Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Iron is essential to the unicellular green alga Chlamydomonas, but the molecular mechanism for response to iron deficiency remains largely unknown. In previous studies, we have identified FOX1 and ATX1 FEREs (Fe deficiency-responsive elements) as important regulation components of iron response in this organism. Here we present another iron regulated gene FEA1, which promoter was analysed by using a 5'-and 3'-end deletion and a scanning mutagenesis assay. The results reveal that the co-existence of -273/-188 and -118/-49 regions from transcriptional start site of FEA1 were sufficient and necessary for Fe deficiency-induced expression. Further deletion analysis indicates both -273/-253 and -103/-85 regions are essential for inducible expression. The scanning mutagenesis analysis of these regions identifies two cis-acting elements: the FeaFeRE1 at -273/-259 (CTGCGGTGGCAAAGT) and FeaFeRE2 at -106/-85 (CCGCCGCNNNTGGCACCAGCCT). Sequence comparison of FeaFeRE1 and FeaFeRE2 reveals a core sequence of TGGCA, which had been found in our previously reported Fe-deficiency-inducible gene ATX1. Moreover, we show that the promoter region of several genes, including FRE1, IRT1, ISCA, ZRT1, ZRT5, NRAMP2 and COPT1, also contains this core sequence, suggesting that at least two classes FeRE elements exist in Clamydomonas, one in FEA1 and ATX1 and others the second in FOX1, FEA2, MTP4, NRAMP3 and RBOL1.
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PMID:An Fe deficiency responsive element with a core sequence of TGGCA regulates the expression of FEA1 in Chlamydomonas reinharditii. 1935 5

The present work describes the effects on iron homeostasis when copper transport was deregulated in Arabidopsis thaliana by overexpressing high affinity copper transporters COPT1 and COPT3 (COPTOE ). A genome-wide analysis conducted on COPT1OE plants, highlighted that iron homeostasis gene expression was affected under both copper deficiency and excess. Among the altered genes were those encoding the iron uptake machinery and their transcriptional regulators. Subsequently, COPTOE seedlings contained less iron and were more sensitive than controls to iron deficiency. The deregulation of copper (I) uptake hindered the transcriptional activation of the subgroup Ib of basic helix-loop-helix (bHLH-Ib) factors under copper deficiency. Oppositely, copper excess inhibited the expression of the master regulator FIT but activated bHLH-Ib expression in COPTOE plants, in both cases leading to the lack of an adequate iron uptake response. As copper increased in the media, iron (III) was accumulated in roots, and the ratio iron (III)/iron (II) was increased in COPTOE plants. Thus, iron (III) overloading in COPTOE roots inhibited local iron deficiency responses, aimed to metal uptake from soil, leading to a general lower iron content in the COPTOE seedlings. These results emphasized the importance of appropriate spatiotemporal copper uptake for iron homeostasis under non-optimal copper supply. The understanding of the role of copper uptake in iron metabolism could be applied for increasing crops resistance to iron deficiency.
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PMID:Deregulated High Affinity Copper Transport Alters Iron Homeostasis in Arabidopsis. 3279 63