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evolution
OsITPK6 belongs to subgroup III, with 12 exons and 11 introns, of the OsITPK gene family. ITPK6 is a unique gene in the ITPK gene family
evolution
phylogenetic tree showing the evolutionary relatedness of GmITPK2 with ITPKs of monocot and dicot species using Entamoeba histolytica (EhITPK) as an outgroup member
malfunction
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required for proper development of the neural tube and axial mesoderm
malfunction
loss of this gene in itpk3-1 does neither affect phytate seed levels, nor seed Zn, Fe, and Mn but the micronutrient bioavailability is strongly reduced by seed phytate that forms complexes with seed cations. Low seed zinc is primarily caused by plant growth in Zn-deficient soil
malfunction
the epidermis structure of seed coat is irregularly formed in seeds of itpk2-1 mutant, resulting in the increased permeability of seed coat to tetrazolium salts. The cell wall shows a dramatic decrease in composition of suberin and cutin, which relate to the permeability of seed coat and the formation of which is accompanied with seed coat development. ITPK2 deficiency results in the distorted seed coat and crumpled columellas. Seed coat of itpk2-1 mutant presents high permeability to 2,3,5-triphenyltetrazolium and has less mucilage
malfunction
although both ipk1-1 and itpk1 mutants exhibit decreased levels of InsP6 (phytate) and diphosphoinositol pentakisphosphate (PP-InsP5, InsP7), disruption of another ITPK family enzyme, ITPK4, which correspondingly causes depletion of InsP6 and InsP7, does not display similar phosphate-related phenotypes, which precludes these InsP species from being effectors. Notably, the level of D/L-Ins(3,4,5,6)P4 is concurrently elevated in both ipk1-1 and itpk1 mutants, which demonstrates a specific correlation with the misregulated phosphate phenotypes. The level of D/L-Ins(3,4,5,6)P4 is not responsive to phosphate starvation that instead manifests a shoot-specific increase in the InsP7 level. ITPK1 overexpression significantly decreases phosphate uptake activity, in contrast to the elevated uptake activity shown by itpk1 mutants. In addition, several PSR genes are downregulated in ITPK1-overexpressing lines compared with the wild-type (e.g. PHT1:2, SPX1, AT4, IPS1 and PAP17)
malfunction
mutation of OsITPK6 not only significantly reduces the accumulation of IP6 in rice grains but also impairs plant growth and tolerance to abiotic stress. Nucleotide substitutions of gene OsITPK6 can significantly lower the phytic acid content in rice grains. Impact of ositpk6 mutations on plant growth and seed germination, panicle phenotype of mutant OsITPK6 and wild-type plants, overview. There is no significant difference in the number of leaves and roots with or without stress treatment between ositpk6_1 and wild-type
malfunction
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loss of this gene in itpk3-1 does neither affect phytate seed levels, nor seed Zn, Fe, and Mn but the micronutrient bioavailability is strongly reduced by seed phytate that forms complexes with seed cations. Low seed zinc is primarily caused by plant growth in Zn-deficient soil
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malfunction
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required for proper development of the neural tube and axial mesoderm
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metabolism
measurement of Fe, Zn, and Mn concentrations in seeds of Arabidopsis thaliana accessions grown in Zn-deficient and Zn-amended conditions, overview. Inositol 1,3,4-trisphosphate 5/6-kinase 3 gene (ITPK3), located close to a significant nucleotide polymorphism associated with relative Zn seed concentrations, is dispensable for seed micronutrients accumulation in ecotype Col-0
metabolism
following the formation of myo-inositol-3-phosphate, sequential phosphorylation reactions via action of various inositol phosphate kinases-myo-inositol kinase (Mik), inositol 1,3,4-trisphosphate kinase (Itpk), inositol 1,4,5-trisphosphate 3/6 kinase (Ipk2), and inositol 1,3,4,5,6-pentakisphosphate kinase (Ipk1) lead to phytic acid (PA, myo-inositol 1,2,3,4,5,6-hexakisphosphate) synthesis via the lipid-independent pathway and fine-tune the phosphorous flux towards PA accumulation
metabolism
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pathways enriched analysis indicates that the ubiquitin-mediated proteolysis pathway (UPP) and phosphatidylinositol (PI) signaling system are crucial for a successful transcriptional response in Gloiopeltis furcata to simulated natural tidal changes with twoconsecutive dehydration-rehydration cycles, overview. Genes encoding ubiquitin-protein ligase E3 (E3-1), SUMO-activating enzyme sub-unit 2 (SAE2), calmodulin (CaM), and inositol-1,3,4-trisphosphate 5/6-kinase (ITPK) are the hub genes which respond positively to two successive dehydration treatments. Network-based interactions with hub genes indicate that transcription factor (e.g. TFIID), RNA modification (e.g. DEAH) and osmotic adjustment (e.g. MIP, ABC1, Bam1) are related to these two pathways. The PI signal connected with Ca2+/CaM pathway responds to dehydration, and the role of CaM and ITPK in signal transduction
metabolism
the kinase activity of inositol pentakisphosphate 2-kinase (IPK1) is required for phytate (inositol hexakisphosphate, InsP6) synthesis, and is indispensable for maintaining phosphate homeostasis under phosphate-replete conditions. Inositol 1,3,4-trisphosphate 5/6-kinase 1 (ITPK1) plays an equivalent role. Genetic dissection of the roles for InsP and PP-InsP biosynthesis enzymes in regulation of phosphate homeostasis, overview
metabolism
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measurement of Fe, Zn, and Mn concentrations in seeds of Arabidopsis thaliana accessions grown in Zn-deficient and Zn-amended conditions, overview. Inositol 1,3,4-trisphosphate 5/6-kinase 3 gene (ITPK3), located close to a significant nucleotide polymorphism associated with relative Zn seed concentrations, is dispensable for seed micronutrients accumulation in ecotype Col-0
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physiological function
T-DNA insertion in a gene encoding a putative inositol 1,3,4-trisphosphate 5/6-kinase, i.e. ITPK2, dsm3, leads to a drought- and salt-hypersensitive mutant. Under drought stress conditions, the mutant has significantly less accumulation of osmolytes such as proline and soluble sugar and shows significantly reduced root volume, spikelet fertility, biomass, and grain yield with concomittant increase in malondialdehyde level Overexpression of DSM3 in rice results in drought- and salt-hypersensitive phenotypes and physiological changes similar to those in the mutant. Inositol trisphosphate level is decreased in the overexpressors under normal condition and drought stress
physiological function
enzyme ITPK2 plays an essential role in seed coat development and lipid polyester barrier formation
physiological function
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enzyme ITPK is the key regulatory enzyme at the branch point for the synthesis of InsP4 isomers [e.g. Ins(1,3,4,5)P4, Ins(1,3,4,6)P4 and Ins(3,4,5,6)P4], inositol pentakisphosphate (InsP5) and inositol hexaphosphate (InsP6). Ins (3,4,5,6)P4 can act as second messenger and play important roles in signal transduction
physiological function
inositol 1,3,4, trisphosphate 5/6 kinase (ITPK), a polyphosphate kinase that converts inositol 1,3,4-trisphosphate to inositol 1,3,4,5/6-tetraphosphate, averting the inositol phosphate pool towards phytic acid (PA) biosynthesis, is a key regulator that exists in four different isoforms in soybean. Role of inositol 1,3,4-trisphosphate 5/6 kinase-2 (GmITPK2) as a dehydration and salinity stress regulator in Glycine max. The significantly higher expression of GmITPK2 under drought and salinity stress suggests its role in providing tolerance mechanism against abiotic stress
physiological function
inositol 1,3,4-trisphosphate kinase-2 (GmItpk2), catalyzing the ATP-dependent phosphorylation of inositol 1,3,4-trisphosphate (IP3) to inositol 1,3,4,5-tetraphosphate or inositol 1,3,4,6-tetraphosphate, is a key enzyme diverting the flux of inositol phosphate pool towards phytate biosynthesis
physiological function
the enzyme is required for phytate (inositol hexakisphosphate, InsP6) synthesis and involved in maintaining phosphate homeostasis under phosphate-replete conditions
additional information
enzyme homology-based modeling and structure comparisons, overview. Active site mapping and molecular docking with ATP
additional information
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enzyme homology-based modeling and structure comparisons, overview. Active site mapping and molecular docking with ATP