Iron deficiency-inducible peptide-coding genes OsIMA1 and OsIMA2 positively regulate a major pathway of iron uptake and translocation in rice

2020 ◽  
Author(s):  
Takanori Kobayashi ◽  
Atsushi J Nagano ◽  
Naoko K Nishizawa
Keyword(s):  
Transcription Factors ◽  
Iron Deficiency ◽  
Iron Uptake ◽  
Ubiquitin Ligases ◽  
Fe Deficiency ◽  
Transporter Gene ◽  
Major Pathway ◽  
Fe Uptake ◽  
Enhanced Expression ◽  
Inducible Genes

Abstract Under low iron (Fe) availability, plants transcriptionally induce various genes responsible for Fe uptake and translocation to obtain adequate amounts of Fe. Although transcription factors and ubiquitin ligases involved in these Fe deficiency responses have been identified, the mechanisms coordinating these pathways have not been clarified in rice. Recently identified Fe-deficiency-inducible IRON MAN (IMA)/FE UPTAKE-INDUCING PEPTIDE (FEP) positively regulates many Fe-deficiency-inducible genes for Fe uptake in Arabidopsis. Here, we report that the expression of two IMA/FEP genes in rice, OsIMA1 and OsIMA2, is strongly induced under Fe deficiency, positively regulated by the transcription factors IDEF1, OsbHLH058, and OsbHLH059, as well as OsIMA1 and OsIMA2 themselves, and negatively regulated by HRZ ubiquitin ligases. Overexpression of OsIMA1 or OsIMA2 in rice conferred tolerance to Fe deficiency and accumulation of Fe in leaves and seeds. These OsIMA-overexpressing rice exhibited enhanced expression of all of the known Fe-deficiency-inducible genes involved in Fe uptake and translocation, except for OsYSL2, a Fe–nicotianamine transporter gene, in roots but not in leaves. Knockdown of OsIMA1 or OsIMA2 caused minor effects, including repression of some Fe uptake- and translocation-related genes in OsIMA1 knockdown roots. These results indicate that OsIMA1 and OsIMA2 play key roles in enhancing the major pathway of the Fe deficiency response in rice.

scholarly journals OsbHLH058 and OsbHLH059 transcription factors positively regulate iron deficiency responses in rice

2019 ◽  
Vol 101 (4-5) ◽  
pp. 471-486 ◽  
Author(s):  
Takanori Kobayashi ◽  
Asami Ozu ◽  
Subaru Kobayashi ◽  
Gynheung An ◽  
Jong-Seong Jeon ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Iron Deficiency ◽  
Iron Uptake ◽  
Iron Concentration ◽  
Sufficient Conditions ◽  
Bhlh Transcription Factor ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix ◽  
Iron Deficient ◽  
Inducible Genes

Abstract Key message Subgroup IVc basic helix-loop-helix transcription factors OsbHLH058 and OsbHLH059 positively regulate major iron deficiency responses in rice in a similar but distinct manner, putatively under partial control by OsHRZs. Abstract Under low iron availability, plants transcriptionally induce the expression of genes involved in iron uptake and translocation. OsHRZ1 and OsHRZ2 ubiquitin ligases negatively regulate this iron deficiency response in rice. The basic helix-loop-helix (bHLH) transcription factor OsbHLH060 interacts with OsHRZ1, and positively regulates iron deficiency-inducible genes. However, the functions of three other subgroup IVc bHLH transcription factors in rice, OsbHLH057, OsbHLH058, and OsbHLH059, have not yet been characterized. In the present study, we investigated the functions of OsbHLH058 and OsbHLH059 related to iron deficiency response. OsbHLH058 expression was repressed under iron deficiency, whereas the expression of OsbHLH057 and OsbHLH060 was moderately induced. Yeast two-hybrid analysis indicated that OsbHLH058 interacts with OsHRZ1 and OsHRZ2 more strongly than OsbHLH060, whereas OsbHLH059 showed no interaction. An in vitro ubiquitination assay detected no OsbHLH058 and OsbHLH060 ubiquitination by OsHRZ1 and OsHRZ2. Transgenic rice lines overexpressing OsbHLH058 showed tolerance for iron deficiency and higher iron concentration in seeds. These lines also showed enhanced expression of many iron deficiency-inducible genes involved in iron uptake and translocation under iron-sufficient conditions. Conversely, OsbHLH058 knockdown lines showed susceptibility to iron deficiency and reduced expression of many iron deficiency-inducible genes. OsbHLH059 knockdown lines were also susceptible to iron deficiency, and formed characteristic brownish regions in iron-deficient new leaves. OsbHLH059 knockdown lines also showed reduced expression of many iron deficiency-inducible genes. These results indicate that OsbHLH058 and OsbHLH059 positively regulate major iron deficiency responses in a similar but distinct manner, and that this function may be partially controlled by OsHRZs.

scholarly journals NRAMP1 promotes iron uptake at the late stage of iron deficiency in poplars

2019 ◽  
Vol 39 (7) ◽  
pp. 1235-1250 ◽  
Author(s):  
Hui-Min Chen ◽  
Yi-Ming Wang ◽  
Hai-Ling Yang ◽  
Qing-Yin Zeng ◽  
Yan-Jing Liu
Keyword(s):  
Iron Deficiency ◽  
Root Growth ◽  
Late Stage ◽  
Iron Uptake ◽  
Shoot Growth ◽  
Chlorophyll Synthesis ◽  
Divalent Metal ◽  
Fe Deficiency ◽  
Divalent Metal Ions ◽  
Fe Homeostasis

Abstract Iron (Fe) is an essential micronutrient for plant survival and proliferation. Plants have evolved complex mechanisms to maintain Fe homeostasis in response to Fe deficiency. In this study, we evaluated the physiological, biochemical and transcriptomic differences between poplars grown under Fe-sufficient and Fe-deficient conditions to elucidate the mechanistic responses of poplars to Fe deficiency. Our results revealed that chlorophyll synthesis and photosynthesis were inhibited under Fe-deficient conditions. The inhibition of these pathways caused chlorosis and reduced shoot growth. Although both photosynthetic systems (PSI and PSII) were inhibited under Fe limitation, PSI was affected more severely and earlier than PSII. Fe deficiency also promoted root growth and increased the accumulation of divalent metal ions in roots. IRT1 and NRAMP1 are both Fe2+ transporters for iron uptake in Arabidopsis. In this study, however, only NRAMP1 was induced to promote Fe2+ uptake in roots at the late stage of Fe deficiency response. It indicated that NRAMP1, rather than the more well-known IRT1, might be a major Fe2+ transporter at the late stage of Fe-deficiency in poplars.

scholarly journals Putative cis-regulatory elements predict iron deficiency responses in Arabidopsis roots

2019 ◽  
Author(s):  
Birte Schwarz ◽  
Christina B. Azodi ◽  
Shin-Han Shiu ◽  
Petra Bauer
Keyword(s):  
Transcription Factor ◽  
Iron Deficiency ◽  
Large Scale ◽  
Computational Models ◽  
Regulatory Elements ◽  
Transport Systems ◽  
Fe Deficiency ◽  
Grass Species ◽  
Bhlh Transcription Factor ◽  
Fe Uptake

AbstractIron (Fe) is a key cofactor in many cellular redox processes, including respiration and photosynthesis. Plant Fe deficiency (-Fe) activates a complex regulatory network which coordinates root Fe uptake and distribution to sink tissues, while avoiding over-accumulation of Fe and other metals to toxic levels. In Arabidopsis (Arabidopsis thaliana), FIT (FER-LIKE FE DEFICIENCY-INDUCED TRANSCRIPTION FACTOR), a bHLH transcription factor (TF), is required for up-regulation of root Fe acquisition genes. However, other root and shoot -Fe-induced genes involved in Fe allocation and signaling are FIT-independent. The cis-regulatory code, i.e. the cis-regulatory elements (CREs) and their combinations that regulate plant -Fe-responses, remains largely elusive. Using Arabidopsis genome and transcriptome data, we identified over 100 putative CREs (pCREs) that were predictive of -Fe-induced up-regulation of genes in root tissue. We used large-scale in vitro TF binding data, association with FIT-dependent or FIT-independent co-expression clusters, positional bias, and evolutionary conservation to assess pCRE properties and possible functions. In addition to bHLH and MYB TFs, also B3, NAC, bZIP, and TCP TFs might be important regulators for -Fe responses. Our approach uncovered IDE1 (Iron Deficiency-responsive Element 1), a -Fe response CRE in grass species, to be conserved in regulating genes for biosynthesis of Fe-chelating compounds also in Arabidopsis. Our findings provide a comprehensive source of cis-regulatory information for -Fe-responsive genes, that advances our mechanistic understanding and informs future efforts in engineering plants with more efficient Fe uptake or transport systems.One sentence summary>100 putative cis-regulatory elements robustly predict Arabidopsis root Fe deficiency-responses in computational models, and shed light on the mechanisms of transcriptional regulation.

scholarly journals The iron deficiency response in Arabidopsis thaliana requires the phosphorylated transcription factor URI

2019 ◽  
Vol 116 (50) ◽  
pp. 24933-24942 ◽  
Author(s):  
Sun A. Kim ◽  
Ian S. LaCroix ◽  
Scott A. Gerber ◽  
Mary Lou Guerinot
Keyword(s):  
Arabidopsis Thaliana ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Iron Deficiency ◽  
Iron Uptake ◽  
Iron Status ◽  
Bhlh Transcription Factor ◽  
Excess Iron ◽  
Phosphorylated Form

Iron is an essential nutrient for plants, but excess iron is toxic due to its catalytic role in the formation of hydroxyl radicals. Thus, iron uptake is highly regulated and induced only under iron deficiency. The mechanisms of iron uptake in roots are well characterized, but less is known about how plants perceive iron deficiency. We show that a basic helix–loop–helix (bHLH) transcription factor Upstream Regulator of IRT1 (URI) acts as an essential part of the iron deficiency signaling pathway in Arabidopsis thaliana. The uri mutant is defective in inducing Iron-Regulated Transporter1 (IRT1) and Ferric Reduction Oxidase2 (FRO2) and their transcriptional regulators FER-like iron deficiency-induced transcription factor (FIT) and bHLH38/39/100/101 in response to iron deficiency. Chromatin immunoprecipitation followed by sequencing (ChIP-seq) reveals direct binding of URI to promoters of many iron-regulated genes, including bHLH38/39/100/101 but not FIT. While URI transcript and protein are expressed regardless of iron status, a phosphorylated form of URI only accumulates under iron deficiency. Phosphorylated URI is subject to proteasome-dependent degradation during iron resupply, and turnover of phosphorylated URI is dependent on the E3 ligase BTS. The subgroup IVc bHLH transcription factors, which have previously been shown to regulate bHLH38/39/100/101, coimmunoprecipitate with URI mainly under Fe-deficient conditions, suggesting that it is the phosphorylated form of URI that is capable of forming heterodimers in vivo. We propose that the phosphorylated form of URI accumulates under Fe deficiency, forms heterodimers with subgroup IVc proteins, and induces transcription of bHLH38/39/100/101. These transcription factors in turn heterodimerize with FIT and drive the transcription of IRT1 and FRO2 to increase Fe uptake.

scholarly journals Iron absorption in hepcidin1 knockout mice

2011 ◽  
Vol 105 (11) ◽  
pp. 1583-1591 ◽  
Author(s):  
Patarabutr Masaratana ◽  
Abas H. Laftah ◽  
Gladys O. Latunde-Dada ◽  
Sophie Vaulont ◽  
Robert J. Simpson ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Iron Absorption ◽  
Fe Deficiency ◽  
Acute Effects ◽  
Regulatory Peptide ◽  
Fe Uptake

Hepcidin, the Fe-regulatory peptide, has been shown to inhibit Fe absorption and reticuloendothelial Fe recycling. The present study was conducted to explore the mechanism of in vivo Fe regulation through genetic disruption of hepcidin1 and acute effects of hepcidin treatment in hepcidin1 knockout (Hepc1− / − ) and heterozygous mice. Hepcidin1 disruption resulted in significantly increased intestinal Fe uptake. Hepcidin injection inhibited Fe absorption in both genotypes, but the effects were more evident in the knockout mice. Hepcidin administration was also associated with decreased membrane localisation of ferroportin in the duodenum, liver and, most significantly, in the spleen of Hepc1− / −  mice. Hypoferraemia was induced in heterozygous mice by hepcidin treatment, but not in Hepc1− / −  mice, 4 h after injection. Interestingly, Fe absorption and serum Fe levels in Hepc1− / −  and heterozygous mice fed a low-Fe diet were not affected by hepcidin injection. The present study demonstrates that hepcidin deficiency causes increased Fe absorption. The effects of hepcidin were abolished by dietary Fe deficiency, indicating that the response to hepcidin may be influenced by dietary Fe level or Fe status.

IRON MAN interacts with BRUTUS to maintain iron homeostasis in Arabidopsis

2021 ◽  
Vol 118 (39) ◽  
pp. e2109063118
Author(s):  
Yang Li ◽  
Cheng Kai Lu ◽  
Chen Yang Li ◽  
Ri Hua Lei ◽  
Meng Na Pu ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Transcription Factors ◽  
Iron Homeostasis ◽  
Fe Deficiency ◽  
Small Peptides ◽  
Interaction Domain ◽  
C Terminus ◽  
Positive Regulators ◽  
Fe Homeostasis ◽  
And Function

IRON MAN (IMA) peptides, a family of small peptides, control iron (Fe) transport in plants, but their roles in Fe signaling remain unclear. BRUTUS (BTS) is a potential Fe sensor that negatively regulates Fe homeostasis by promoting the ubiquitin-mediated degradation of bHLH105 and bHLH115, two positive regulators of the Fe deficiency response. Here, we show that IMA peptides interact with BTS. The C-terminal parts of IMA peptides contain a conserved BTS interaction domain (BID) that is responsible for their interaction with the C terminus of BTS. Arabidopsis thaliana plants constitutively expressing IMA genes phenocopy the bts-2 mutant. Moreover, IMA peptides are ubiquitinated and degraded by BTS. bHLH105 and bHLH115 also share a BID, which accounts for their interaction with BTS. IMA peptides compete with bHLH105/bHLH115 for interaction with BTS, thereby inhibiting the degradation of these transcription factors by BTS. Genetic analyses suggest that bHLH105/bHLH115 and IMA3 have additive roles and function downstream of BTS. Moreover, the transcription of both BTS and IMA3 is activated directly by bHLH105 and bHLH115 under Fe-deficient conditions. Our findings provide a conceptual framework for understanding the regulation of Fe homeostasis: IMA peptides protect bHLH105/bHLH115 from degradation by sequestering BTS, thereby activating the Fe deficiency response.

scholarly journals Inoculation with Efficient Nitrogen Fixing and Indoleacetic Acid Producing Bacterial Microsymbiont Enhance Tolerance of the Model LegumeMedicago truncatulato Iron Deficiency

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Nadia Kallala ◽  
Wissal M’sehli ◽  
Karima Jelali ◽  
Zribi Kais ◽  
Haythem Mhadhbi
Keyword(s):  
Oxidative Stress ◽  
Iron Deficiency ◽  
Medicago Truncatula ◽  
Sinorhizobium Meliloti ◽  
Plant Biomass ◽  
High Growth ◽  
Fe Deficiency ◽  
Nitrogen Fixing ◽  
Bacterial Strains ◽  
Negative Effect

The aim of this study was to assess the effect of symbiotic bacteria inoculation on the response ofMedicago truncatulagenotypes to iron deficiency. The present work was conducted on threeMedicago truncatulagenotypes: A17, TN8.20, and TN1.11. Three treatments were performed: control (C), direct Fe deficiency (DD), and induced Fe deficiency by bicarbonate (ID). Plants were nitrogen-fertilized (T) or inoculated with two bacterial strains:Sinorhizobium melilotiTII7 andSinorhizobium medicaeSII4. Biometric, physiological, and biochemical parameters were analyzed. Iron deficiency had a significant lowering effect on plant biomass and chlorophyll content in allMedicago truncatulagenotypes. TN1.11 showed the highest lipid peroxidation and leakage of electrolyte under iron deficiency conditions, which suggest that TN1.11 was more affected than A17 and TN8.20 by Fe starvation. Iron deficiency affected symbiotic performance indices of allMedicago truncatulagenotypes inoculated with bothSinorhizobiumstrains, mainly nodules number and biomass as well as nitrogen-fixing capacity. Nevertheless, inoculation withSinorhizobiumstrains mitigates the negative effect of Fe deficiency on plant growth and oxidative stress compared to nitrogen-fertilized plants. The highest auxin producing strain, TII7, preserves relatively high growth and root biomass and length when inoculated to TN8.20 and A17. On the other hand, both TII7 and SII4 strains improve the performance of sensitive genotype TN1.11 through reduction of the negative effect of iron deficiency on chlorophyll and plant Fe content. The bacterial inoculation improved Fe-deficient plant response to oxidative stress via the induction of the activities of antioxidant enzymes.

scholarly journals MNB1 gene is involved in regulating the iron-deficiency stress response in Arabidopsis thaliana

2021 ◽  
Author(s):  
Hui Song ◽  
Feng Chen ◽  
Xi Wu ◽  
Min Hu ◽  
Qingliu Geng ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Arabidopsis Thaliana ◽  
Normal Growth ◽  
Developmental Changes ◽  
Fe Deficiency ◽  
Oxygen Species ◽  
Mineral Element ◽  
Wild Type ◽  
Transcription Level ◽  
Fe Uptake

Abstract Abstract Iron (Fe) is an indispensable mineral element for normal growth of plants. Fe deficiency induces a complex series of responses in plants, involving physiological and developmental changes, to increase Fe uptake from soil. However, the molecular mechanism involved in plant Fe-deficiency is not well understood. Here, we found that the MNB1 gene is involved in modulating Fe-deficiency response in Arabidopsis thaliana . The expression of MNB1 was inhabited by Fe-deficiency stress. Knockout of MNB1 led to enhanced Fe accumulation and tolerance, whereas the MNB1-overexpressing plants were sensitive to Fe-deficiency stress. Lower H 2 O 2 concentrations in mnb1 mutant plants were examined under Fe deficiency circumstances compared to wild-type. On the contray, higher H 2 O 2 concentrations were found in MNB1-overexpressing plants, which was adversely linked with malondialdehyde (MDA) concentrations. Furthermore, in mnb1 mutants, the transcription level of the Fe-uptake and translocation genes, FIT , IRT1 , FRO2 , Z IF , FRD3 , NAS4 , PYE and MYB72 , were considerably elevated during Fe-deficiency stress, resulting in higher Fe accumulation. Together, our findings show that the MNB1 gene negatively controls the Fe-deficiency response in Arabidopsis via modulating reactive oxygen species (ROS) levels and the ROS-mediated signaling pathway, thereby affecting the expression of Fe-uptake and translocation genes.

scholarly journals Understanding the Transferrin Receptor and Cellular Iron Deficiency Outside the Erythron

Blood ◽  
2017 ◽  
Vol 130 (Suppl_1) ◽  
pp. SCI-42-SCI-42
Author(s):  
Nancy C. Andrews
Keyword(s):  
Iron Deficiency ◽  
Missense Mutation ◽  
Transferrin Receptor ◽  
Iron Uptake ◽  
Clinical Manifestations ◽  
Cell Types ◽  
Conditional Knockout ◽  
Deficiency Anemia ◽  
Transferrin Receptor 1

Our laboratory showed that mouse embryos lacking the classical transferrin receptor, Tfrc, experienced anemia, pericardial effusion and a kinking of the neural tube, but otherwise appeared to be developing normally, suggesting that Tfrc was not needed by most tissues (Levy et al. 1999). Subsequently, we reported that Tfrc was essential for hematopoiesis but seemed to be dispensable in other tissues (Ned et al., 2003). A recent paper showing that a missense mutation in the TFRC internalization motif resulted in immunodeficiency without other clinical manifestations was consistent with this idea (Jabara et al., 2016). Nonetheless, we were not entirely convinced. More than thirty years ago, Larrick and Hyman described a patient with an anti-TFRC autoantibody who suffered from a broader range of clinical problems, suggesting that TFRC might have other roles (Larrick and Hyman, 1984). To help resolve the issue, we developed mice carrying an allele of Tfrc that can be conditionally inactivated, and used Cre/lox-mediated recombination to disrupt that allele in vivo, in several key cell types. We asked two questions: (1) is Tfrc important in those cell types and, if so, (2) what are the cellular consequences of Tfrc loss? We found that some cell types do not need Tfrc but others are highly dependent upon it. Those cell types that depend upon Tfrc generally need it for iron uptake, as expected, with one exception. Tfrc is critically important for normal development of the intestinal epithelium, but our data indicate that its essential role does not involve iron uptake. While surprising in view of our earlier results, the roles of Tfrc that we have unmasked through conditional knockout experiments would not have been apparent prior to the death of global Tfrc knockout embryos in mid-gestation. Nonetheless those roles are important, and our results give insight into why iron deficiency exacerbates heart failure, how muscle iron deficiency leads to disruption of systemic carbon metabolism, and how iron deficiency, rather than iron excess, may play a role in the pathogenesis of neurodegenerative disorders. Levy JE, Jin O, Fujiwara Y, Kuo F, Andrews NC. Transferrin receptor is necessary for development of erythrocytes and the nervous system. Nat Genet. 1999;21:396-9. Ned RM, Swat W, Andrews NC. Transferrin receptor 1 is differentially required in lymphocyte development. Blood. 2003;102:3711-8. Jabara HH, Boyden SE, Chou J et al. A missense mutation in TFRC, encoding transferrin receptor 1, causes combined immunodeficiency. Nat Genet. 2016;48:74-8. Larrick JW, Hyman ES. Acquired iron-deficiency anemia caused by an antibody against the transferrin receptor. N Engl J Med. 1984;311:214-8. Disclosures Andrews: Novartis: Membership on an entity's Board of Directors or advisory committees.

scholarly journals FIT, a regulatory hub for iron deficiency and stress signaling in roots, and FIT-dependent and -independent gene signatures

2020 ◽  
Vol 71 (5) ◽  
pp. 1694-1705 ◽  
Author(s):  
Birte Schwarz ◽  
Petra Bauer
Keyword(s):  
Transcription Factor ◽  
Protein Interactions ◽  
Fe Deficiency ◽  
Bhlh Transcription Factor ◽  
Root Cells ◽  
Gene Signatures ◽  
Helix Loop Helix ◽  
Independent Gene ◽  
Fe Uptake ◽  
Fe Acquisition

Abstract Iron (Fe) is vital for plant growth. Plants balance the beneficial and toxic effects of this micronutrient, and tightly control Fe uptake and allocation. Here, we review the role of the basic helix–loop–helix (bHLH) transcription factor FIT (FER-LIKE FE DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) in Fe acquisition. FIT is not only essential, it is also a central regulatory hub in root cells to steer and adjust the rate of Fe uptake by the root in a changing environment. FIT regulates a subset of root Fe deficiency (–Fe) response genes. Based on a combination of co-expression network and FIT-dependent transcriptome analyses, we defined a set of FIT-dependent and FIT-independent gene expression signatures and co-expression clusters that encode specific functions in Fe regulation and Fe homeostasis. These gene signatures serve as markers to integrate novel regulatory factors and signals into the –Fe response cascade. FIT forms a complex with bHLH subgroup Ib transcription factors. Furthermore, it interacts with key regulators from different signaling pathways that either activate or inhibit FIT function to adjust Fe acquisition to growth and environmental constraints. Co-expression clusters and FIT protein interactions suggest a connection of –Fe with ABA responses and root cell elongation processes that can be explored in future studies.

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