Gene expression of cytosolic glutamine synthetase 1;1 knock-out mutant rice
Ontology highlight
ABSTRACT:
ORGANISM(S): Oryza sativa Oryza sativa Japonica Group
PROVIDER: GSE15122 | GEO | 2010/03/01
SECONDARY ACCESSION(S): PRJNA114877
REPOSITORIES: GEO
Similar Datasets
Project description:Goal of the study is to characterize distinct function(s) of two cytosolic glutamine synthetase (GS) in rice plants. We grew rice lacking GS1;1 and GS1;2 under the ammonium sufficient condition. We harvested roots from the two mutants as well as those of the corresponding control.
2019-04-01 | E-MTAB-6303 | biostudies-arrayexpress
Project description:Goal of the study is to characterize specific function(s) of the cytosolic glutamine synthetase (GS) 1;2 for apical meristem induction in rice plants. To address the issue, we conducted transcript profiling toward basal parts of the knockout mutant lacking GS1;2. We used microarrays conduct transcript profiling of gs1;2 plants. Wild-type samples were used as control.
2014-11-28 | GSE62124 | GEO
Project description:Nitrogen (N) is a critical limiting element in the provision of important components, e.g., chlorophylls, to plants. Organic N synthesized by glutamine synthetase (GS) may help regulate metabolic networks for plant growth and development. However, how multiple isoforms of cytosolic GSs act for metabolic regulation remain unclear. Using the knockout mutants, Osgs1;1 and Osgs1;2, we compared the effects of two cytosolic GSs on metabolism and cell differentiation in rice roots using reverse genetic-, metabolite- and transcript profiling- and microscopic analyzes together with integrated metabolite-transcript network analysis. We used microarrays to detail the global programme of gene expression in rice Osgs1;1 and Osgs1;2 roots.
2020-04-20 | GSE49789 | GEO
Project description:Glutamine synthetase (GS), a key enzyme in biological nitrogen assimilation, is regulated in multiple ways in response to varying nitrogen sources and levels. Here we show a small regulatory RNA, NsiR4 (nitrogen stress induced RNA 4), which plays an important role in the regulation of GS in cyanobacteria. NsiR4 expression in the unicellular Synechocystis sp. PCC 6803 and in the filamentous, nitrogen-fixing Anabaena sp. PCC 7120 is stimulated through nitrogen-limitation via NtcA, the global transcriptional regulator of genes involved in nitrogen metabolism. NsiR4 is widely conserved throughout the cyanobacterial phylum, suggesting a conserved function. In silico target prediction, transcriptome profiling upon pulse overexpression and site-directed mutagenesis experiments using a heterologous reporter system showed that NsiR4 interacts with the 5’UTR of gifA mRNA, which encodes glutamine synthetase inactivating factor IF7. In Synechocystis, we observed an inverse relationship between the levels of NsiR4 and the accumulation of IF7 in vivo. This NsiR4-dependent modulation of gifA (IF7) mRNA accumulation influenced the glutamine pool and thus NH4+ assimilation via glutamine synthetase. As a second target, we identified ssr1528, a hitherto uncharacterized nitrogen-regulated gene. Competition experiments between wild type and an NsiR4 knock-out mutant showed that the lack of NsiR4 led to decreased acclimation capabilities of Synechocystis towards oscillating nitrogen levels. These results suggest a role for NsiR4 in the regulation of nitrogen metabolism in cyanobacteria, especially for the adaptation to rapid changes in available nitrogen sources and concentrations. NsiR4 is the first identified bacterial sRNA regulating the primary assimilation of a macronutrient.
2015-10-20 | GSE73840 | GEO
Project description:There are two major subtype of cells in breast cancer. These cancer cells response differently to glutamine deprivation, here we use one luminal type of breast cancer cell (MCF7) and one basal type of breast cancer cell (MDAMB231) to compare the gene expression differences of these two types of cancer cells in glutamine deprivation. Many cancer cells depend on glutamine for survival and oncogenic transformation. Although targeting glutamine metabolism is proposed as novel therapies, their heterogeneity among different tumors is unknown. Here, we found only basal-type, but not luminal-type breast cancer cells, exhibited phenotypes of glutamine dependency and may benefit from glutamine-targeting therapeutics. The glutamine independence of luminal-type cells is caused by the specific expression of glutamine synthetase (GS), a pattern recapitulated in luminal breast cancers. The co-culture of luminal cells partially rescued the basal cells under glutamine deprivation, suggesting glutamine symbiosis. The luminal-specific expression of GS is directly induced GATA3 and down-regulates glutaminase expression to maintain subtype-specific glutamine metabolism. Collectively, these data indicate the distinct glutamine phenotypes among breast cells and enable the rational design of glutamine targeted therapies.
2012-01-01 | GSE26370 | GEO
Project description:The PI3K-PKB/c-akt-FOXO signalling network provides a major intracellular hub for regulation of cell proliferation, survival and stress resistance1. Here we report a novel function for FOXO transcription factors in regulating autophagy through modulation of intracellular glutamine levels. To identify novel transcriptional targets of this module we performed an unbiased microarray analysis after conditional activation of the key components PI3K, PKB, FOXO3 and FOXO4. Utilising this global pathway approach we identified glutamine synthetase (GS) as being transcriptionally regulated by PI3K-PKB-FOXO signalling. FOXO-mediated increase in GS expression specifically induced glutamine production independently of cell type, and this was evolutionary conserved. FOXO activation resulted in mTOR inhibition by preventing the translocation of mTOR to lysosomal membranes, which was dependent on GS activity. Increased GS activity resulted in increased autophagosome turnover as measured by LC3 lipidation, p62 degradation, and confocal imaging of LC3, p62, WIPI-1, ULK2 and Atg12. Inhibition of FOXO3-mediated autophagy resulted in increased apoptosis, suggesting that the induction of autophagy by FOXO3-mediated upregulation of GS is important for cellular survival. These findings reveal a novel signalling network that can directly modulate autophagy through regulation of glutamine metabolism.
2012-07-22 | GSE35703 | GEO
Project description:The PI3K-PKB/c-akt-FOXO signalling network provides a major intracellular hub for regulation of cell proliferation, survival and stress resistance1. Here we report a novel function for FOXO transcription factors in regulating autophagy through modulation of intracellular glutamine levels. To identify novel transcriptional targets of this module we performed an unbiased microarray analysis after conditional activation of the key components PI3K, PKB, FOXO3 and FOXO4. Utilising this global pathway approach we identified glutamine synthetase (GS) as being transcriptionally regulated by PI3K-PKB-FOXO signalling. FOXO-mediated increase in GS expression specifically induced glutamine production independently of cell type, and this was evolutionary conserved. FOXO activation resulted in mTOR inhibition by preventing the translocation of mTOR to lysosomal membranes, which was dependent on GS activity. Increased GS activity resulted in increased autophagosome turnover as measured by LC3 lipidation, p62 degradation, and confocal imaging of LC3, p62, WIPI-1, ULK2 and Atg12. Inhibition of FOXO3-mediated autophagy resulted in increased apoptosis, suggesting that the induction of autophagy by FOXO3-mediated upregulation of GS is important for cellular survival. These findings reveal a novel signalling network that can directly modulate autophagy through regulation of glutamine metabolism.
2012-07-22 | GSE35701 | GEO
Project description:Corynebacterium glutamicum, a gram-positive soil bacterium used for the industrial production of amino acids such as L-glutamate and L-lysine, is able to use a number of different nitrogen sources, such as ammonium, urea, or creatinine. In this communication, we show that L-glutamine serves as an excellent nitrogen source for C. glutamicum and allows similar growth rates in glucose minimal medium as ammonium. A transcriptome comparison revealed a strong induction of the nitrogen starvation response when glutamine was used as nitrogen source. Subsequent growth experiments with a variety of mutants defective in nitrogen metabolism showed that glutamate synthase is crucial for glutamine utilization, while a putative glutaminase is dispensable under the experimental conditions used. The fact that the glutamate synthase encoding gltBD operon is under strict nitrogen control explains the necessity for induction of the nitrogen starvation response. The paradox situation that the nitrogen starvation response is induced although intracellular L-glutamine levels are high has implications on nitrogen sensing. In contrast to other gram-positive and gram-negative bacteria such as Bacillus subtilis, Salmonella typhimurium, and Klebsiella pneumoniae, a drop in glutamine concentration obviously does not serve as a nitrogen starvation signal in C. glutamicum. Three biological replicates were performed. To analyse how L-glutamine influences global gene expression when used as sole nitrogen source instead of ammonium, DNA microarray analyses were performed. For this purpose RNA was isolated from exponentially growing cells cultivated in CgXII medium containing glucose as carbon source and either L-glutamine or ammonium sulphate as nitrogen source.
2010-10-05 | E-GEOD-19779 | biostudies-arrayexpress
Project description:There are two major subtype of cells in breast cancer. These cancer cells response differently to glutamine deprivation, here we use one luminal type of breast cancer cell (MCF7) and one basal type of breast cancer cell (MDAMB231) to compare the gene expression differences of these two types of cancer cells in glutamine deprivation. Many cancer cells depend on glutamine for survival and oncogenic transformation. Although targeting glutamine metabolism is proposed as novel therapies, their heterogeneity among different tumors is unknown. Here, we found only basal-type, but not luminal-type breast cancer cells, exhibited phenotypes of glutamine dependency and may benefit from glutamine-targeting therapeutics. The glutamine independence of luminal-type cells is caused by the specific expression of glutamine synthetase (GS), a pattern recapitulated in luminal breast cancers. The co-culture of luminal cells partially rescued the basal cells under glutamine deprivation, suggesting glutamine symbiosis. The luminal-specific expression of GS is directly induced GATA3 and down-regulates glutaminase expression to maintain subtype-specific glutamine metabolism. Collectively, these data indicate the distinct glutamine phenotypes among breast cells and enable the rational design of glutamine targeted therapies. Gene expression analysis in MCF7 and MDAMB231 cultured with or without glutamine for 24h
2012-01-01 | E-GEOD-26370 | biostudies-arrayexpress
Project description:Enteric bacteria use up to 15% of their cellular energy for ammonium assimilation via glutamine synthetase (GS)/glutamate synthase (GOGAT) and glutamate dehydrogenase (GDH), in response to low or high ammonium availability. However, the sensory mechanisms for effective and appropriate coordination between carbon metabolism and ammonium assimilation are not fully elucidated. Here, we report that, in Salmonella, carbon metabolism coordinates the activities of GS/GDH via functional reversible protein lysine acetylation. Glucose simultaneously promotes acetyltransferase Pat-mediated acetylation on Lys164 and Lys353 of GS to activate the adenylylated-GS by inducing its conformation change, while on Lys128 of GDH to inactivate the enzyme by impeding its catalytic center, respectively, which are reversed by deacetylase CobB-mediated deacetylation. Molecular dynamic (MD) simulations indicated that the acetylation activation of GS activity was adenylylation-dependent. Acetylation and deacetylation occur within minutes of ‘glucose shock’ to promptly adapt to ammonium/carbon variation and finely balance glutamine/glutamate synthesis. Acetylation can rehabilitate the growth tardiness of Salmonella mutant with chromosomal mimetic mutation of adenylylated-GS and thus help its survival in mice. Thus, glucose-driven acetylation integrates the signals of assimilation and carbon metabolism for proper growth control.
2023-06-21 | PXD039658 | Pride