Iron deficiency induces sulfate uptake and modulates redistribution of reduced sulfur pool in barley plants

2006 ◽  
Vol 33 (11) ◽  
pp. 1055 ◽  
Author(s):  
Stefania Astolfi ◽  
Sabrina Zuchi ◽  
Stefano Cesco ◽  
Luigi Sanità di Toppi ◽  
Daniela Pirazzi ◽  
...  

We studied the possibility that the sulfur (S) assimilatory pathway might be modulated by iron (Fe) starvation in barley, as a consequence of plant requirement for an adequate amount of reduced S to maintain methionine and, in turn, phytosiderophore biosynthesis. Barley seedlings were grown with or without 100 µm FeIII–EDTA, at three S levels in the nutrient solution (S2 = 1200, S1 = 60, and S0 = 0 µm sulfate) in order to reproduce conditions of optimal supply, latent and severe deficiency, respectively. Fe deprivation increased root cysteine content irrespective of the S supply. However, this increase was not associated with either higher rates of 35SO42– uptake or increased expression of the gene for the high-affinity sulfate transporter, HvST1, and these roots failed to increase their activities of ATP sulfurylase (ATPS) and O-acetylserine(thiol) lyase (OASTL). We observed a significant increase in 35SO42– uptake rate (+76%) only in Fe-deficient S1 plants and we found an increase in root ATPS activity only in S0 plants. We observed an increase of ATPS enzyme activity in leaves of S1 and S2 plants, most likely suggesting increased S assimilation followed by translocation of thiols (Cys) to the root. Taken together, our results suggest that Fe deficiency affects the partitioning from the shoot to the root of the reduced S pool within the plant and can affect SO42– uptake under limited S supply.

Blood ◽  
1998 ◽  
Vol 92 (8) ◽  
pp. 2959-2962 ◽  
Author(s):  
Arthur Schneider ◽  
Linda Forman ◽  
Beryl Westwood ◽  
Catherine Yim ◽  
James Lin ◽  
...  

Abstract In 424 African-American and 75 white subjects, we found that the −5 (TPI 592 A→G), −8 (TPI 589 G→A), and −24 (TPI 573 T→G) variants in the triosephosphate isomerase (TPI) gene occurred frequently (41.0%) in the African-American subjects but did not occur in the whites. These data suggest that this set of polymorphisms may turn out to be one of the higher-incidence molecular markers of African lineage, a surprising finding because others had reported that these nucleotide substitutions were restricted to a small subset of African Americans who had been characterized as TPI-deficiency heterozygotes. Additionally, we investigated the relationship of these variants to TPI-enzyme activity. Although the variant substitutions (occurring in three haplotypes: −5 alone, −5 −8, and −5 −8 −24) were associated with moderate reduction in enzyme activity, severe-deficiency heterozygotes could not be identified with certainty, and none of the haplotypes were restricted to subjects with marked reduction of enzyme activity. Three subjects were homozygous for the −5 −8 haplotype, a finding inconsistent with the putative role of this haplotype as the cause of a null variant incompatible with life in homozygotes. Despite these findings, the possibility remains that the −5 −8 or −5 −8 −24 haplotypes may in some instances contribute to compound heterozygosity and clinical TPI deficiency. © 1998 by The American Society of Hematology.


2006 ◽  
Vol 35 (3) ◽  
pp. 726-733 ◽  
Author(s):  
Stormy Dawn Lindblom ◽  
Salah Abdel-Ghany ◽  
Brady R. Hanson ◽  
Seongbin Hwang ◽  
Norman Terry ◽  
...  

1984 ◽  
Vol 102 (1) ◽  
pp. 57-61 ◽  
Author(s):  
H. Humphries ◽  
S. MacNeil ◽  
D. S. Munro ◽  
S. Tomlinson

ABSTRACT Recent evidence suggests that epidermal growth factor (EGF) may play an important role in the regulation of thyroid growth and function. We have examined the interaction of murine EGF (mEGF) with human and porcine thyroid membranes and compared this with the binding of bovine TSH (bTSH) using 125I-labelled hormones as tracers. The characteristics of the binding of mEGF were found to be similar for human and porcine thyroid membranes. Epidermal growth factor bound with high affinity (affinity constant = 1·4 × 109 l/mol); the density of binding sites was low compared with the TSH receptor. At 37 °C, the binding of 125I-labelled EGF was maximal at 1 h and was saturable in the presence of unlabelled EGF; half-maximal inhibition was at 1 ng EGF/tube (0·5 nmol/l) using 0·5 mg membrane protein/tube. Unlabelled bTSH had no effect on the binding of labelled EGF. Similarly, unlabelled EGF did not affect the binding of labelled TSH; hence it was concluded that mEGF and bTSH bound to independent sites. Epidermal growth factor had no effect on adenylate cyclase activity in membranes prepared from human non-toxic goitre; increasing concentrations of EGF did not affect basal, TSH-stimulated or fluoride-stimulated enzyme activity. J. Endocr. (1984) 102, 57–61


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ying He ◽  
Yinhui Zhang ◽  
Xionghao Chen ◽  
Qiong Wang ◽  
Lifen Ling ◽  
...  

Abstract Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common hereditary disorder in China. The existing prevalence and molecular epidemiology of G6PD deficiency in China were geographically limited. In this study, the spectrum of G6PD gene mutations was well characterized in a large and diverse population all over the country; and the correlation of genotype and enzyme activity phenotype was explored for the first time. The results showed that the overall prevalence of G6PD deficiency in China was 2.10% at the national level. The top six common mutations were c.1388 G>A, c.1376 G>T, c.95 A>G, c.392 G>T, c.871 G>A and c.1024 C>T, accounting for more than 90% of G6PD deficient alleles. Compound mutation patterns were frequently observed in females with severe deficiency. The distribution of G6PD activities depended on the type of mutation patterns and genders. Hemizygote, homozygote, and compound heterozygote were predominantly associated with severe G6PD deficiency, whereas heterozygotes with single mutation mainly presented moderate enzyme deficiency. A significant gap between G6PD activities in hemizygous and normal males was observed, and yet, the overall distribution of that in females carrying missense mutations was a continuum from G6PD severely deficient to normal. This is the first report of discussing the association between G6PD genetic variants in the Chinese and enzyme activity phenotypes.


Crop Science ◽  
1998 ◽  
Vol 38 (1) ◽  
pp. 254-259 ◽  
Author(s):  
Shun‐Fu Lin ◽  
James S. Baumer ◽  
Drew Ivers ◽  
Silvia Rodriguez Cianzo ◽  
Randy C. Shoemaker

1986 ◽  
Vol 18 (2) ◽  
pp. 156???161 ◽  
Author(s):  
FREDRIK CELSING ◽  
EVA BLOMSTRAND ◽  
BJ??RN WERNER ◽  
PETER PIHLSTEDT ◽  
BJ??RN EKBLOM

2010 ◽  
Vol 37 (1) ◽  
pp. 74 ◽  
Author(s):  
Michael Frei ◽  
Yunxia Wang ◽  
Abdelbagi M. Ismail ◽  
Matthias Wissuwa

Zinc deficiency reduces rice growth and yield, and this is, in part, due to leaf damage caused by reactive oxygen species (ROS). The aim of this study was to identify biochemical mechanisms conferring tolerance to Zn deficiency-induced oxidative stress. A field experiment and three nutrient solution experiments were conducted with the intolerant genotype IR74 and recombinant inbred lines (RILs) derived from a cross between IR74 and the tolerant landrace Jalmagna. After 2 weeks of growth in low Zn soil, stress symptoms developed in leaves of IR74, but not in the tolerant RIL46. Activity of antioxidant enzymes showed clear treatment effects, but did not explain tolerance of RIL46. On the contrary, the intolerant IR74 showed higher activities of superoxide dismutase (SOD), guaiacol peroxidase (POX), ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR) and glutathione reductase (GR) under Zn deficiency. This contrasted with a constitutively higher level of total and reduced ascorbic acid (AsA) in RIL46. Three further nutrient solution experiments focussed on enzymes and reducing substrates of the ascorbate–glutathione cycle. The first experiment included the highly sensitive RIL76 in addition to the genotypes used in the field trial, to test whether the patterns of antioxidant response observed in the field were specific to the genotypes used. This genotype had similarly low AsA level as IR74, but did not respond to Zn deficiency with an increase in enzyme activity, leading to even more pronounced leaf symptoms. In a second experiment, co-segregation of AsA concentration and Zn deficiency tolerance was confirmed in five genotypes from the IR74/Jalmagna quantitative trait loci (QTL) mapping population. A third experiment was conducted to determine whether the observed patterns of antioxidant response were specific to Zn deficiency or would also apply to oxidative stress caused by iron deficiency. Although high AsA level apparently conferred tolerance under both types of stress, the enzymatic response to iron deficiency differed from that to Zn deficiency. In particular, APX activity showed a decrease instead of an increase under low iron stress. In conclusion, we suggest that a high AsA level is a promising target for developing rice genotypes with tolerance to oxidative stress.


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