A series of well-defined phosphine-ligated diarylgold­(III) complexes cis-[Au­(L)­(ArF)­(Ar′)­(Cl)] were prepared, and detailed kinetics of the C­(sp2)–C­(sp2) reductive elimination from these complexes were studied. The mechanism of the reductive elimination from the complexes cis-[Au­(L)­(ArF)­(Ar′)­(Cl)] was further studied by theoretical calculations. The combination of experimental and theoretical results suggests that the biaryl reductive elimination from organogold­(III) complexes cis-[Au­(L)­(ArF)­(Ar′)­(Cl)] proceeds through a concerted biaryl-forming pathway from the four-coordinated Au­(III) metal center. These studies also disclose that the steric hindrance of the phosphine ligands plays a major role in promoting the biaryl-forming reductive elimination from diarylgold­(III) complexes cis-[Au­(L)­(ArF)­(Ar′)­(Cl)], while electronic properties of these ligands have a much smaller effect. Futhermore, it was found that the complexes with more weakly electron withdrawing aryl ligands undergo reductive elimination more quickly and the elimination rate is not sensitive to the polarity of the solvents.

The preparation of the difluoromethylated organogold-(III) complex cis-[Au(PCy 3 )(4-F-C 6 H 4 )(CF 2 H)(Cl)] (3) and its Ar− CF 2 H reductive elimination are described. In the presence of 1.0 equiv of AgSbF 6 or AgPF 6 , compound 3 underwent a quantitative Ar− CF 2 H reductive elimination in less than 1.0 min at 25 °C, while the lack of silver salt resulted in Ar−CF 2 H reductive elimination from complex 3 in 1,1,2,2-tetrachloroethane (CCl 2 HCCl 2 H) after 80 min at 115 °C to afford the elimination product p-F-PhCF 2 H (4) and (Cy 3 P)Au(Cl) in quantitative yields. On the basis of the mechanistic studies of the kinetics of the reaction and DFT calculation, a concerted Ar−CF 2 H bond-forming pathway for the Ar−CF 2 H reductive elimination from organogold(III) complex 3 is proposed.

Earlier studies reveal that Small protein B (SmpB), a class of well-conserved tmRNA-binding proteins, is essential for the trans-translation process, which functions as a system for translation surveillance and ribosome rescue. Here, we report a previously unrecognized mechanism by which SmpB alone positively regulates the expression of a sensor kinase, BvgS, in Aeromonas veronii. A reporter plasmid was constructed in which the promoter of bvgS was used to control the expression of the enhanced green fluorescent protein (eGFP) gene. When the reporter plasmid was co-transformed with a SmpB expression construct into E. coli, the relative fluorescence intensity increased about threefold. Transformation with a truncated form of smpB gene showed that the C-terminus had little effect, while N-terminus unexpectedly increased eGFP production. Next, a series of SmpB mutants were generated by site-directed mutagenesis. When the mutants SmpB (G11S) or SmpB (E32AG) was used in the experiment, eGFP expression dropped significantly compared with that of wild type SmpB. Further, purified SmpB was shown to bind the promoter regions of bvgS in the agarose gel retardation assay. Quantitative RT-PCR analysis showed that eGFP transcript levels increased approximately 25-fold in the presence of SmpB. Likewise, smpB knockout decreased bvgS transcripts significantly in A. veronii, and also displayed a reduced capability in salt tolerance. Collectively, the data presented here will facilitate a deeper understanding of SmpB-mediated regulatory circuits as a transcriptional factor in A. veronii.

Haloxylon ammodendron, an important shrub for desert afforestation, can adapt to harsh ecological environments such as drought, saline and extreme high temperature. Therefore, the study of H. ammodendron stress adaptation mechanism is of great practical signi cance for ecological improvement in desert areas. Previously, a heat stress (HS) responsive H. ammodendron 14-3-3 protein gene HaFT-1 with HS memory characteristics found in transcriptome was cloned and its transgenic Arabidopsis lines were obtained. In this study, its role in HS tolerance was further investigated. qRT-PCR analysis showed that HS priming enhanced the expression of HaFT-1 under the second HS and subsequent recovery treatment, indicating expression of HaFT-1 had transcriptional memory to HS. Subcellular localization showed that YFP-HaFT-1 fusion protein located in the cytoplasm of protoplasts. The survival rates of HaFT-1 overexpression seedlings were higher than that of WT after priming-andtriggering and non-primed control treatments. Cell death staining showed that cell death in HaFT-1 overexpression lines was more signi cantly inhibited than that in WT seedlings when treated with HS. Transcriptome analysis showed that energy generation, protein metabolism, signal transduction, biosynthesis, proline metabolism, autophagy, chlorophyll metabolism, and peroxisome were related to resistance of HaFT-1 transgenic plants to the second HS. Growth physiology analysis showed that priming-and-triggering treatment in HaFT-1 overexpression Arabidopsis promoted regulation on proline content and strengthened reactive oxygen species (ROS) scavenging activity. These results demonstrated that overexpression of HaFT-1 strengthened not only HS priming but also tolerance to the second HS of transgenic Arabidopsis, suggesting HaFT-1 as a positive regulator in acquired thermotolerance.

A mild, efficient and practical Co-catalyzed cross coupling reaction of a variety of activated heteroaryl chlorides and bromides with lithium aryl zincates that were in situ generated from lithium aryl boronates with ZnBr2 was described.