Uptake of zinc from chelate-buffered nutrient solutions by wheat genotypes differing in zinc efficiency

Zinc-efficient Triticum aestivum (cv. Warigal) and Zn-inefficientTriticum turgidum conv. durum (cv. Durati) were grown in chelate-buffered,complete nutrient solutions providing either deficient or sufficientZn supply. When transferred to fresh chelatebuffered nutrientsolutions containing a wide range of Zn supplies (0–1.28µmol m^–3 Zn²⁺ activity) for 24–48 h, bothgenotypes increased net Zn uptake linearly with an increasein solution Zn²⁺ activities. Zincefficient Warigal accumulatedZn at a greater rate than Zn-inefficient Durati. The greaterrate of net Zn uptake was observed by plants of both genotypeswhen pretreated at deficient Zn supply. Net loss of Zn to thesolution was higher in plants pretreated with sufficient Znand was inversely related to Zn²⁺ activity in the external solution.When continuously supplied with 40 nmol m^–3 Zn²⁺, netZn uptake by Zn-efficient Warigal was significantly greaterthan that of Zn-inefficient Durati, but the difference diminishedwith plant age. Shoot concentrations of Fe, Mn and Cu were higherwhen plants were grown at deficient than at sufficient Zn supply.The Zn-efficient genotype transported less Zn and Fe to shootsand had higher Fe concentrations in roots than the Zn-inefficientgenotype, supporting the hypothesis that Zn efficiency may beconnected with inefficient transport of Fe from roots to shootsand thus initiation of the Fe-deficiency response resultingin increased release of Zn- and Fe-binding phytosiderophores.It is concluded that differential Zn efficiency of wheat genotypesis at least partly due to a greater ability of efficient genotypesto accumulate Zn. Key words: Chelate-buffering, genotypes, micronutrients, Triticum spp., uptake, zinc efficiency     

Short chemoenzymatic synthesis of S-enantiomers of two systemic fungicides

Summary 2-Methyl-(4-tert-butyl)cinnamaldehyde (1) was reduced by Saccharomyces cerevisiae (baker's yeast) to S-3-(4-tert-butyl)-phenyl-2-propanol (4) in high chemical and very high optical yield (e.e. 99%). Chlorination of 4 to 5, and alkylation of the corresponding cyclic amines complete this short enantioselective synthesis of S-1-(l'-pyperidino)-2-methyl-3-(4tert-butyl)-phenyl-propane (6) and S-1-(1'-(3,5-cisdimethyl)morpholino)-2-methyl-3-(4-tert-butyl)-phenyl-propane (7), the S-enantiomers of fenpropidine and fenpropimorph, commercialy important systemic fungicides.     

Organisation of Photosystem I and Photosystem II in red alga Cyanidium caldarium: encounter of cyanobacterial and higher plant concepts

Structure and organisation of Photosystem I and Photosystem II isolated from red alga Cyanidium caldarium was determined by electron microscopy and single particle image analysis. The overall structure of Photosystem II was found to be similar to that known from cyanobacteria. The location of additional 20 kDa (PsbQ') extrinsic protein that forms part of the oxygen evolving complex was suggested to be in the vicinity of cytochrome c-550 (PsbV) and the 12 kDa (PsbU) protein. Photosystem I was determined as a monomeric unit consisting of PsaA/B core complex with varying amounts of antenna subunits attached. The number of these subunits was seen to be dependent on the light conditions used during cell cultivation. The role of PsaH and PsaG proteins of Photosystem I in trimerisation and antennae complexes binding is discussed.     

Identification of a DNA methylome signature of esophageal squamous cell carcinoma and potential epigenetic biomarkers

Esophageal squamous cell carcinoma (ESCC) is believed to arise from esophageal mucosa through accumulation of both genetic and epigenetic changes. DNA methylation is a critical epigenetic mechanism involved in key cellular processes and its deregulation has been linked to many human cancers, including ESCC. The aim of this study is to examine the global deregulation of methylation states in ESCC and identify potential early biomarkers. With this purpose, we performed a bead array analysis of more than 800 cancer-related genes in ten ESCC samples, ten matched surrounding tissues and four esophageal mucosa from healthy individuals. Pyrosequencing was used for validation of DNA methylation changes in up to 106 cases and 27 controls. A total of 37 CpG sites were found to be differentially methylated between tumors and surrounding tissues. These CpG sites were significantly enriched in genes related to several pathways including IL-10 anti-inflammatory signaling pathway and cell communication pathway. In addition, by comparing with healthy esophageal mucosa, we identified TFF1 gene as a potential early marker of ESCC. This is the first study to address methylation changes in ESCC in a large set of genes. Methylome analysis is shown as a sensitive and powerful tool to identify molecular players in ESCC. These data should prove to be the reference for future studies identifying potential biomarkers and molecular targets in ESCC.     

Dynamic imbalance between cancer cell subpopulations induced by Transforming Growth Factor Beta (TGF-β) is associated with a DNA methylome switch

Background

Distinct subpopulations of neoplastic cells within tumors, including hepatocellular carcinoma (HCC), display pronounced ability to initiate new tumors and induce metastasis. Recent evidence suggests that signals from transforming growth factor beta (TGF-β) may increase the survival of these so called tumor initiating cells leading to poor HCC prognosis. However, how TGF-β establishes and modifies the key features of these cell subpopulations is not fully understood.

Results

In the present report we describe the differential DNA methylome of CD133-negative and CD133-expressing liver cancer cells. Next, we show that TGF-β is able to increase the proportion of CD133+ cells in liver cancer cell lines in a way that is stable and persistent across cell division. This process is associated with stable genome-wide changes in DNA methylation that persist through cell division. Differential methylation in response to TGF-β is under-represented at promoter CpG islands and enriched at gene bodies, including a locus in the body of the de novo DNA methyl-transferase DNMT3B gene. Moreover, phenotypic changes induced by TGF-β, including the induction of CD133, are impaired by siRNA silencing of de novo DNA methyl-transferases.

Conclusions

Our study reveals a self-perpetuating crosstalk between TGF-β signaling and the DNA methylation machinery, which can be relevant in the establishment of cellular phenotypes. This is the first indication of the ability of TGF-β to induce genome-wide changes in DNA methylation, resulting in a stable change in the proportion of liver cancer cell subpopulations.

Electronic supplementary material

The online version of this article (doi:10.1186/1471-2164-15-435) contains supplementary material, which is available to authorized users.     

Failure of Poly(ADP-Ribose) Polymerase Cleavage by Caspases Leads to Induction of Necrosis and Enhanced Apoptosis

Activation of poly(ADP-ribose) polymerase (PARP) by DNA breaks catalyzes poly(ADP-ribosyl)ation and results in depletion of NAD+ and ATP, which is thought to induce necrosis. Proteolytic cleavage of PARP by caspases is a hallmark of apoptosis. To investigate whether PARP cleavage plays a role in apoptosis and in the decision of cells to undergo apoptosis or necrosis, we introduced a point mutation into the cleavage site (DEVD) of PARP that renders the protein resistant to caspase cleavage in vitro and in vivo. Here, we show that after treatment with tumor necrosis factor alpha, fibroblasts expressing this caspase-resistant PARP exhibited an accelerated cell death. This enhanced cell death is attributable to the induction of necrosis and an increased apoptosis and was coupled with depletion of NAD+ and ATP that occurred only in cells expressing caspase-resistant PARP. The PARP inhibitor 3-aminobenzamide prevented the NAD+ drop and concomitantly inhibited necrosis and the elevated apoptosis. These data indicate that this accelerated cell death is due to NAD+ depletion, a mechanism known to kill various cell types, caused by activation of uncleaved PARP after DNA fragmentation. The present study demonstrates that PARP cleavage prevents induction of necrosis during apoptosis and ensures appropriate execution of caspase-mediated programmed cell death.     

Comparisons of microRNA Patterns in Plasma before and after Tumor Removal Reveal New Biomarkers of Lung Squamous Cell Carcinoma

Lung cancer is the major human malignancy, accounting for 30% of all cancer-related deaths worldwide. Poor survival of lung cancer patients, together with late diagnosis and resistance to classic chemotherapy, highlights the need for identification of new biomarkers for early detection. Among different cancer biomarkers, small non-coding RNAs called microRNAs (miRNAs) are considered the most promising, owing to their remarkable stability, their cancer-type specificity, and their presence in body fluids. However, results of multiple previous attempts to identify circulating miRNAs specific for lung cancer are inconsistent, likely due to two main reasons: prominent variability in blood miRNA content among individuals and difficulties in distinguishing tumor-relevant miRNAs in the blood from their non-tumor counterparts. To overcome these impediments, we compared circulating miRNA profiles in patients with lung squamous cell carcinoma (SCC) before and after tumor removal, assuming that the levels of all tumor-relevant miRNAs would drop after the surgery. Our results revealed a specific panel of the miRNAs (miR-205, -19a, -19b, -30b, and -20a) whose levels decreased strikingly in the blood of patients after lung SCC surgery. Interestingly, miRNA profiling of plasma fractions of lung SCC patients revealed high levels of these miRNA species in tumor-specific exosomes; additionally, some of these miRNAs were also found to be selectively secreted to the medium by cultivated lung cancer cells. These results strengthen the notion that tumor cells secrete miRNA-containing exosomes into circulation, and that miRNA profiling of the exosomal plasma fraction may reveal powerful cancer biomarkers.