Protein phosphorylation, especially serine/threonine and tyrosine phosphorylation, plays significant roles in signalling during plant growth and development as well as plant responses to biotic or abiotic stresses. Dual-specificity protein tyrosine phosphatases dephosphorylate components of these signalling pathways. Here, we report that an atypical dual-specificity protein tyrosine phosphatase, AtPFA-DSP3 (DSP3), negatively affects the response of plants to high-salt conditions. A DSP3 loss-offunction mutant showed reduced sensitivity to salt treatment. DSP3 was primarily localized in nuclei and was degraded during salt treatment. Compared to wild type, the level of ROS was lower in the dsp3 mutant and higher in plants ectopically expressing DSP3, indicating that higher DSP3 level was associated with increased ROS production. DSP3 interacted with and dephosphorylated MPK3 and MPK6.Genetic analyses of a dsp3mpk3 double mutant revealed that DSP3's effect on salt stress depends on MPK3. Moreover, the phosphatase activity of DSP3 was required for its role in salt signalling. These results indicate that DSP3 is a negative regulator of salt responses in Arabidopsis by directly modulating the accumulation of phosphorylated MPK3 and MPK6.

In this paper, three commercial polymers (polytetrafluoroethylene [PTFE], polyetheretherketone [PEEK], and polyimide [PI]) were irradiated by gamma rays in the ambient air. The changes in microstructure, mechanical, and tribological properties of these three polymers after irradiation were investigated comparatively. The results display that both the surface and internal structures of PTFE are degraded due to the irradiation chemical reaction, and the molecular chain scission at the surface is more severe than that at its internal as a result of the involvement of oxygen. The oxidative degradation also plays a dominant role in the PEEK surface, but the molecular chain crosslink is dominant in the PEEK internal. The top layer of PI also shows the characteristics of oxidative irradiation degradation, but its internal exhibits excellent irradiation resistance and no structure change occurs even at irradiation doses up to 20 MGy. The microhardness and scratch resistance of irradiated surfaces for all three polymers decrease but only the scratching damage mode of PTFE changes after irradiation. Friction experiments show that the friction coefficients of PTFE increase but that of PEEK decrease after irradiation. The wear rates on the irradiated surfaces of all three polymers increase compared with the unirradiated samples. Moreover, there is a depth gradient effect on the wear properties of both irradiated PTFE and PEEK polymers. The changes in wear rates of irradiated surfaces are consistent with the structural variations of all three polymers.

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I t has been shown(l,2) that Vit. E-deficient diet caused rabbits to excrete 1-methylhistidine in large amounts. Appeuance of this amino acid in urine generally precedes that of creatine making it one of the earliest detectable symptoms of nutritional muscular dystrophy. McManus( 1) has shown a diminished concentration af muscle carnosine and anserine suggesting an abnormality in the metabolism of these dipeptides. She believes that Vit. E-deficiency results in a hydrolysis of muscle anserine to beta-alanine and 1-methylhistidine as well as a decreased synthesis of anserine.Regardless of the causative mechanism, the loss of large amounts of 1-methylhistidine might itself produce secondary effects such as a significant drain on the body's reserve of the essential amino acid histidine. Our studies describe the effect of dietary L-histidine on excretion of creatine, histidine, and 1-methylhistidine of normal and Vit. E-deficient rabbits.Methods. Twelve male rabbits, divided into 4 equal groups, were fed the following diets ud Zib.: A. Dystrophy-producing diet of Young and Dinning(3) plus 8 rng alphatocopherol acetate thrice weekly: R. Dystrophy-producing diet containing 1 % L-histidine plus 8 mg oral alpha-tocopherol acetate thrice weekly: C. Dystrophy-producing diet: D. Dystrophy-producing diet containing 1 % L-histidine. When histidine was inmrporated into the diet, an equivalent weight of sucrose was deducted.Twenty-four hour urine samples were collected occasionally in a rabbit metabolism cage. Creatine and creatinine were determined by the method of Folin(4) while quantitative determinations of histidine and 1methylhistidine were made by Dowex-50 chromatography using the method of Tallan et a l . ( 5 ) .