Expression data from Arabidopsis Col and rglg1/2 mutant in response to Fe deficiency
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE63946 | GEO | 2016/10/30
SECONDARY ACCESSION(S): PRJNA269581
REPOSITORIES: GEO
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Project description:Pericycle specific transcriptional profiles were generated by FACS (Fluorescence Activated Cell Sorting) of roots that express a pericycle-specific GFP-reporter. FACS cell populations were isolated from roots grown under standard conditions or roots that had been transferred to -Fe media for 24 hours. 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: Cell-type specific analysis of stress response using FACS
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Project description:This study was designed to identify candidate genes associated with iron efficiency in soybeans. Two genotypes, Clark (PI548553) and IsoClark (PI547430), were grown in both iron sufficient (100uM Fe(NO3)3) and iron deficient (50uM Fe(NO3)3) hydroponics conditions. The second trifoliate was harvested for RNA extraction for the microarray experiment. Candidate genes were identified by comparing gene expression profiles within genotypes between the two iron growth conditions. Experiment Overall Design: This experiment was designed to compare expression profiles of Clark grown in iron sufficient and deficient iron conditions and of IsoClark grown in the same conditions. Plants grown in iron sufficient conditions were used as controls and plants grown in iron deficient conditions were considered experimental. For the Clark genotype, There were two biological replicates of iron deficient plants, and three biological replicates of iron sufficient plants. The IsoClark genotype had three biological replicates for both iron sufficient and deficient conditions.
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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.
2016-10-01 | GSE74515 | GEO
