ABSTRACT
Deep eutectic solvents (DESs) dissolve metal salts or oxides and are used as solvent and carbon source for the preparation of supported palladium catalysts. After dissolving of the palladium salt in the DES, the pyrolysis of the mixture under nitrogen atmosphere yields catalytically active palladium on supporting material composed of carbon, nitrogen and oxygen (CNO) by a simple single step preparation method without further activation. The catalysts were characterized by scanning electron microscopy (SEM) and X-ray photoelectron spectroscopy (XPS), X-ray diffraction (XRD), Brunauer-Emmett-Teller (BET) and CHNS/O elementary analysis. The amount of functional groups on the surface of the supporting material was determined by Boehm titrations. Moreover, the activity of the prepared catalysts was evaluated in the hydrogenation of linear alkenes and compared with a commercial Pd/C catalyst.
ABSTRACT
The recently identified P6A promoter of the anaerobically inducible focApfl operon of Escherichia coll overlaps the Fnr (fumarate-nitrate reduction regulator)-dependent P6 promoter. The Fnr-binding site of P6 and the -35 hexamer sequence of P6A are shared between the promoters. Inactivation of P6A, through introduction of a -10 hexamer mutation, resulted in enhanced anaerobic induction of operon expression. The dependence on the ArcA (aerobic respiration control regulator) and Fnr transcription factors for anaerobic induction was tested for several focA-lacZ and pfl-lacZ gene fusions. Anaerobic induction became more dependent on Fnr in derivatives lacking a functional P6A promoter compared with wild-type constructs. Moreover, aerobic expression of the focA gene was reduced by the p6A mutation, as was the dependence on ArcA for anaerobic induction. Inactivation of P6 severely reduced Fnr-dependent anaerobic induction, in accord with previous findings. Transcription analyses demonstrated that a mutation in the -10 hexamer sequence of either P6A or P6 did not adversely affect transcription from the remaining promoter. Taken together, these results indicate that the P6A promoter moderates the Fnr-dependent activation of P6 through competition for RNA polymerase binding.
