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Wheat stem rust was once the most destructive plant disease, but it has been largely controlled. However, to prevent future problems, the ongoing development of resistant wheat varieties requires knowledge of the changing virulence patterns for Pgt virulence of the fungus that causes wheat stem rust and the detection of new races. Surveys were conducted from 2013-2014 to determine the races of the Pgt present in China. Low levels of stem rust infections were found in China during this investigation and 11 Puccinia graminis f. sp. tritici (Pgt) samples were obtained. In addition, 22 Pgt samples collected from the alternate host (Berberis) were obtained and have been reported for the first time. Fifty-three isolates were obtained from all samples. Four race groups, including 13 physiological races, were identified. They included the most prevalent races, 34C3MTGQM and 34C6MRGQM, with 13.2% predominance, followed by 34C0MRGQM at 11.3%. Six new races that were virulent against the resistance genes, Sr5 + Sr11, were found for the first time in China, namely 34C0MRGQM, 34C3MTGQM, 34C3MKGQM, 34C3MKGSM, 34C6MTGSM, and 34C6MRGQM, with a predominance of 11.3, 13.2, 9.4, 9.4, 1.9, and 13.2%, respectively. Most of the genes studied were ineffective against one or more of the tested isolates, except Sr9e, Sr21, Sr26, Sr31, Sr33, Sr38, Sr47, and SrTt3. Genes Sr35, SrTmp, Sr30, Sr37, Sr17, and Sr36 were effective in 92.5, 86.8, 84.9, 84.9, 79.3, and 77.4% of the tested isolates, respectively. In contrast, all of the isolates were virulent against Sr6, Sr7b, Sr9a, Sr9b, Sr9d, Sr9g, and SrMcN. Our results indicate that remarkable differences exist among the categories of the races in this study (i.e., their known virulence gene spectra) and the Pgt races reported previously. In addition, the sexual cycle of Pgt may contribute to its diversity in China.

Peroxiredoxins (Prxs) act against hydrogen peroxide (H2O2), organic peroxides, and peroxynitrite. Thermococcus kodakaraensis KOD1, an anaerobic archaeon, contains many antioxidant proteins, including three Prxs (Tk0537, Tk0815, and Tk1055). Only Tk0537 has been found to be induced in response to heat, osmotic, and oxidative stress. Tk0537 was found to belong to a 1-Cys Prx6 subfamily based on sequence analysis and was named 1-Cys TkPrx. Using gel filtration chromatography, electron microscopy, and blue-native polyacrylamide gel electrophoresis, we observed that 1-Cys TkPrx exhibits oligomeric forms with reduced peroxide reductase activity as well as decameric and dodecameric forms that can act as molecular chaperones by protecting both proteins and DNA from oxidative stress. Mutational analysis showed that a cysteine residue at the N-terminus (Cys46) was responsible for the peroxide reductase activity, and cysteine residues at the C-terminus (Cys205 and Cys211) were important for oligomerization. Based on our results, we propose that interconversion between different oligomers is important for regulating the different functions of 1-Cys TkPrx.

High blood sugar is a symptom of diabetes mellitus (DM). Vascular endothelial cells (VECs) directly contact the blood and are damaged when blood sugar levels are high. However, the molecular mechanism underlying this process remains elusive. To analyze the effects of DM on migration, we simulated DM by applying high glucose (HG) to the human VEC. HG delayed cell migration and induced phosphorylation of MAPKs (JNK and ERK). By contrast, in presence of bFGF, cell migration was promoted and MAPK phosphorylation levels were reduced. Furthermore, treatment with JNK and ERK inhibitors rescued HG-mediated delay of cell migration. Molecular and cell biological studies demonstrated that HG increased ROS production, whereas treatment with bFGF or JNK/ERK inhibitors blocked HG-induced ROS accumulation. Addition of MnTMPyP, a ROS scavenger, reduced HG-induced ROS production and accelerated cell migration, suggesting that the influence of HG on bFGF-MAPK signaling causes accumulation of ROS, which in turn regulate cell migration. This is the first study to elucidate the molecular mechanism of HG-mediated VEC migration; these findings could facilitate the development of novel therapies for DM.

One of the major symptoms of diabetes mellitus (DM) is delayed wound healing, which affects large populations of patients worldwide. However, the underlying mechanism behind this illness remains elusive. Skin wound healing requires a series of coordinated processes, including fibroblast cell proliferation and migration. Here, we simulate DM by application of high glucose (HG) in human foreskin primary fibroblast cells to analyze the molecular mechanism of DM effects on wound healing. The results indicate that HG, at a concentration of 30 mM, delay cell migration, but not cell proliferation. bFGF is known to promote cell migration that partially rescues HG effects on cell migration. Molecular and cell biology studies demonstrated that HG enhanced ROS production and repressed JNK phosphorylation, but did not affect Rac1 activity. JNK and Rac1 activation were known to be important for bFGF regulated cell migration. To further confirm DM effects on skin repair, a type 1 diabetic rat model was established, and we observed the efficacy of bFGF on both normal and diabetic rat skin repair. Furthermore, proteomic studies identified an increase of Annexin A2 protein nitration in HG-stressed fibroblasts and the nitration was protected by activation of bFGF signaling. Treatment with FGFR1 and JNK inhibitors delayed cell migration and increased Annexin A2 nitration levels, indicating that Annexin A2 nitration is modulated by bFGF signaling via activation of JNK. Together with these results, our data suggests that the HG-mediated delay of cell migration is linked to the inhibition of bFGF signaling, specifically through JNK suppression.