ABSTRACT: Comparison 39ox and wt samples with or without fe-bHLH039 overexpression results in iron accumulation dependent on the FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (FIT)
Project description:au13-06_fit - Fe-FIT-Diff - FIT (FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) is a regulator of Fe deficiency responses in the root. FIT is a basic helix-loop-helix protein. Here, we investigated the transcriptome changes in response to Fe deficiency (- Fe) versus the control condition (+ Fe) in wild type, the fit-3 loss of function mutant and in FIT overexpression plants.
Project description:au15-01_iron-fit - fe-fit-diff_6d - Changes in gene expression profiles between fit knock-out, wild-type and FIT overexpressor seedlings under sufficient iron supply and under iron deficiency. - Col-0, HA-FIT and fit-3.
Project description:au15-05_fit - differential gene expression in a.tha. depending on mutation in fit - Transcriptomical changes in transgenic plants that carry a point mutation in FIT. - Differential gene expression in A. thaliana seedlings depending on the introduction of a point mutation in FIT (FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) under iron deficient conditions.
Project description:au15-01_iron-fit - fe-fit-diff_6d - Changes in gene expression profiles between fit knock-out, wild-type and FIT overexpressor seedlings under sufficient iron supply and under iron deficiency. - Col-0, HA-FIT and fit-3. 21 dye-swap - gene knock in (transgenic),gene knock out,treated vs untreated comparison
Project description:fe-fit-diff_6d-Differential gene expression in A. thaliana roots depending on iron supply and FIT (FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) abundance
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.
Project description:Iron (Fe) is an essential micronutrient for the survival and proliferation of plants. Plants have evolved complex mechanisms to maintain Fe homeostasis in response of Fe deficiency conditions. To explore the mechanisms of Populus tomentosa response to Fe deficiency, we evaluated the physiological, biochemical and transcriptome differences of P. tomentosa between Fe-sufficient and Fe-deficient conditions. The results showed that, under Fe-free conditions, the chlorophyll synthesis and photosynthesis pathways in shoots were extremely depressed. The inhibition of these pathways caused chlorosis and reduced shoot growth. Meanwhile, although both two photosynthetic systems (PSI and PSII) were inhibited under Fe limited conditions, PSI is affected more serious and earlier than PSII. In order to maintain Fe homeostasis, several genes involved in Fe regulation network were differentially expressed. At the late period of Fe deficiency response, some genes (BTS, bHLH38/39 and PYE) in PYE regulatory network were up-regulated in roots, while some root-specific ethylene-dependent FIT regulatory genes (EIN3, ERF and FIT) were down-regulated. Moreover, FRO2 was induced in P. tomentosa roots to reduce more Fe3+, which is similar with other strategy I plants. It is interest that we found another Fe2+ transporter gene (NRAMP1) was induced, instead of the well-known Fe2+ transporter gene (IRT1) for strategy I plants, to promote Fe2+ absorption at the Fe deficiency late stage.
Project description:Iron-sulfur (Fe-S) clusters play an essential role in plants as protein co-factors mediating diverse electron transfer reactions. Because they can react with oxygen to form reactive oxygen species (ROS) and cause cellular damage, the biogenesis of Fe-S clusters is highly regulated. A newly discovered group of 2Fe-2S proteins, termed NEET proteins, was recently proposed to coordinate iron-sulfur, iron, and ROS homeostasis in mammalian cells. Here we report that disrupting the function of AtNEET, the sole member of the NEET protein family in Arabidopsis thaliana, triggers a leaf-associated Fe- and Fe-S-deficiency responses, iron overload in chloroplasts (1.2-1.5 fold), chlorosis, structural damage to chloroplasts, and a high seedling mortality rate. Our findings suggest that disrupting AtNEET function disrupts the transfer of 2Fe-2S clusters from the chloroplastic 2Fe-2S biogenesis pathway to Fe-S proteins, and that uncoupling this process triggers a leaf-associated Fe-deficiency response that results in iron overload in chloroplasts and enhanced ROS accumulation
Project description:This SuperSeries is composed of the following subset Series:; GSE10496: Expression analysis of the effect of protoplasting and FACS sorting in roots exposed to iron deficiency (-Fe); GSE10497: Expression analysis of root developmental zones after iron deficiency (-Fe) treatment; GSE10501: Expression analysis of root cell-types after iron deficiency (-Fe) treatment; GSE10502: Time course expression analysis of the iron deficiency (-Fe) response in Arabidopsis roots Experiment Overall Design: Refer to individual Series
Project description:Several phytohormones and other small molecules have been demonstrated to be involved in iron (Fe) homeostasis. However, how salicylic acid (SA), an essential hormone in plant immunity and defense responses, participates in Fe-deficiency responses in plants is largely unknown. Here, we took advantage of a SA biosynthesis defect mutant phytoalexin deficient 4 (pad4: T-DNA Salk_089936) to explore the possible effects of endogenous SA on the morphological and physiological responses to Fe deprivation. Under a Fe-deficiency treatment, Col-0 showed more severe leaf chlorosis and root growth inhibition compared with the pad4 mutant. The soluble Fe concentrations were significant higher in pad4 than Col-0 under the Fe-deficiency treatment, suggesting that a mutation in the PAD4 gene may alleviate the Fe-deficiency-induced symptoms by regulating the soluble Fe concentrations. Furthermore, a SA signaling maker line (PR1promoter: GUS) was used to investigate how Fe deficiency affects endogenous SA biosynthesis and metabolism. The data showed that Fe deficiency significantly induced SA accumulation in Col-0, and the loss function of PAD4 blocked this process. The requirement of endogenous SA accumulation for Fe-deficiency responses was confirmed using a series of SA biosynthetic mutants and transgenic lines.
