No abstract

No abstract

Selenoprotein K (SelK) is a newly identified selenoprotein. We showed that selenium incorporation into SelK was dependent on the 3 0 UTR of SelK mRNA. Sec insertion sequence (SECIS) RNA binding assays demonstrated that human SBP2 bound to the SelK SECIS element through the conserved nonWatson-Crick base pair quartet but not the AAT motif. Examination of the expression pattern revealed that human SelK mRNA was highly expressed in heart. Immunofluorescence analysis showed that SelK localized to the endoplasmic reticulum. Using SelK recombinant adenovirus, we found that overexpression of SelK attenuated the intracellular reactive oxygen species level and protected cells from oxidative stress-induced toxicity in cardiomyocytes. Our findings indicated that SelK is a novel antioxidant in cardiomyocytes and is related to the regulation of cellular redox balance.

Biodiesel can replace petroleum diesel as it is produced from animal fats and vegetable oils, and it produces about 10 % (w/w) glycerol, which is a promising new industrial microbial carbon, as a major by-product. One of the most potential applications of glycerol is its biotransformation to high value chemicals such as 1,3-propanediol (1,3-PD), dihydroxyacetone (DHA), succinic acid, etc., through microbial fermentation. Glycerol dehydratase, 1,3-propanediol dehydrogenase (1,3-propanediol-oxydoreductase), and glycerol dehydrogenase, which were encoded, respectively, by dhaB, dhaT, and dhaD and with DHA kinase are encompassed by the dha regulon, are the three key enzymes in glycerol bioconversion into 1,3-PD and DHA, and these are discussed in this review article. The summary of the main research direction of these three key enzyme and methods of glycerol bioconversion into 1,3-PD and DHA indicates their potential application in future enzymatic research and industrial production, especially in biodiesel industry.

The wheat blast fungus (Triticum pathotype of Pyricularia oryzae) first arose in Brazil in 1985 and has recently spread to Asia. Resistance genes against this new pathogen are very rare in common wheat populations. We screened 520 local landraces of common wheat collected worldwide with Br48, a Triticum isolate collected in Brazil, and found a highly resistant, unique accession, GR119. When F seedlings derived from a cross between GR119 and Chinese Spring (CS, susceptible control) were inoculated with Br48, resistant and susceptible seedlings segregated in a 15:1 ratio, suggesting that GR119 carries two resistance genes. When the F seedlings were inoculated with Br48ΔA8 carrying a disrupted allele of AVR-Rmg8 (an avirulence gene corresponding to a previously reported resistance gene, Rmg8), however, the segregation fitted a 3:1 ratio. These results suggest that one of the two genes in GR119 was Rmg8. The other, new gene was tentatively designated as RmgGR119. GR119 was highly resistant to all Triticum isolates tested. Spikes of GR119 were highly resistant to Br48, moderately resistant to Br48ΔA8 and a hybrid culture carrying avr-Rmg8 (nonfunctional allele), and highly resistant to its transformant carrying AVR-Rmg8. The strong resistance of GR119 was attributed to the combined effects of Rmg8 and RmgGR119.

Rmg8 and Rmg7 are genes for resistance to the wheat blast fungus (Pyricularia oryzae), located on chromosome 2B in hexaploid wheat and chromosome 2A in tetraploid wheat, respectively. AVR-Rmg8, an avirulence gene corresponding to Rmg8, was isolated from a wheat blast isolate through a map-based strategy. The cloned fragment encoded a small protein containing a putative signal peptide. AVR-Rmg8 was recognized not only by Rmg8, but also by Rmg7, suggesting that these two resistance genes are equivalent to a single gene from the viewpoint of resistance breeding.

No abstract

In this paper we consider chemotherapy in a spatial model of tumor growth. The model, which is of reaction-diffusion type, takes into account the complex interactions between the tumor and surrounding stromal cells by including densities of endothelial cells and the extra-cellular matrix. When no treatment is applied the model reproduces the typical dynamics of early tumor growth. The initially avascular tumor reaches a diffusion limited size of the order of millimeters and initiates angiogenesis through the release of vascular endothelial growth factor (VEGF) secreted by hypoxic cells in the core of the tumor. This stimulates endothelial cells to migrate towards the tumor and establishes a nutrient supply sufficient for sustained invasion. To this model we apply cytostatic treatment in the form of a VEGF-inhibitor, which reduces the proliferation and chemotaxis of endothelial cells. This treatment has the capability to reduce tumor mass, but more importantly, we were able to determine that inhibition of endothelial cell proliferation is the more important of the two cellular functions targeted by the drug. Further, we considered the application of a cytotoxic drug that targets proliferating tumor cells. The drug was treated as a diffusible substance entering the tissue from the blood vessels. Our results show that depending on the characteristics of the drug it can either reduce the tumor mass significantly or in fact accelerate the growth rate of the tumor. This result seems to be due to complicated interplay between the stromal and tumor cell types and highlights the importance of considering chemotherapy in a spatial context.