Transcriptomic analysis reveals the participation of NTRC in iron homeostasis throughout Arabidopsis development
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PROVIDER: PRJNA1201152 | ENA |
REPOSITORIES: ENA
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Project description:NADPH-dependent thioredoxin reductase C (NTRC) plays a central role in redox regulation of chloroplast photosynthetic metabolism. Accordingly, Arabidopsis (Arabidopsis thaliana) NTRC null mutants show defective photosynthetic performance and growth inhibition. Remarkably, these mutants show almost wild type phenotype at the seedling stage, which raises the question of whether NTRC plays different functions throughout plant development. In this work, we have addressed this issue by performing transcriptome comparisons of Arabidopsis wild type and ntrc mutant lines at seedling and adult stages of development. In contrast with the high impact of NTRC on leaves from adult plants, the low transcriptomic differences in seedlings suggested a less-relevant function of NTRC at this stage of plant development. Notably, the ntrc mutant showed transcriptomic changes resembling the response to Fe excess throughout plant development, though this response was almost unique at the seedling stage. The lack of NTRC caused altered levels of Mn, Zn, Cu, S, P, K and Na, but no significant differences in the content of Fe, as compared with the wild type. Moreover, at the seedling stage, the lack of NTRC caused hypersensitivity to Fe deficit, but a protective effect in response to Fe excess, most likely due to lower ROS accumulation in the mutant seedlings. Our results reveal the different impact of NTRC throughout plant development and identify Fe homeostasis as a process highly affected by NTRC, most notably at the seedling stage.
2025-04-11 | GSE285082 | GEO
Project description:Thiol-dependent redox regulation is essential for the rapid adaptation of chloroplast metabolism to unpredictable changes of light intensity. The disulfide reductase activity of thioredoxins (Trxs), which relies on photo-reduced ferredoxin (Fdx) and a Fdx-dependent Trx reductase (FTR), constitutes the Fdx-FTR-Trxs system, which links chloroplast redox regulation to light. In addition, chloroplasts harbor an NADPH-dependent Trx reductase (NTR) with a joint Trx domain, NTRC. The activity of these two redox systems is integrated by the balance of the hydrogen peroxide scavenging enzyme 2-Cys peroxiredoxin (2-Cys Prx), which thus plays a key role in maintaining the reducing capacity of chloroplast Trxs in response to light intensity. Based on the severe phenotype of mutant lines lacking NTRC, it is clear that this enzyme plays an essential role in chloroplast redox homeostasis. However, whether the function of NTRC depends on its capacity of reduce 2-Cys Prxs or has additional targets remains unknown. Here, we have addressed this issue by a comparative analysis of the triple mutant of Arabidopsis thaliana, ntrc-2cpab, simultaneously lacking 2-Cys Prxs and NTRC, and the double mutant 2cpab lacking 2-Cys Prxs. The phenotype of the ntrc-2cpab mutant is indistinguishable of the 2cpab mutant, as shown by growth rate, photosynthesis performance, light-dependent redox regulation of enzyme activity and comparative transcriptomics based RNA-Seq. Based on these results, we propose that the function of NTRC in chloroplast redox homeostasis is exerted by the regulation of the redox balance of 2-Cys Prxs rather than by the direct reduction of additional targets.
2021-09-09 | GSE147793 | GEO
Project description:The study of gene expression profile of iron homeostasis-related genes using Affymetrix GeneChips in conjunction with the pathological assessment of hepatic iron content in hepatocellular carcinoma (HCC) samples offers a new strategy to understand the role of hepatic iron overload in hepatocarcinogenesis.
2007-01-10 | E-MEXP-84 | biostudies-arrayexpress
Project description:Disruption of local iron homeostasis is a common feature of neurodegenerative diseases. We focused on dopaminergic neurons, asking how iron transport proteins modulate iron homeostasis in vivo. Inactivation of the transmembrane iron exporter ferroportin had no apparent consequences. However, loss of the transferrin receptor 1, involved in iron uptake, caused profound, age-progressive neurodegeneration with features similar to Parkinson’s disease. There was gradual loss of dopaminergic projections in the striatum with subsequent death of dopaminergic neurons in the substantia nigra. After depletion of 30% of the neurons the mice developed neurobehavioral parkinsonism, with evidence of mitochondrial dysfunction and impaired mitochondrial autophagy. Molecular analysis revealed strong signatures indicative of attempted axonal regeneration, a metabolic switch to glycolysis and the unfolded protein response. We speculate that cellular iron deficiency may contribute to neurodegeneration in human patients Using Ribotag technology, from mouse ventral midbrain lysates, we isolated actively translated mRNA species from control and Transferrin receptor 1-null dopaminergic neurons. Two mouse ages were used 3 wks (early neurodegeration) 10 wks (late neurodegeneration)
2015-03-11 | E-GEOD-66730 | biostudies-arrayexpress
Project description:Disruption of local iron homeostasis is a common feature of neurodegenerative diseases. We focused on dopaminergic neurons, asking how iron transport proteins modulate iron homeostasis in vivo. Inactivation of the transmembrane iron exporter ferroportin had no apparent consequences. However, loss of the transferrin receptor 1, involved in iron uptake, caused profound, age-progressive neurodegeneration with features similar to Parkinson’s disease. There was gradual loss of dopaminergic projections in the striatum with subsequent death of dopaminergic neurons in the substantia nigra. After depletion of 30% of the neurons the mice developed neurobehavioral parkinsonism, with evidence of mitochondrial dysfunction and impaired mitochondrial autophagy. Molecular analysis revealed strong signatures indicative of attempted axonal regeneration, a metabolic switch to glycolysis and the unfolded protein response. We speculate that cellular iron deficiency may contribute to neurodegeneration in human patients
2015-03-11 | GSE66730 | GEO
Project description:Strict iron regulation is essential for normal brain function. The iron homeostasis, determined by the milieu of available iron compounds, is impaired in aging, neurodegenerative diseases and cancer. However, non-invasive assessment of different molecular iron environments implicating brain tissue's iron homeostasis remains a challenge. We present a novel magnetic resonance imaging (MRI) technology sensitive to the iron homeostasis of the living brain (the r1-r2*relaxivity). In vitro, our MRI approach reveals the distinct paramagnetic properties of ferritin, transferrin and ferrous iron. In the in vivo human brain, we validate our approach against ex vivo iron compounds quantification and gene expression. Our approach varies with the iron mobilization capacity across brain regions and in aging. It reveals brain tumors’ iron homeostasis, and enhances the distinction between tumor tissue and non- pathological tissue without contrast agents. Therefore, our approach may allow for non-invasive research and diagnosis of iron homeostasis in living human brains.
2023-08-11 | GSE240204 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE29704: Two transcription factors are necessary for iron homeostasis in a salt-dwelling archaeon [gene expression data] GSE29705: Two transcription factors are necessary for iron homeostasis in a salt-dwelling archaeon [ChIP-chip data] Refer to individual Series
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Project description:Transcriptional profiling of low-iron stimulon and XibR influenced regulon using wild-type Xcc 8004 and xibR mutant grown under iron-replete and iron-deplete conditions. Trancriptional analysis under iron-deplete condition, mimicking in planta environment, provides greater insights into expression pattern of several virulence-associated functions under low-iron. A genetic screen sggested the involvement of XibR (Xanthomonas iron binding regulator) in iron-uptake and metabolism. Present transcriptional analysis suggested the co-regulation of virulence associated functions including siderophore biosynthesis, motility, chemotaxis and typeIII effectors by a novel transcriptional regulator of NtrC family protein XibR and iron avability.
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Project description:Microvascular endothelial cells (EC) display a high degree of phenotypic and functional heterogeneity among different organs. Organ-specific EC control their tissue microenvironment by angiocrine factors in health and disease. Liver sinusoidal EC (LSEC) are uniquely differentiated to fulfil important organ-specific functions in development, under homeostatic conditions, and in regeneration and liver pathology. Recently, Bmp2 has been identified by us as an organ-specific angiokine derived from LSEC. To study angiocrine Bmp2 signaling in the liver, we conditionally deleted Bmp2 in LSEC using EC subtype-specific Stab2-Cre mice. Genetic inactivation of hepatic angiocrine Bmp2 signaling in Stab2-Cre;Bmp2fl/fl (Bmp2LSECKO) mice caused massive iron overload in the liver, and increased serum iron levels and iron deposition in several organs similar to classic hereditary hemochromatosis. Iron overload was mediated by decreased hepatic expression of hepcidin, a key regulator of iron homeostasis. Thus, angiocrine Bmp2 signaling within the hepatic vascular niche represents a constitutive pathway indispensable for iron homeostasis in vivo that is non-redundant with Bmp6. Notably, we demonstrate that organ-specific angiocrine signaling is essential not only for the homeostasis of the respective organ, but also for the homeostasis of the whole organism.
2017-01-31 | GSE90506 | GEO