Effect of Thermal Exposure on Microstructure Evolution and Mechanical Properties of TC25G Alloy.

The microstructure and room temperature tensile properties of heat-treated TC25G alloy after thermal exposure were investigated. The results show that the α2 phase dispersed in the α phase, and silicide precipitated firstly at the α/ß phase boundary and then at the dislocation of the αp phase and on the ß phase. When thermal exposure was 0-10 h at 550 °C and 600 °C, the decrease of alloy strength was mainly due to the dominant effect of dislocations recovery. With the rise and extension of thermal exposure temperature and time, the increasing quantity and size of precipitates played an important role in the improvement of alloy strength. When thermal exposure temperature rose to 650 °C, the strength was always lower than that of heat-treated alloy. However, since the decreasing rate of solid solution strengthening was smaller than the increasing rate of dispersion strengthening, alloy still showed an increasing trend in the range of 5-100 h. When thermal exposure time was 100-500 h, the size of the α2 phase increased from the critical value of 3 nm to 6 nm, and the interaction between the moving dislocations and the α2 phase changed from the cutting mechanism to the by-pass mechanism (Orowan mechanism), and thus alloy strength decreased rapidly.

The rsmA-like gene rsmA(Xoo) of Xanthomonas oryzae pv. oryzae regulates bacterial virulence and production of diffusible signal factor.

The plant-pathogenic prokaryote Xanthomonas oryzae pv. oryzae (Xoo) causes bacterial leaf blight, one of the most destructive diseases of rice. A nonpolar mutant of the rsmA-like gene rsmA(Xoo) of the Xoo Chinese strain 13751 was constructed by homologous integration with a suicide plasmid. Virulence tests on a host plant, namely the hybrid rice cultivar Teyou 63, showed that the mutant had lost its virulence almost completely, whereas tests on a nonhost, namely castor-oil plant (Ricinus communis), showed that the mutant had also lost the ability to induce a hypersensitive response in the nonhost. In addition, the rsmA(Xoo) mutant produced significantly smaller amounts of the diffusible signal factor, extracellular endoglucanase, amylase and extracellular polysaccharide, but showed significantly higher glycogen accumulation, bacterial aggregation and cell adhesion. The expression of most hrp genes, genes encoding AvrBs3/PthA family members, rpfB, xrvA, glgA, eglXoB and XOO0175 (encoding an α-amylase) was down-regulated in the rsmA(Xoo) mutant. All phenotypes and expression levels of the tested genes in the rsmA(Xoo) mutant were restored to their levels in the wild-type by the presence of rsmA(Xoo) in trans. These results indicate that rsmA(Xoo) is essential for the virulence of Xoo.