Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A high-affinity K+ transporter PutHKT2;1 cDNA was isolated from the salt-tolerant plant Puccinellia tenuiflora. Expression of PutHKT2;1 was induced by both 300 mM NaCl and K+-starvation stress in roots, but only slightly regulated by those stresses in shoots. PutHKT2;1 transcript levels in 300 mM NaCl were doubled by the depletion of potassium. Yeast transformed with PutHKT2;1, like those transformed with PhaHKT2;1 from salt-tolerant reed plants (Phragmites australis), (i) were able to take up K+ in low K+ concentration medium or in the presence of NaCl, and (ii) were permeable to Na+. This suggests that PutHKT2;1 has a high affinity K+-Na+ symport function in yeast. Arabidopsis over-expressing PutHKT2;1 showed increased sensitivities to Na+, K+, and Li+, while Arabidopsis over-expressing OsHKT2;1 from rice (Oryza sativa) showed increased sensitivity only to Na+. In contrast to OsHKT2;1, which functions in Na+-uptake at low external K+ concentrations, PutHKT2;1 functions in Na+-uptake at higher external K+ concentrations. These results show that the modes of action of PutHKT2;1 in transgenic yeast and Arabidopsis differ from the mode of action of the closely related OsHKT2;1 transporter.
J Exp Bot 2009
PMID:Cloning of a high-affinity K+ transporter gene PutHKT2;1 from Puccinellia tenuiflora and its functional comparison with OsHKT2;1 from rice in yeast and Arabidopsis. 1952 29

The effect of the S nutritional status on a plant's capability to cope with Fe shortage was studied in solution cultivation experiments in barley (Hordeum vulgare L. cv. Europa). Barley is a Strategy II plant and responds to Fe deficiency by secretion of chelating compounds, phytosiderophores (PS). All PS are derived from nicotianamine whose precursor is methionine. This suggests that a long-term supply of an inadequate amount of S could reduce a plant's capability to respond to Fe deficiency by limiting the rate of PS biosynthesis. The responses of barley (Hordeum vulgare L. cv. Europa) plants grown for 12 d on Fe-free nutrient solutions (NS) containing 0 or 1.2 mM SO(4)(2-), was examined after 24 h or 48 h from transfer to NS containing 1.2 mM SO(4)(2-). After the supply of S was restored to S-deprived plants, an increase in PS release in root exudates was evident after 24 h of growth in S-sufficient NS and the increment reached values up to 4-fold higher than the control 48 h after S resupply. When S was supplied to S-deficient plants, leaf ATPS (EC 2.7.7.4) and OASTL (EC 4.2.99.8) activities exhibited a progressive recovery. Furthermore, root HvST1 transcript abundance remained high for 48 h following S resupply and a significant increase in the level of root HvYS1 transcripts was also found after only 24 h of S resupply. Data support the idea that the extent to which the plant is able to cope with Fe starvation is strongly associated with its S nutritional status. In particular, our results are indicative that barley plants fully recover their capability to cope with Fe shortage after the supply of S is restored to S-deficient plants.
J Exp Bot 2010 Mar
PMID:Supply of sulphur to S-deficient young barley seedlings restores their capability to cope with iron shortage. 2001 4

The effect of water stress on stomatal closure in sunflower plants has been found to be dependent on K(+) nutrient status. When plants with different internal K(+) content were subjected to a water-stress period, stomatal conductance was reduced more markedly in plants with an adequate K(+) supply than in K(+)-starved plants. K(+) starvation promoted the production of ethylene by detached leaves, as well as by the shoot of whole plants. Water stress had no significant effect on this synthesis. The effect on stomatal conductance of adding 5 microM cobalt (an ethylene synthesis inhibitor) to the growing medium of plants subjected to water stress was also dependent on their K(+) nutritional status: conductance was not significantly affected in normal K(+) plants whereas it was reduced in K(+)-starved plants. Cobalt had no harmful effects on growth, and did not alter the internal K(+) content in the plants. These results suggest that ethylene may play a role in the inhibiting effect of K(+) starvation on stomatal closure.
J Exp Bot 2010 Feb
PMID:K+ starvation inhibits water-stress-induced stomatal closure via ethylene synthesis in sunflower plants. 2005 30

Aluminium is well known to inhibit plant elongation, but the role in this inhibition played by water relations remains unclear. To investigate this, tobacco (Nicotiana tabacum L.) suspension-cultured cells (line SL) was used, treating them with aluminium (50 microM) in a medium containing calcium, sucrose, and MES (pH 5.0). Over an 18 h treatment period, aluminium inhibited the increase in fresh weight almost completely and decreased cellular osmolality and internal soluble sugar content substantially; however, aluminium did not affect the concentrations of major inorganic ions. In aluminium-treated cultures, fresh weight, soluble sugar content, and osmolality decreased over the first 6 h and remained constant thereafter, contrasting with their continued increases in the untreated cultures. The rate of sucrose uptake, measured by radio-tracer, was reduced by approximately 60% within 3 h of treatment. Aluminium also inhibited glucose uptake. In an aluminium-tolerant cell line (ALT301) isogenic to SL, all of the above-mentioned changes in water relations occurred and tolerance emerged only after 6 h and appeared to involve the suppression of reactive oxygen species. Further separating the effects of aluminium on elongation and cell survival, sucrose starvation for 18 h inhibited elongation and caused similar changes in cellular osmolality but stimulated the production of neither reactive oxygen species nor callose and did not cause cell death. We propose that the inhibition of sucrose uptake is a mechanism whereby aluminium inhibits elongation, but does not account for the induction of cell death.
J Exp Bot 2010 Jun
PMID:Aluminium reduces sugar uptake in tobacco cell cultures: a potential cause of inhibited elongation but not of toxicity. 2021 76

Rice has the unique ability to express alpha-amylase under anoxic conditions, a feature that is critical for successful anaerobic germination and growth. Previously, anaerobic conditions were shown to up-regulate the expression of Amy3 subfamily genes (Amy3B/C, 3D, and 3E) in rice embryos. These genes are known to be feedback regulated by the hydrolytic products of starchy endosperm such as the simple sugar glucose. It was found that oxygen deficiency interferes with the repression of Amy3D gene expression imposed by low concentrations of glucose but not with that imposed by higher amounts. This differential anoxic de-repression depending on sugar concentration suggests the presence of two distinct pathways for sugar regulation of Amy3D gene expression. Anoxic de-repression can be mimicked by treating rice embryos with inhibitors of ATP synthesis during respiration. Other sugar-regulated rice alpha-amylase genes, Amy3B/C and 3E, behave similarly to Amy3D. Treatment with a respiratory inhibitor or anoxia also relieved the sugar repression of the rice CIPK15 gene, a main upstream positive regulator of SnRK1A that is critical for Amy3D expression in response to sugar starvation. SnRK1A accumulation was previously shown to be required for MYBS1 expression, which transactivates Amy3D by binding to a cis-acting element found in the proximal region of all Amy3 subfamily gene promoters (the TA box). Taken together, these results suggest that prevention of oxidative phosphorylation by oxygen deficiency interferes with the sugar repression of Amy3 subfamily gene expression, leading to their enhanced expression in rice embryos during anaerobic germination.
J Exp Bot 2010 Jul
PMID:Interference with oxidative phosphorylation enhances anoxic expression of rice alpha-amylase genes through abolishing sugar regulation. 2053 Jan 96

In plants, carbon (C) molecules provide building blocks for biomass production, fuel for energy, and exert signalling roles to shape development and metabolism. Accordingly, plant growth is well correlated with light interception and energy conversion through photosynthesis. Because water deficits close stomata and thus reduce C entry, it has been hypothesised that droughted plants are under C starvation and their growth under C limitation. In this review, these points are questioned by combining literature review with experimental and modelling illustrations in various plant organs and species. First, converging evidence is gathered from the literature that water deficit generally increases C concentration in plant organs. The hypothesis is raised that this could be due to organ expansion (as a major C sink) being affected earlier and more intensively than photosynthesis (C source) and metabolism. How such an increase is likely to interact with C signalling is not known. Hence, the literature is reviewed for possible links between C and stress signalling that could take part in this interaction. Finally, the possible impact of water deficit-induced C accumulation on growth is questioned for various sink organs of several species by combining published as well as new experimental data or data generated using a modelling approach. To this aim, robust correlations between C availability and sink organ growth are reported in the absence of water deficit. Under water deficit, relationships weaken or are modified suggesting release of the influence of C availability on sink organ growth. These results are interpreted as the signature of a transition from source to sink growth limitation under water deficit.
J Exp Bot 2011 Mar
PMID:Water deficits uncouple growth from photosynthesis, increase C content, and modify the relationships between C and growth in sink organs. 2123 76

Sugar responsiveness of genes for both paths of sucrose metabolism could provide a mechanism not only for transcriptional regulation of the first step in the use of imported carbon, but also for altering signals to the sugar-sensing system. This hypothesis was examined by comparison of (1) sugar regulation among maize genes for sucrose synthase and invertase, (2) their contrasting patterns of tissue expression, and (3) their influence on production of effectors for other sugar-responsive genes. Cloning and characterization of the Ivr1 and Ivr2 invertase genes of maize indicated that these genes belong to distinct subfamilies of the maize soluble invertase gene family. In addition, maize invertases can be grouped with the sucrose synthases (Sh1 and Sus1) on the basis of shared patterns of differential sugar-responsiveness and tissue-specific expression. Extension of this comparison to include genes for sucrose metabolism from other species revealed a more widespread association between starvation-tolerant expression and restricted patterns of tissue distribution. Consideration of current models for plant sugar-sensing systems and transport pathways suggested that the site and mechanism of sucrose cleavage in the cell could affect the magnitude and type of signal generated.
J Exp Bot 1996 Aug
PMID:Sugar and metabolic regulation of genes for sucrose metabolism: potential influence of maize sucrose synthase and soluble invertase responses on carbon partitioning and sugar sensing. 2124 46

Suspension-cultured tobacco cells express a cell wall invertase (CWI) and a proteinaceous invertase inhibitor. Both proteins have been purified and characterized. A CWI cDNA clone has been isolated. The N-terminal protein sequence of the inhibitor has been determined showing high similarity with the N-terminal sequence of a tomato invertase inhibitor. A polyclonal antiserum has been raised against the denatured inhibitor protein. The observed changes of CWI activity during cell culture are partially the result of changes in gene expression, however, evidence has accumulated for further regulation by the inhibitor protein. In vivo regulation of CWI by the inhibitor is likely for the following reasons: (1) CWI inhibition is dependent on pH within the range relevant for the apoplasmic space, (2) divalent cations in the millimolar range affect CWI inhibition, (3) substrate protects CWI (but not vacuolar invertase) against inhibition, (4) CWI and inhibitor are co-expressed and co-localized in the apoplasmic space, (5) addition of inhibitor to intact cells causes substrate-protectable inhibition of CWI, (6) an in situ formation of tight complexes between CWI and inhibitor upon starvation of cells could be demonstrated. The results indicate that suspension-cultured tobacco cells are a suitable system to study the effects of an invertase inhibitor on CWI.
J Exp Bot 1996 Aug
PMID:Regulation of cell wall invertase by a proteinaceous inhibitor. 2124 48

The energy status of plant cells strongly depends on the energy metabolism in chloroplasts and mitochondria, which are capable of generating ATP either by photosynthetic or oxidative phosphorylation, respectively. Another energy-rich metabolite inside plastids is the glycolytic intermediate phosphoenolpyruvate (PEP). However, chloroplasts and most non-green plastids lack the ability to generate PEP via a complete glycolytic pathway. Hence, PEP import mediated by the plastidic PEP/phosphate translocator or PEP provided by the plastidic enolase are vital for plant growth and development. In contrast to chloroplasts, metabolism in non-green plastids (amyloplasts) of starch-storing tissues strongly depends on both the import of ATP mediated by the plastidic nucleotide transporter NTT and of carbon (glucose 6-phosphate, Glc6P) mediated by the plastidic Glc6P/phosphate translocator (GPT). Both transporters have been shown to co-limit starch biosynthesis in potato plants. In addition, non-photosynthetic plastids as well as chloroplasts during the night rely on the import of energy in the form of ATP via the NTT. During energy starvation such as prolonged darkness, chloroplasts strongly depend on the supply of ATP which can be provided by lipid respiration, a process involving chloroplasts, peroxisomes, and mitochondria and the transport of intermediates, i.e. fatty acids, ATP, citrate, and oxaloacetate across their membranes. The role of transporters involved in the provision of energy-rich metabolites and in pathways supplying plastids with metabolic energy is summarized here.
J Exp Bot 2011 Apr
PMID:The role of transporters in supplying energy to plant plastids. 2151 15

Our understanding of plant growth in response to nitrogen (N) supply is mainly based on studies of mutants and transformants. This study explored the natural variability of Arabidopsis thaliana first to find out its global response to N availability and secondly to characterize the plasticity for growth and N metabolism among 23 genetically distant accessions under normal (N+), limited (N-), and starved (N0) N supplies. Plant growth was estimated by eight morphological traits characterizing shoot and root growth and 10 metabolic parameters that represented N and carbon metabolism. Most of the studied traits showed a large variation linked to genotype and nutrition. Furthermore, Arabidopsis growth was coordinated by master traits such as the shoot to root ratio of nitrate content in N+, root fresh matter and root amino acids in N-, and shoot fresh matter together with root thickness in N0. The 23 accessions could be gathered into four different groups, according to their growth in N+, N-, and N0. Phenotypic profiling characterized four different adaptative responses to N- and N0. Class 1 tolerated N limitation with the smallest decrease in shoot and root biomass compared with N+, while class 2 presented the highest resistance to N starvation by preferential increased root growth, huge starch accumulation, and high shoot nitrate content. In contrast, class 3 plants could tolerate neither N limitation nor N starvation. Small plants of class 4 were different, with shoot biomass barely affected in N- and root biomass unaffected in N0.
J Exp Bot 2012 Jan
PMID:Natural variation of Arabidopsis response to nitrogen availability. 2191 59


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