Asparaginase 2 gene expression as a biomarker in response to nitrate ans sucrose during bud outgrowth in Rosa hybrida
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ABSTRACT:
PROVIDER: PRJNA551889 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9621940.fastq.gz | Fastqsanger.gz | |||
| SRR9621938.fastq.gz | Fastqsanger.gz | |||
| SRR9621939.fastq.gz | Fastqsanger.gz |
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Project description:Axillary bud outgrowth is an essential process of plant branching to set-up its architecture. Nitrogen is implicated in the development of young organs such as secondary axes (axes II) resulting from bud outgrowth. We have previously shown in planta that asparagine concentration increases in the sap and in the tissues during axes II elongation. In vitro, we demonstrated that this amino acid is the sole at its physiological concentration able to evoke an efficient elongation of axes II in the presence of different sugars. To go further, we performed in this work a transcriptomic analysis through RNA sequencing and obtained 848 annotated sequences that are potentially implicated in bud outgrowth in response to nitrate in the presence of sucrose. Among them, the expression of Asparaginase 2 gene takes place during dormancy while, in contrast, Asparagine synthase 2 gene is active during bud outgrowth. So we have established through qRT-PCR the expression level of the main growth regulators related genes in the permissive condition in the presence of asparagine and sucrose. We confirmed using conceptually different experiments that asparagine has a strong involvement in bud outgrowth and demonstrated that the genes implicated in its metabolism could be consider as new biomarkers in the process in rosebush.
2019-07-01 | GSE133559 | GEO
Project description:Resistance to asparaginase, an antileukemic enzyme that depletes asparagine, is a common clinical problem. Using a genome-wide CRISPR/Cas9 screen, we found a synthetic lethal interaction between Wnt pathway activation and asparaginase in acute leukemias resistant to this enzyme. Wnt pathway activation induced asparaginase sensitivity in distinct treatment-resistant subtypes of acute leukemia, but not in normal hematopoietic progenitors. Sensitization to asparaginase was mediated by Wnt-dependent stabilization of proteins (Wnt/STOP), which inhibits GSK3-dependent protein ubiquitination and proteasomal degradation, a catabolic source of asparagine. Inhibiting the alpha isoform of GSK3 phenocopied this effect, and pharmacologic GSK3 inhibition profoundly sensitized drug-resistant leukemias to asparaginase. Our findings provide a molecular rationale for activation of Wnt/STOP signaling to improve the therapeutic index of asparaginase. To gain further insights into mechanisms of cytotoxicity of this combination, we applied unbiased mass spectrometry proteomics to CCRF-CEM cells, a human T-cell acute lymphoblastic leukemia cell line, treated with vehicle, asparaginase alone, the GSK3 inhibitor BRD0705 (which phenocopies Wnt/STOP pathway activation), or the combination of asparaginase and BRD0705.
2019-03-29 | PXD013061 | Pride
Project description:To identify genes affected by L-asparaginase, we treated with L-asparaginase 1U/ml. After 2 days, RNA was extracted, and then expression analysis was performed using agilent microarray.
2017-01-31 | GSE94289 | GEO
Project description:Abstract: To investigate the effect of l-asparaginase on acute lymphoblastic leukemia (ALL), we used cDNA microarrays to obtain a genome-wide view of gene expression both at baseline and after in vitro exposure to l-asparaginase in cell lines and pediatric ALL samples. In 16 cell lines, a baseline gene expression pattern distinguished l-asparaginase sensitivity from resistance. However, for 28 pediatric ALL samples, no consistent baseline expression pattern was associated with sensitivity to l-asparaginase. In particular, baseline expression of asparagine synthetase (ASNS) was not predictive of response to l-asparaginase. After exposure to l-asparaginase, 5 cell lines and 10 clinical samples exhibited very similar changes in the expression of a large number of genes. However, the gene expression changes occurred more slowly in the clinical samples. These changes included a consistent increase in expression of tRNA synthetases and solute transporters and activating transcription factor and CCAAT/enhancer binding protein family members, a response similar to that observed with amino acid starvation. There was also a consistent decrease in many genes associated with proliferation. Taken together, the changes seem to reflect a consistent coordinated response to asparagine starvation in both cell lines and clinical samples. Importantly, in the clinical samples, increased expression of ASNS after l-asparaginase exposure was not associated with in vitro resistance to l-asparaginase, indicating that ASNS-independent mechanisms of in vitro l-asparaginase resistance are common in ALL. These results suggest that targeting particular genes involved in the response to amino acid starvation in ALL cells may provide a novel way to overcome l-asparaginase resistance. This SuperSeries is composed of the SubSeries listed below.
2006-03-08 | GSE4397 | GEO
Project description:Sugar has only recently been identified as a key player in triggering bud outgrowth, while hormonal control of bud outgrowth is already well established. To get a better understanding of sugar control, the present study investigated how sugar availability modulates the hormonal network during bud outgrowth in Rosa hybrida. Other plant models, for which mutants are available, were used when necessary. Buds were grown in vitro to manipulate available sugars. The temporal patterns of the hormonal regulatory network were assessed in parallel with bud outgrowth dynamics. Sucrose determined bud entrance into sustained growth in a concentration-dependent manner. Sustained growth was accompanied by sustained auxin production in buds, and sustained auxin export in a DR5::GUS-expressing pea line. Several events occurred ahead of sucrose-stimulated bud outgrowth. Sucrose upregulated early auxin synthesis genes (RhTAR1, RhYUC1) and the auxin efflux carrier gene RhPIN1, and promoted PIN1 abundance at the plasma membrane in a pPIN1::PIN1-GFP-expressing tomato line. Sucrose downregulated both RwMAX2, involved in the strigolactone-transduction pathway, and RhBRC1, a repressor of branching, at an early stage. The presence of sucrose also increased stem cytokinin content, but sucrose-promoted bud outgrowth was not related to that pathway. In these processes, several non-metabolizable sucrose analogues induced sustained bud outgrowth in R. hybrida, Pisum sativum, and Arabidopsis thaliana, suggesting that sucrose was involved in a signalling pathway. In conclusion, we identified potential hormonal candidates for bud outgrowth control by sugar. They are central to future investigations aimed at disentangling the processes that underlie regulation of bud outgrowth by sugar.
| S-EPMC4986866 | biostudies-other