Saccharomyces cerevisiae
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PROVIDER: PRJNA106737 | ENA |
REPOSITORIES: ENA
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Project description:The metabolic responce to iron deficiency in Saccharomyces cerevisiae
| PRJNA121085 | ENA
Project description:Iron plays the central role in the oxygen transport by the erythrocyte as a constituent of heme and hemoglobin. The importance of iron and heme also resides in their regulatory roles during erythroblast maturation. The transcription factor Bach1 may be involved in their regulatory roles since it is inactivated by direct binding of heme. To address whether Bach1 is involved in the responses of erythroblasts to iron status, low iron conditions that induced severe iron deficiency in mice were established. Under iron deficiency, extensive gene expression changes and mitophagy disorder were induced during maturation of erythroblasts. Bach1 mice showed more severe iron deficiency anemia in the developmental phase of mice and a retarded recovery once iron was replenished when compared with wild-type mice. In the absence of Bach1, the expression of globin genes and Hmox1 (encoding heme oxygenase-1) was de-repressed in erythroblasts under iron deficiency, suggesting that Bach1 represses these genes in erythroblasts under iron deficiency to balance the levels of heme and globin. Moreover, an increase in genome-wide DNA methylation was observed in erythroblasts of Bach1–/– mice under iron deficiency. These findings reveal the principle role of iron as a regulator of gene expression in erythroblast maturation and suggest that the iron-heme-Bach1 axis is important for a proper adaptation of erythroblast to iron deficiency to avoid toxic aggregates of non-heme globin.
2016-12-14 | GSE78955 | GEO
Project description:Iron deficiency-induced anemia is generally a representative nutritional problem in most populations. We reported that the anemia due to dietary iron deficiency causes a variety of changes in nutrient metabolism, even leading to apoptosis as a result of associated endoplasmic reticulum (ER) stress in the rat liver. On the other hand, it appears that non-anemic iron-deficiency causes no serious problem because no appreciable down-regulation of hemoglobin synthesis occurs. Biochemically, iron is essential for activation of cytochrome-related enzymes and its deficiency should yield some physiological problems. We performed a comprehensive transcriptome analysis to define the effects of non-anemic iron deficiency on hepatic gene expression. Four-week-old rats were fed a low-iron diet (ca. 3 ppm iron) for 2 days. These rats were compared with those fed a control diet (48 ppm iron) by pair feeding. On day 3, the rats were sacrificed under anesthesia, and their livers were dissected for DNA microarray analysis. Rats in the iron-deficient diet group, showed that their serum ferritin and iron levels decreased with an increase in the serum total iron binding capacity (TIBC) level, while the hemoglobin level was not changed. In the DNA microarray study, we identified 91 up-regulated and 186 down-regulated probe sets that characterized the iron-deficient diet group. In the up-regulated probe sets, genes involved in glucose and lipid metabolic processes were significantly enriched, whereas genes related to organic acid metabolic process, cellular ketone metabolic process, lipid metabolic process, oxidation reduction, response to drug, response to extracellular stimulus and gas transport were significantly enriched in the down-regulated probe sets. These results suggest that even the non-anemic iron-deficiency exerts various influences on nutrient metabolisms in the liver.
2013-03-21 | GSE30533 | GEO
Project description:Iron deficiency-induced anemia is generally a representative nutritional problem in most populations. We reported that the anemia due to dietary iron deficiency causes a variety of changes in nutrient metabolism, even leading to apoptosis as a result of associated endoplasmic reticulum (ER) stress in the rat liver. On the other hand, it appears that non-anemic iron-deficiency causes no serious problem because no appreciable down-regulation of hemoglobin synthesis occurs. Biochemically, iron is essential for activation of cytochrome-related enzymes and its deficiency should yield some physiological problems. We performed a comprehensive transcriptome analysis to define the effects of non-anemic iron deficiency on hepatic gene expression. Four-week-old rats were fed a low-iron diet (ca. 3 ppm iron) for 2 days. These rats were compared with those fed a control diet (48 ppm iron) by pair feeding. On day 3, the rats were sacrificed under anesthesia, and their livers were dissected for DNA microarray analysis. Rats in the iron-deficient diet group, showed that their serum ferritin and iron levels decreased with an increase in the serum total iron binding capacity (TIBC) level, while the hemoglobin level was not changed. In the DNA microarray study, we identified 91 up-regulated and 186 down-regulated probe sets that characterized the iron-deficient diet group. In the up-regulated probe sets, genes involved in glucose and lipid metabolic processes were significantly enriched, whereas genes related to organic acid metabolic process, cellular ketone metabolic process, lipid metabolic process, oxidation reduction, response to drug, response to extracellular stimulus and gas transport were significantly enriched in the down-regulated probe sets. These results suggest that even the non-anemic iron-deficiency exerts various influences on nutrient metabolisms in the liver. Three-week-old male rats (Sprague Dawley) were purchased from Charles River Japan (Kanagawa, Japan) and housed in a room maintained at 24 M-BM-1 1M-BM-0C and 40 M-BM-1 5% humidity with a 12-h light/dark cycle (light 08:00M-bM-^@M-^S20:00; dark 20:00M-bM-^@M-^S08:00). Rats were given a normal diet (Research Diets, Inc., New Brunswick, NJ, USA) as control and water for 24 h ad libitum. The composition of the control diet, 48 ppm iron, was based on the AIN-93G diet; Avicel was used in place of cellulose which may contain a trace amount of iron. On day 3, diet was removed at 18:00 and the feeding was conducted between 09:00 and 17:00 for another 4 days to synchronize the feeding behaviors. On day 8, rats were divided into two groups with similar average body weights. Rats in the one group (n = 5) were given ad libitum an iron-deficient diet, ca. 3 ppm iron, that was prepared by removal of iron (ferric citrate) from the control diet, and those in the other group (n = 5) were fed the control diet by pair feeding. On day 1 and day 3 of feeding with the experiment diet, the hemoglobin level of each rat was measured for the blood samples collected from the tail vein. On day 3, each rat was sacrificed under anesthesia after 1.5 h feeding, prior to excising the liver which was soon immersed in RNAlater.
2013-03-21 | E-GEOD-30533 | 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:Transcriptional profile of whole roots of wild-type and pye-1 mutants exposed to 24 hours -Fe were generated Global population increases and climate change underscore the need for better comprehension of how plants acquire and process nutrients such as iron. A systems biology approach was taken to elucidate novel regulatory mechanisms involved in plant responses to iron deficiency (-Fe). Using cell-type specific transcriptional profiling we identified a pericycle-specific iron deficiency response, and a previously uncharacterized transcription factor, POPEYE (PYE), that plays an important role in this response. Functional analysis of PYE suggests that it positively regulates growth and development under iron deficient conditions. ChIP-on-chip analysis and transcriptional profiling reveal that PYE helps maintain iron homeostasis by directly and indirectly regulating the expression of ferric reductases, metal ion transporters, iron storage proteins, and other key iron homeostasis genes. In addition to PYE, we also identified a second protein BRUTUS (BTS), which appears to negatively regulate the response to iron deficiency. BTS is a unique putative E3 ligase protein, with metal ion binding and DNA binding domains. PYE and BTS are tightly co-regulated and physically interact with PYE paralogs, one of which is thought to positively regulate expression of genes involved in iron homeostasis. We propose that iron content is sensed within the pericycle where PYE, perhaps in conjunction with BTS and other regulatory proteins, is then activated to control a regulatory network involved in maintaining proper iron distribution in plants. Keywords: Expression analysis To determine how loss of PYE expression affects the transcriptional profile of whole roots, pye-1 mutants and wild-type seeds were germinated under standard growth conditions then transferred to standard media (control, MS media) or iron deficient media (-Fe, 0.3mM Ferrozine in MS media containing no ferrous sulfate). After 24 hours of exposure to +Fe or -Fe whole roots were collected and analyzed.
2010-10-12 | E-GEOD-21443 | biostudies-arrayexpress
Project description:Transcriptional profile of whole roots of wild-type and pye-1 mutants exposed to 24 hours -Fe were generated Global population increases and climate change underscore the need for better comprehension of how plants acquire and process nutrients such as iron. A systems biology approach was taken to elucidate novel regulatory mechanisms involved in plant responses to iron deficiency (-Fe). Using cell-type specific transcriptional profiling we identified a pericycle-specific iron deficiency response, and a previously uncharacterized transcription factor, POPEYE (PYE), that plays an important role in this response. Functional analysis of PYE suggests that it positively regulates growth and development under iron deficient conditions. ChIP-on-chip analysis and transcriptional profiling reveal that PYE helps maintain iron homeostasis by directly and indirectly regulating the expression of ferric reductases, metal ion transporters, iron storage proteins, and other key iron homeostasis genes. In addition to PYE, we also identified a second protein BRUTUS (BTS), which appears to negatively regulate the response to iron deficiency. BTS is a unique putative E3 ligase protein, with metal ion binding and DNA binding domains. PYE and BTS are tightly co-regulated and physically interact with PYE paralogs, one of which is thought to positively regulate expression of genes involved in iron homeostasis. We propose that iron content is sensed within the pericycle where PYE, perhaps in conjunction with BTS and other regulatory proteins, is then activated to control a regulatory network involved in maintaining proper iron distribution in plants. Keywords: Expression analysis
2010-10-12 | GSE21443 | GEO
Project description:Iron-Heme-Bach1 Axis Is Involved In Erythroblast Adaptation To Iron Deficiency
| PRJNA314505 | ENA
Project description:Arsenic metalloid is a double-edge sword. On the one hand it is a very toxic and powerful carcinogen, and on the other it has been successfully used in the treatment of acute promyelocytic leukemia. In order to prevent the deleterious effects caused by arsenic compounds, almost all living organisms have developed mechanisms to eliminate it. In this study genome-wide response of S. cerevisiae to arsenic shows that this metal interferes with genes involved in the iron homeostasis including those encoding proteins that function in iron uptake, incorporation into Fe–S clusters, and more. In addition our data indicate that Yap1 transcriptionally controls the iron homeostasis regulator AFT2 as well as its direct target, MRS4. Most importantly in response to arsenate exposure Yap1 strongly regulates the expression of several genes involved in the Fe-S proteins biosynthesis, namely NBP35 and YFH1. Interestingly mRNA levels encoding Fet3, Ferro-O2-oxidoreductase required for high-affinity iron uptake, are drastically destabilized upon arsenic exposure. Such destabilization is due to the 5’ to 3’ exonuclease Xrn1 localized in the P Bodies. Moreover FET3 mRNA decay is not mediated by Cth2 and is independent on the formation of ROS responsible for the toxic effects of arsenic compounds. Strikingly, in presence of arsenate fet3 mutant shows resistance over the wild-type which leads us to suggest that Fet3 has a role in arsenic toxicity. Unexpectedly arsenic treatment seems to activate the non-reductive iron uptake in order to maintain the cellular iron homeostasis. Furthermore our genetic, biochemical, and physiological analysis demonstrate that aft1 mutant is sensitive to arsenic compounds and such phenotype is reversible upon addition of iron. We also show that arsenic exposure induces iron deficiency in aft1 mutant. In conclusion this work shows for the first time that arsenic, a chemotherapy drug used to treat a specific type of acute promyelocytic leukemia (APL), disrupts iron homeostasis and our results suggest that this disruption is independent on ROS generation. Finally we provide preliminary data confirming that such disruption also takes place in mammalian cells, an observation that can be very relevant in term of clinical applications.
2011-11-04 | GSE33427 | GEO
Project description:Iron (Fe) plays a pivotal role in several metabolic and biosynthetic pathways essential for plant growth. Fe deficiency in plants severely affects the overall crop yield. Despite several studies on iron deficiency responses in different plant species, these mechanisms remain unclear in the allohexaploid wheat, which is the most widely cultivated commercial crop. In order to gain a comprehensive insight into molecular responses of bread wheat when exposed to iron deficiency, we studied transcriptomic changes in the roots and flag leaves of wheat plants subjected to iron-deficient and iron-sufficient conditions during early grain filling.
2020-11-24 | GSE162027 | GEO