Comparison of gene expression of WT and PerM mutant M. tuberculosis H37Rv grown in high and reduced magnesium
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ABSTRACT:
ORGANISM(S): Mycobacterium tuberculosis Mycobacterium tuberculosis H37Rv
PROVIDER: GSE57263 | GEO | 2015/01/05
SECONDARY ACCESSION(S): PRJNA246114
REPOSITORIES: GEO
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Project description:M. tuberculosis membrane protein PerM is required for persistence in chronic mouse infection. In vitro, the perM mutant requires increased magnesium for replication and survival, with elongation and lysis in low-magnesium media. To gain insight into the function of PerM, we compared the transcriptomes of wt and perM mutant Mtb grown in high (2000 M-NM-<M) and reduced (250 M-NM-<M) Mg2+ in three independent experiments. Transcriptome analysis of the perM mutant grown in reduced magnesium revealed upregulation of cell division and cell wall biosynthesis genes. Bacteria were grown for 5 days in SautonM-bM-^@M-^Ys media containing 250 or 2000 M-NM-<M MgCl2 and 0.05% Tween 80. Three independent experiments were performed.
2015-01-05 | E-GEOD-57263 | biostudies-arrayexpress
Project description:By chance, we discovered a window of extracellular magnesium (Mg2+) availability that modulates Bacillus subtilis division frequency without affecting growth rate. In this window, cells grown with excess Mg2+ produce shorter cells than those grown in unsupplemented medium. The Mg2+-responsive adjustment in cell length occurs in both rich and minimal media and in domesticated and undomesticated strains. Of other divalent cations tested, manganese (Mn2+) and zinc (Zn2+) also resulted in cell shortening, but only at concentrations that affected growth. Cell length decreased proportionally with increasing Mg2+ from 0.2 mM to 4.0 mM, with little or no detectable change in labile, intracellular Mg2+ based on a riboswitch reporter. Cells grown in excess Mg2+ had fewer nucleoids and possessed more FtsZ-rings per unit cell length, consistent with increased division frequency. Remarkably, when shifting cells from unsupplemented to supplemented medium, more than half of the cell length decrease occurred in the first 10 min, consistent with rapid division onset. Relative to unsupplemented cells, cells growing at steady-state with excess Mg2+ showed enhanced expression of a large number of SigB-regulated genes and activation of the Fur, MntR, and Zur regulons. Thus, by manipulating the availability of one nutrient, we were able to uncouple growth rate from division frequency and identify transcriptional changes suggesting cell division is accompanied by the general stress response and an enhanced demand to sequester and/or increase uptake of iron, Mn2+, and Zn2+.
2022-12-06 | GSE219221 | GEO
Project description:Physiological mechanisms involved in root hair development in response to magnesium (Mg) availability are unclear. This study investigated the influence of Mg availability on root hair development in arabidopsis grown in different Mg concentrations ranging from 0.5 μM to 10 mM. After 7-d treatment, root hair development was enhanced in roots exposed to low Mg but was inhibited severely in roots grown in high Mg. Low Mg (0.5 µM) enhanced many genes like LRX1, COW1, EXP7 and ROP2 that control root hair development. Low Mg supply also increased concentrations of total Ca2+ and ROS in roots, but application of either BAPTA or DPI to low Mg treatment blocked the enhanced development of root hairs. The opposite was true when the plants under high Mg (3 mM) were supplied with Ca2+ or PMS. Besides, in roots under low Mg and high Mg, the most significant biological function enrichment were in the ‘oxidation reduction’, ‘cell wall organization’, ‘ion response’. This study demonstrated that Ca2+ and ROS played critically in controlling the Mg-induced development of root hairs. Meanwhile, transcriptome analysis associated with Mg supply contributed to a better understanding of molecular events responsible for sensing Mg status. Roots were sampled from five-week-cultivated Arabidopsis after 7 d treatment of low Mg (supplied with 0.5 μM Mg2+) and high Mg (supplied with 10 mM Mg2+).
2012-12-14 | E-GEOD-42899 | biostudies-arrayexpress
Project description:In many Gram-negative bacteria, the stress sigma factor of RNA polymerase, σS/RpoS, remodels global gene expression to reshape the physiology of quiescent cells and ensure their survival under non-optimal growth conditions. In the foodborne pathogen Salmonella enterica serovar Typhimurium, σS is also required for biofilm formation and virulence. We have recently shown that a ΔrpoS mutation affects the magnesium content of Salmonella and expression of the primary Mg2+-transporter CorA. The other two Mg2+-transporters of Salmonella are encoded by the PhoP-activated mgtA and mgtB genes expressed under magnesium starvation, whereas the corA gene is expressed constitutively. The σS control of corA prompted us to evaluate the impact CorA in quiescent Salmonella cells, by using global and analytical proteomic analyses and physiological assays. The ΔcorA mutation conferred a competitive disadvantage to exit from stationary phase, and slightly impaired motility, but had no effect on total and free cellular magnesium contents. In contrast to the wild type strain, the ΔcorA mutant produced MgtA, but not MgtB, in the presence of high extracellular magnesium concentration. Under these conditions, MgtA production in the ΔcorA mutant did not require PhoP and, consistently, a ΔmgtA, but not a ΔphoP, mutation slightly reduced the magnesium content of the ΔcorA mutant. Nevertheless, the ΔphoP mutation strongly impaired growth and motility, in the absence of CorA only and independently of the extracellular magnesium concentration, unraveling the importance of PhoP-dependent functions in the absence of CorA. Under these conditions, several proteins involved in flagella formation, chemotaxis and secretion were affected by the ΔcorA and ΔphoP mutations in combination, but not alone. Altogether, our data pinpoint a regulatory network, where the absence of CorA is sensed and its physiological consequences alleviated by induction of MgtA- and PhoP- dependent compensatory mechanisms.
2023-10-24 | PXD041489 | Pride
Project description:To learn about the cellular processes involved in Mg2+ transport and the mechanisms allowing cells to cope with low Mg2+ availability, we performed RNA expression profiling experiments, and followed changes in gene activity upon Mg2+ depletion on a genome-wide scale. A striking portion of genes up-regulated under Mg2+ depletion is also induced by high Ca2+ and/or alkalinization. Among the genes significantly up-regulated by Mg2+ starvation, Ca2+ stress and alkalinization are ENA1 (encoding a P-type ATPase sodium pump) and PHO89 (encoding a sodium/phosphate cotransporter). We show that up-regulation of these genes is dependent on the calcineurin/Crz1p signaling pathway. Similarly to Ca2+ stress, Mg2+ starvation induces translocation of the transcription factor Crz1p from the cytoplasm into the nucleus. The up-regulation of ENA1 and PHO89 upon Mg2+ starvation depends on extracellular Ca2+. Using fluorescence resonance energy transfer microscopy we demonstrate that removal of Mg2+ results in an immediate increase in free cytoplasmic Ca2+. This effect is dependent on external Ca2+. Results presented indicate that Mg2+ depletion in yeast cells leads to enhanced cellular Ca2+ concentrations, which activate the Crz1p/calcineurin pathway. We provide evidence that calcineurin/Crz1p signaling is crucial for yeast cells to cope with Mg2+ depletion stress. Keywords: stress response (magnesium starvation)
2007-03-08 | GSE6687 | GEO
Project description:The distal convoluted tubule (DCT) plays a key role in the fine-tuning of renal Mg2+ reabsorption. In recent years, hereditary magnesium (Mg2+) transport disorders have helped to identify important players in DCT Mg2+ homeostasis. Here, we report the Mg2+-sensitive transcriptional expression of the DCT transcriptome using gene expression microarray analysis. Mice expressing eGFP under a DCT-specific promoter were subjected to Mg2+-deficient or Mg2+-enriched diets. Subsequently, the Complex Object Parametric Analyzer and Sorter (COPAS) allowed isolation of eGFP-positive DCT cells. RNA extracts were subjected to pair-wise microarray analysis, high vs. low Mg2+. Of all genes in the genome, 46 were shown to be differentially expressed with a minimal fold-change of 2. Several known magnesiotropic genes, such as Trpm6 and Parvalbumin, were upregulated in the low Mg2+ fraction. Moreover, new genes were identified that are potentially involved in renal Mg2+ homeostasis. To confirm that the selected candidate genes are regulated by dietary Mg2+ availability, the expression levels of Slc41a3, Pcbd1, Tbc1d4 and Umod were determined by RT-PCR analysis. Indeed, all four genes were shown to be significantly upregulated in mice fed the Mg2+-deficient diet. In conclusion, by elucidating the Mg2+-sensitive DCT transcriptome, new candidate players in renal Mg2+ homeostasis were identified. RNA samples were isolated from PV-eGFP-positive tubules from mice fed on a low (L-samples) or high (H-samples) magnesium diet. Littermate H and L samples were labeled and put on mouse microarrays together. Two of the four sample sets were analyzed in dye-swap to compensate for dye-biases.
2013-12-13 | E-GEOD-40208 | biostudies-arrayexpress
Project description:Klotho knock-out mice are an important model for CKD-induced calcification. In CKD, serum magnesium (Mg2+) inversely correlates with vascular calcification. This study aims to determine the effects of Mg2+ on aortic calcification in Klotho knock-out mice. Klotho knock-out mice were treated with either a minimal or a high Mg2+ diet from birth. After eight weeks, serum biochemistry was studied and organs were harvested. Protective effects of Mg2+ were characterized by RNA-sequencing of aortic tissue. Micro-CT analysis was performed to study bone integrity. High Mg2+ diet prevented vascular calcification and reduced aortic gene expression of Runx2 and matrix Gla protein, demonstrating the protective effect on pro-osteogenic signaling. Differential expression of inflammation and extracellular matrix remodeling genes accompany the beneficial effects of Mg2+ on calcification. High dietary Mg2+ did not affect serum parathyroid hormone, vitamin D3 and calcium. High Mg2+ intake prevented calcification despite increasing fibroblast growth factor-23 and phosphate concentration in knock-out mice. In addition, mice on the high Mg2+ diet had a 20% reduced femoral bone mineral density and increased osteoid formation indicating osteomalacia, while osteoclast activity was decreased in Klotho knock-out mice. In Saos-2 osteoblasts, Mg2+ supplementation reduced mineralization independent of osteoblastic matrix production, alkaline phosphatase activity and maturation markers alpha-1 type-I collagen and sclerostin. In conclusion, high dietary Mg2+ prevents calcification in Klotho knock-out mice. These effects are potentially mediated by reduction of inflammatory and extracellular matrix remodeling pathways in the aorta. Mg2+ treatment is promising to prevent vascular calcification, but the risk for osteomalacia should be considered.
2019-11-04 | GSE136593 | GEO
Project description:In response to low levels of magnesium (Mg2+), the PhoQP two component system induces the transcription of two convergent genes, one encoding a 31-amino acid protein denoted MgtS and the second encoding a small, regulatory RNA (sRNA) denoted MgrR. Previous studies showed that the MgtS protein interacts with and stabilizes the MgtA Mg2+ importer to increase intracellular Mg2+ levels, while the MgrR sRNA base pairs with the eptB mRNA thus affecting lipopolysaccharide modification. Surprisingly, we found overexpression of the MgtS protein also leads to induction of the PhoRB regulon. Studies to understand this activation showed that MgtS forms a complex with a second protein, PitA, a cation-phosphate symporter. Given that the additive effect of ∆mgtA and ∆mgtS mutations on intracellular Mg2+ concentrations seen previously is lost in the ∆pitA mutant, we suggest that MgtS binds to and blocks Mg2+ leakage through PitA under Mg2+-limiting conditions. Consistent with a detrimental role of PitA in low Mg2+, we also observe MgrR sRNA repression of PitA synthesis. Thus, PhoQP induces the expression of two convergent small genes in response to Mg2+ limitation whose products both repress PitA activity and levels to increase intracellular Mg2+ levels. Funded by NIH Intramural Program ZIA HD008855-11.
2018-10-03 | GSE120726 | GEO
Project description:The distal convoluted tubule (DCT) plays a key role in the fine-tuning of renal Mg2+ reabsorption. In recent years, hereditary magnesium (Mg2+) transport disorders have helped to identify important players in DCT Mg2+ homeostasis. Here, we report the Mg2+-sensitive transcriptional expression of the DCT transcriptome using gene expression microarray analysis. Mice expressing eGFP under a DCT-specific promoter were subjected to Mg2+-deficient or Mg2+-enriched diets. Subsequently, the Complex Object Parametric Analyzer and Sorter (COPAS) allowed isolation of eGFP-positive DCT cells. RNA extracts were subjected to pair-wise microarray analysis, high vs. low Mg2+. Of all genes in the genome, 46 were shown to be differentially expressed with a minimal fold-change of 2. Several known magnesiotropic genes, such as Trpm6 and Parvalbumin, were upregulated in the low Mg2+ fraction. Moreover, new genes were identified that are potentially involved in renal Mg2+ homeostasis. To confirm that the selected candidate genes are regulated by dietary Mg2+ availability, the expression levels of Slc41a3, Pcbd1, Tbc1d4 and Umod were determined by RT-PCR analysis. Indeed, all four genes were shown to be significantly upregulated in mice fed the Mg2+-deficient diet. In conclusion, by elucidating the Mg2+-sensitive DCT transcriptome, new candidate players in renal Mg2+ homeostasis were identified.
2013-12-13 | GSE40208 | GEO
Project description:The poor osseointegration of dental implants in diabetic patients has become a long-standing clinical problem. Magnesium has been proved to promote bone healing under normal conditions. Here, we elucidate the mechanism by which Mg2+ promotes vascularized osseointegration in diabetic status. We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised, with significantly decreased angiogenesis. We then developed Mg-coating implants with hydrothermal synthesis. These implants sucessfully improved the vascularization and osseointegration in diabetic status. Mechanically, Mg2+ promoted the degradation of Kelch-like ECH associated protein 1 (Keap1) and the nucleation of nuclear factor erythroid 2-related factor 2 (Nrf2) by up-regulating the expression of sestrin 2 (SESN2) in endothelial cells, thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia. Altogether, our data proved that Mg2+ promoted vascularized osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.
2024-02-07 | GSE236139 | GEO