Gene expression profiling of wiltype and Ctr1 knockout MEFs with depleted cellular Cu levels
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE121322 | GEO | 2020/01/01
REPOSITORIES: GEO
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Project description:Gene expression profiling of wiltype and Ctr1 knockout MEFs with depleted cellular Cu levels
| PRJNA497055 | ENA
Project description:We used digital gene expression (NlaIII sequence tags) and RNA-Seq to compare the transcriptomes of Cu-replete vs. Cu–deficient Chlamydomonas wild-type cells to reveal dozens of mRNAs whose abundance is modified. Half of the corresponding genes are targets of CRR1, a master regulator of nutritional copper sensing, and are associated with candidate CRR1 binding sites. The targets include many plastid-localized proteins, like FDX5 encoding a ferredoxin isoform, and CGL78, encoding a protein conserved in the green lineage, indicative of modified plastid metabolism. Immunoblot analysis and proteome profiles recapitulate the transcriptome profiles. New evidence for Cu sparing is suggested by up-regulation of AOF1 encoding a copper-independent but flavin-dependent amine oxidase and down-regulation of two metal- binding proteins. Genes encoding redox proteins, many of which function in lipid metabolism, are over-represented, which is compatible with the role of Cu in biology. Lipid profiles indicate a CRR1-dependent increase in Cu-deficient cells in the proportion of unsaturated (16:2, 16:3, 16:4, 18:2) fatty acids at the expense of the more saturated (16:0, 16:1, 18:0) precursors, especially on plastid galactolipids, which validates the increased expression of acyl-ACP and plastid-localized w-6 desaturases. CRR1-independent changes in the transcriptome suggest a role for Cu in oxygen sensing in Chlamydomonas. Sampling of Chlamydomonas CC-1021 (2137) and crr1-2, crr1:CRR1 mutant cells (the mutant is knock-down for the transcription factor crr1, which plays a key role in the transcriptional response to copper levels) cultivated in TAP or minimal medium under Cu-sufficient (control) and Cu-defficient conditions. poly-A purification, NlaIII digestion/random fragmentation
2011-10-23 | E-GEOD-25124 | biostudies-arrayexpress
Project description:Iron (Fe) and copper (Cu) are essential metal micronutrients that are necessary for many redox reactions. The uptake of these metals is tightly regulated in plants. Some redox processes can alternatively use Fe-containing proteins or Cu-containing proteins, depending on nutritional status. Copper deficiency can rescue a Cucumis melo Fe uptake deficient mutant, and Fe deficiency can result in increased accumulation of Cu. However, the system responsible for Fe-deficiency-regulated Cu-uptake is unknown. To understand the genes and gene networks associated with Fe-deficiency regulated Cu uptake and Fe-Cu cross-talk, we conducted transcriptomic profiling of roots and rosettes of spl7 (a Cu uptake deficient mutant in arabidopsis) and Col-0 (WT) grown under Fe, Cu and simultaneous Fe and Cu deficiency conditions.
2018-03-01 | GSE104916 | GEO
Project description:We used digital gene expression (NlaIII sequence tags) and RNA-Seq to compare the transcriptomes of Cu-replete vs. Cu–deficient Chlamydomonas wild-type cells to reveal dozens of mRNAs whose abundance is modified. Half of the corresponding genes are targets of CRR1, a master regulator of nutritional copper sensing, and are associated with candidate CRR1 binding sites. The targets include many plastid-localized proteins, like FDX5 encoding a ferredoxin isoform, and CGL78, encoding a protein conserved in the green lineage, indicative of modified plastid metabolism. Immunoblot analysis and proteome profiles recapitulate the transcriptome profiles. New evidence for Cu sparing is suggested by up-regulation of AOF1 encoding a copper-independent but flavin-dependent amine oxidase and down-regulation of two metal- binding proteins. Genes encoding redox proteins, many of which function in lipid metabolism, are over-represented, which is compatible with the role of Cu in biology. Lipid profiles indicate a CRR1-dependent increase in Cu-deficient cells in the proportion of unsaturated (16:2, 16:3, 16:4, 18:2) fatty acids at the expense of the more saturated (16:0, 16:1, 18:0) precursors, especially on plastid galactolipids, which validates the increased expression of acyl-ACP and plastid-localized w-6 desaturases. CRR1-independent changes in the transcriptome suggest a role for Cu in oxygen sensing in Chlamydomonas.
2011-10-24 | GSE25124 | GEO
Project description:Copper (Cu) is an essential micronutrient required as a co-factor in the catalytic center of many enzymes in bacteria. However, excess Cu is hazardous and can generate pleiotropic effects. Cu has been the metal of choice for piping used in household water distribution systems. Due to its leaching from pipelines, Cu is present at an elevated concentration in groundwater and in soil which is of public health concern. Sulfate-reducing bacteria (SRB) have been demonstrated to remove toxic levels of Cu. However, reports on the toxicity of Cu towards SRB have primarily focused on the degree of toxicity and subsequent elimination. In this study, we show in detail the Cu(II) stress-related effects on a model sulfate reducing bacteria, Desulfovibrio alaskensis G20. Cu(II) stress effects were assessed as alterations in the transcriptome through RNA-Seq at varying Cu(II) concentrations (5µM and 15µM). In the pairwise comparison of control vs 5µM, 61.43% of genes were downregulated and 38.57% genes were upregulated. In 15µM vs control, 49.51% genes were downregulated, and 50.5% genes were upregulated. The results indicated that the expression of inorganic ion transporters and translation machinery was massively modulated. Moreover, changes in important biological processes such as DNA transcription and signal transduction were observed at high Cu(II) concentration. In addition, metabolomics analysis indicated the effect of certain organic acids and amino acids in cellular metal buffering system and reducing oxidative damage to cells. These results will help us better understand the mechanism of Cu(II) stress response and provide avenues for future research.
2022-05-31 | GSE191076 | GEO
Project description:Given that transition metals are essential cofactors in central biological processes, misallocation of the wrong metal ion to a metalloprotein can have resounding and often detrimental effects on diverse aspects of cellular physiology. Therefore, in an attempt to characterize unique and shared responses to chemically similar metals we have reconstructed physiological behaviors of Halobacterium NRC-1, an archaeal halophile, in sub-lethal levels of Mn(II), Fe(II), Co(II), Ni(II), Cu(II) and Zn(II). Over 20% of all genes responded transiently within minutes of exposure to Fe(II), perhaps reflecting immediate large scale physiological adjustments to maintain homeostasis. At steady state, each transition metal induced growth arrest, attempts to minimize oxidative stress, toxic ion scavenging, increased protein turnover and DNA repair, and modulation of active ion transport. While several of these constitute generalized stress responses, up regulation of active efflux of Co(II), Ni(II), Cu(II), and Zn(II), down regulation of Mn(II) uptake and up regulation of Fe(II) chelation, confer resistance to the respective metals. We have synthesized all these discoveries into a unified systems level model to provide an integrated perspective of responses to six transition metals with emphasis on experimentally verified regulatory mechanisms. Finally, through comparisons across global transcriptional responses to different metals we provide insights into putative in vivo metal selectivity of metalloregulatory proteins and demonstrate that a systems approach can help rapidly unravel novel metabolic potential and regulatory programs of poorly studied organisms. Keywords: stress response, dose response, gene knockout
2006-05-31 | GSE4900 | GEO
Project description:Abnormal metal accumulation is associated with Alzheimer’s disease (AD) and has a relevant role in affecting amyloid beta-peptide (Abeta) aggregation and neurotoxicity.In the present study, employing a microarray analysis of 35,129 genes, we analyzed gene expression profile changes due to exposure to Abeta-Zn or Abeta-Cu complexes in neuronal-like cells (SH-SY5Y). Microarray data indicated that Abeta-Zn or Abeta-Cu complexes selectively alter expression of genes mainly related to cell death, inflammatory responses, and apoptosis.Taken together these findings indicate that Abeta-Zn or Abeta-Cu show some commonalities in affecting AD-related target functions. The overall modulatory activity on these genes supports the idea of a possible net result leading to mechanisms that counteract toxic effects of Abeta-Zn or Abeta-Cu.
2012-05-01 | GSE37661 | GEO
Project description:The essential yet toxic nature of Cu ions in living cells requires exquisite control of Cu homeostasis. The fungal pathogen C. neoformans regulates Cu homeostasis for survival during a complex host colonization process. During pulmonary infection host innate immune cells use Cu in an attempt to toxify C. neoformans, which responds by activating expression of Cu detoxifying proteins. However, during brain colonization expression of the fungal Cu import machinery is activated and required for virulence. To achieve the genetic plasticity required for adaptation to a continuum of distinct Cu environments within the host, C. neoformans utilizes the Cu-responsive transcription factor, Cuf1. Cuf1 is unique as it senses and responds to both high and low Cu environments, activating different sets of genes dependent on environmental Cu status. Cells lacking Cuf1 are compromised for colonization of the lungs and brain, highlighting Cuf1 as an important virulence factor. A genome-wide assessment of the Cuf1 binding sites in the genome of C. neoformans driven by Cu status identified novel genes required for adaptation to high and low Cu environments. These genes and their regulation provide new insights with respect to adaptive responses to changes in host Cu availability and could reveal new targets for therapeutic intervention in cryptococcosis.
2018-10-29 | GSE110120 | GEO
Project description:Transcriptional profiling of Paracoccus denitrificans PD1222 wild type grown to mid-exponential phase in minimal media with either 13 uM (Cu-H) or 0.5 uM (Cu-L) Cu regimes. The goal was to define the effects of Cu-limitation on denitrification genes Two growth conditions, three biological replicates of each condition. Each sample hybridised in a two-channel hybridization against Paracoccus denitrificans genomic DNA as the comparator/reference, which also acted as a control for spot quality. Cu-concentration 13 uM (Cu-H) versus 0.5 uM Cu (Cu-L) in anaerobic growth conditions.
2013-11-18 | E-GEOD-48577 | biostudies-arrayexpress
Project description:Transcriptional profiling of Paracoccus denitrificans PD1222 wild type grown to mid-exponential phase in minimal media with either 13 uM (Cu-H) or 0.5 uM (Cu-L) Cu regimes. The goal was to define the effects of Cu-limitation on denitrification genes
2013-11-18 | GSE48577 | GEO