Arabidopsis inositol phosphate kinases IPK1 and ITPK1 constitute a metabolic pathway in maintaining phosphate homeostasis

AbstractTargeted protein degradation is essential for physiological development and adaptation to stress. Mammalian INOSITOL PENTAKISPHOSPHATE KINASE (IP5K) and INOSITOL HEXAKISPHOSPHATE KINASE 1 (IP6K1) pair modulates functions of Cullin RING Ubiquitin E3 ligases (CRLs) that execute targeted degradation of substrates. Coordinated activities of these kinases protect CRLs on a COP9 signalosome (CSN) platform and stimulates deneddylation-dependent disassembly to maintain continuity of its functions. In plants, CRL regulations on CSN by inositol phosphate (InsP) kinases are not known. Here, we show interactions of Arabidopsis thaliana INOSITOL PENTAKISPHOSPHATE 2-KINASE 1 (IPK1) and INOSITOL 1,3,4-TRISPHOSPHATE 5/6-KINASE 1 (ITPK1), counterparts of the above InsP-kinase pair, with CSN subunits and its positive influences on the dynamics of cullin deneddylation. We identify neddylation enhancements on CRLs as an early response to phosphate-starvation and its orchestration by perturbed IPK1/ITPK1 activities. At a molecular level, specific kinetics of CSN5 deneddylase is affected by the above InsP-kinases. Overall, our data reveal conserved InsP-kinase involvements on CRL-CSN synergism in plants.

Download Full-text

Arabidopsis inositol phosphate kinases, IPK1 and ITPK1, constitute a metabolic pathway in maintaining phosphate homeostasis

10.1101/270355 ◽

2018 ◽

Cited By ~ 2

Author(s):

Hui-Fen Kuo ◽

Yu-Ying Hsu ◽

Wei-Chi Lin ◽

Kai-Yu Chen ◽

Teun Munnik ◽

...

Keyword(s):

Inositol Phosphates ◽

Inositol Phosphate ◽

Phosphate Limitation ◽

Phosphate Metabolism ◽

Adaptive Responses ◽

Phosphate Homeostasis ◽

Close Link ◽

Inositol Phosphate Metabolism ◽

Evolutionarily Conserved ◽

Specific Increase

SummaryEmerging studies have implicated a close link between inositol phosphate (InsP) metabolism and cellular phosphate (Pi) homeostasis in eukaryotes; however, whether a common InsPspecies is deployed as an evolutionarily conserved metabolic messenger to mediate Pisignaling remains unknown. Here, using genetics and InsPprofiling combined with Pistarvation response (PSR) analysis inArabidopsis thaliana, we showed that the kinase activity of inositol pentakisphosphate 2-kinase (IPK1), an enzyme required for phytate (inositol hexakisphosphates; InsP6) synthesis, is indispensable for maintaining Pihomeostasis under Pi-replete conditions, and inositol 1,3,4-trisphosphate 5/6-kinase 1 (ITPK1) plays an equivalent role. Although bothipk1-1anditpk1mutants exhibited decreased levels of InsP6and diphosphoinositol pentakisphosphate (PP-InsP5; InsP7), disruption of another ITPK family enzyme, ITPK4, which correspondingly caused depletion of InsP6and InsP7, did not display similar Pi-related phenotypes, which precludes these InsPspecies as effectors. Notably, the level of D/L-Ins(3,4,5,6)P4was concurrently elevated in bothipk1-1anditpk1mutants, which implies a potential role for InsP4in regulating Pihomeostasis. However, the level of D/L-Ins(3,4,5,6)P4is not responsive to Pistarvation that instead manifests a shoot-specific increase in InsP7level. This study demonstrates a more nuanced picture of intersection of InsPmetabolism and Pihomeostasis and PSR than has previously been elaborated, and additionally establishes intermediate steps to phytate biosynthesis in plant vegetative tissues.Significance StatementRegulation of phosphate homeostasis and adaptive responses to phosphate limitation is critical for plant growth and crop yield. Accumulating studies implicate inositol phosphates as regulators of phosphate homeostasis in eukaryotes; however, the relationship between inositol phosphate metabolism and phosphate signaling in plants remain elusive. This study dissected the step where inositol phosphate metabolism intersects with phosphate homeostasis regulation and phosphate starvation responses.

Download Full-text

Functional Gene and Metabolic Changes of Marine Microbial Populations Involved in Hydrocarbon Degradation Under Different Enrichment Conditions

10.21203/rs.3.rs-457199/v1 ◽

2021 ◽

Author(s):

Bingkui Song ◽

Zhongzhen Zhang ◽

Si Li ◽

Qitong Fu ◽

Shuting Qi ◽

...

Keyword(s):

Carbon Dioxide ◽

Metabolic Pathway ◽

Inositol Phosphate ◽

Culture Conditions ◽

Functional Gene ◽

Microbial Populations ◽

Phosphate Metabolism ◽

Inositol Phosphate Metabolism ◽

High Nutrient ◽

Nutrient Conditions

Abstract In this study, seawater from the area of an oil extraction platform in Bohai Bay was subjected to experimental treatments with oil as the only carbon source to understand the transcriptional responses of seawater microbial populations to oil degradation treatments. Twelve enrichment conditions were used, and fluorescent in situ hybridization (FISH) along with metatranscriptomic analyses were used to understand functional changes within each treatment. RNA from the petroleum-degrading bacterial enrichments was extracted after cultivation and FISH was used to evaluate overall activity, while changes in gene expression among different culture conditions were analyzed based on eight hydrocarbon-specific gene probes and flow cytometry. Concomitantly, 1,066 metabolic pathways were identified as being expressed in the populations through RNA sequencing, metatranscriptomic analysis, and metabolic pathway enrichment analysis. The addition of oil led to the inhibition of carbohydrate metabolism and inositol phosphate metabolism, while also reducing extracellular signaling pathway transcription levels. When low- and high-nutrient conditions were compared, low-nutrient conditions inhibited taurine and hypotaurine metabolism in addition to inositol phosphate metabolism. Among oxygen-treated, carbon dioxide-treated, and air-treated conditions, oxygen-treated conditions inhibited taurine and hypotaurine metabolism but promoted galactose metabolism, while carbon dioxide-treated conditions promoted inositol phosphate metabolism. Overall, metabolic pathway expression and functional gene changes indicated that high-nutrient, oil-free, and aerobic culture conditions best promoted the growth and reproduction of marine microbial communities.

Download Full-text

Simultaneous HPLC determination of four key metabolites in the metabolic pathway for production of 1,3-propanediol from glycerol

Chromatographia ◽

10.1016/s0009-5893(07)82072-8 ◽

2007 ◽

Vol 65 (9-10) ◽

pp. 629-632

Author(s):

H CHEN ◽

B FANG ◽

Z HU

Keyword(s):

Metabolic Pathway ◽

Hplc Determination

Download Full-text

SLC34A3 Mutations in Patients with Hereditary Hypophosphatemic Rickets with Hypercalciuria Predict a Key Role for the Sodium-Phosphate Cotransporter NaPi-IIc in Maintaining Phosphate Homeostasis

Yearbook of Endocrinology ◽

10.1016/s0084-3741(08)70143-4 ◽

2007 ◽

Vol 2007 ◽

pp. 317-319

Author(s):

B.L. Clarke

Keyword(s):

Sodium Phosphate ◽

Hypophosphatemic Rickets ◽

Phosphate Homeostasis

Download Full-text

Eicosapentaenoic Acid Interferes with U46619-Stimulated Formation of Inositol Phosphates in Washed Rabbit Platelets

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647129 ◽

1989 ◽

Vol 62 (04) ◽

pp. 1116-1120 ◽

Cited By ~ 9

Author(s):

N Chetty ◽

J D Vickers ◽

R L Kinlough-Rathbone ◽

M A Packham ◽

J F Mustard

Keyword(s):

Signal Transduction ◽

Fatty Acid Composition ◽

Eicosapentaenoic Acid ◽

Inositol Phosphates ◽

Inositol Phosphate ◽

Dense Granule ◽

Detectable Change ◽

Membrane Phospholipids ◽

Rabbit Platelets ◽

Stimulation Of

SummaryEicosapentaenoic acid (EPA) inhibits platelet responsiveness to aggregating agents. To investigate the reactions that are affected by EPA, we examined the effect of preincubating aspirintreated rabbit platelets with EPA on stimulation of inositol phosphate formation in response to the TXA2 analogue U46619. Stimulation of platelets with U46619 (0.5 μM) caused aggregation and slight release of dense granule contents; aggregation and release were inhibited by preincubation of the platelets with EPA (50 μM) for 1 h followed by washing to remove unincorporated EPA. Incubation with EPA (50 μM) for 1 h did not cause a detectable increase in the amount of EPA in the platelet phospholipids. When platelets were prelabelled with [3H]inositol stimulation with U46619 of control platelets that had not been incubated with EPA significantly increased the labelling of mos1tol phosphates. The increases in inositol phosphate labelling due to U46619 at 10 and 60 s were partially inhibited by premcubat10n of the platelets with 50 μM EPA. Since the activity of cyclo-oxygenase was blocked with aspirin, inhibition of inositol phosphate labelling in response to U46619 indicates either that there may be inhibition of signal transduction without a detectable change in the amount of EPA in platelet phospholipids, that changes in signal transduction require only minute changes in the fatty acid composition of membrane phospholipids, or that after a 1 h incubation with EPA, activation of phospholipase C is affected by a mechanism that is not directly related to incorporation of EPA.

Download Full-text

Trimucytin: A Collagen-Like Aggregating Inducer Isolated from Trimeresurus mucrosquamatus Snake Venom

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651597 ◽

1993 ◽

Vol 69 (03) ◽

pp. 286-292 ◽

Cited By ~ 13

Author(s):

Che-Ming Teng ◽

Feng-Nien Ko ◽

Inn-Ho Tsai ◽

Man-Ling Hung ◽

Tur-Fu Huang

Keyword(s):

Platelet Aggregation ◽

Snake Venom ◽

Inositol Phosphate ◽

Shape Change ◽

Platelet Activating Factor ◽

Atp Release ◽

Platelet Membrane ◽

Thromboxane B2 ◽

Dependent Manner ◽

Concentration Dependent Manner

SummaryTrimucytin is a potent platelet aggregation inducer isolated from Trimeresurus mucrosquamatus snake venom. Similar to collagen, trimucytin has a run of (Gly-Pro-X) repeats at the N-terminal amino acids sequence. It induced platelet aggregation, ATP release and thromboxane formation in rabbit platelets in a concentration-dependent manner. The aggregation was not due to released ADP since it was not suppressed by creatine phosphate/creatine phosphokinase. It was not either due to thromboxane A2 formation because indomethacin and BW755C did not have any effect on the aggregation even thromboxane B2 formation was completely abolished by indomethacin. Platelet-activating factor (PAF) was not involved in the aggregation since a PAF antagonist, kadsurenone, did not affect. However, RGD-containing peptide triflavin inhibited the aggregation, but not the release of ATP, of platelets induced by trimucytin. Indomethacin, mepacrine, prostaglandin E1 and tetracaine inhibited the thromboxane B2 formation of platelets caused by collagen and trimucytin. Forskolin and sodium nitroprusside inhibited both platelet aggregation and ATP release, but not the shape change induced by trimucytin. In quin-2 loaded platelets, the rise of intracellular calcium concentration caused by trimucytin was decreased by 12-O-tetradecanoyl phorbol-13 acetate, imipramine, TMB-8 and indomethacin. In the absence of extracellular calcium, both collagen and trimucytin caused no thromboxane B2 formation, but still induced ATP release which was completely blocked by R 59022. Inositol phosphate formation in platelets was markedly enhanced by trimucytin and collagen. MAB1988, an antibody against platelet membrane glycoprotein Ia, inhibited trimucytinand collagen-induced platelet aggregation and ATP release. However, trimucytin did not replace the binding of 125I-labeled MAB1988 to platelets. Platelets pre-exposed to trimucytin were resistant to the second challenge with trimucytin itself or collagen. It is concluded that trimucytin may activate collagen receptors on platelet membrane, and cause aggregation and release mainly through phospholipase C-phosphoinositide pathway.

Download Full-text