs, we identified one Pi starvation-induced DCL1-dependent small RNA derived from the long terminal repeat of a retrotransposon and a group of 19-nucleotide small RNAs corresponding to the 5' end of tRNA and expressed at a high level in Pi-starved roots. Interestingly, we observed an increased abundance of TAS4-derived trans-acting siRNAs (ta-siRNAs) in Pi-deficient shoots and uncovered an autoregulatory mechanism of PAP1/MYB75 via miR828 and TAS4-siR81(-) that regulates the biosynthesis of anthocyanin. This finding sheds light on the regulatory network between miRNA/ta-siRNA and its target gene. Of note, a substantial amount of miR399* accumulated under Pi deficiency. Like miR399, miR399* can move across the graft junction, implying a potential biological role for miR399*. This study represents a comprehensive expression profiling of Pi-responsive small RNAs and advances our understanding of the regulation of Pi homeostasis mediated by small RNAs. Keywords: Transcriptome analysis Examination of 4 samples from root and shoot tissues of Arabidopsis in either phosphate-sufficient or phosphate-deficient condition
2009-12-01 | E-GEOD-17741 | biostudies-arrayexpress
Project description:FGF23 is a bone-derived hormone that mediates renal phosphate reabsorption and 1,25(OH)2 vitamin D metabolism via its required co-receptor alpha-Klotho (KL). The functional pathways guiding this hormone’s activity in kidney have not been studied extensively, and whether using other factors with overlapping signaling profiles to produce FGF23-like responses is unclear. To map FGF23-related genes, gene array and single-cell RNA sequencing were utilized on wild type mouse kidneys. After identifying Heparin-binding EGF-like growth factor (HBEGF) as an up-regulated gene in response to FGF23 delivery, KL-null and phosphate-deficient diet fed mouse models and in vitro experiments were utilized to further test HBEGF bioactivity in kidney. Gene array demonstrated that HBEGF was significantly up-regulated following FGF23 delivery to wild type (WT) mice. Next, mice injected with HBEGF had phenotypes consistent with partial FGF23-mimetic activity including robust induction of EGR1, and increased CYP24A1 mRNAs. Single cell RNA sequencing showed overlapping HBEGF and EGFR expression in the proximal tubule (PT), and KL expression in PT and distal tubule (DT) segments. In KL-null mice devoid of canonical FGF23 signaling, HBEGF injections significantly increased EGR1 and CYP24A, and correction of basally-elevated CYP27B1 was observed. In addition, mice placed on a phosphate deficient diet to suppress FGF23 had endogenously increased CYP27B1 mRNA, which was rescued in mice receiving HBEGF. In HEK293 renal epithelial cells, HBEGF and FGF23 increased CYP24A1 mRNA. Targeting pathways known to be downstream of FGF23 in kidney may help to control renal phosphate handling in diseases of altered FGF23 bioactivity.
2020-10-01 | GSE138992 | GEO