Generation of surface active sites with tailormade structure is a promising way to enhance catalytic properties of inexpensive metal oxides, as a replacement to noble metals. In the abatement of NH 3 emissions through selective oxidation to N 2 , the nature of active sites over Cubased catalysts plays a decisive role in determining activity and avoiding formation of NO x from excessive oxidation. In the present work, CuO nanoclusters are homogeneously confined in small pore zeolitic SAPO-34 crystals by a Trojan Horse approach, i.e, through combined use of Cu 2+ containing complex and morpholine as structure-directing agents in the hydrothermal synthesis stage and a sequential Cu 2+ cation impregnation followed by calcination, is presented. Nitrogen activation and reoxidation treatment lead to the formation of encapsulated CuO@SAPO-34 structure that showed promoted activities and N 2 selectivity for NH 3 selective catalytic oxidation at relatively low temperatures (250 °C), with respect to catalysts obtained from ion-exchange or simple impregnation routes. The structure of catalytically active sites was unveiled to be Cu(II) superoxo species by a panoply of characterization techniques, including in situ Raman spectra, in situ DRIFT, as well as X-ray absorption spectroscopy. The catalytic activity at low temperatures (165−175 °C) was found to scale proportionally with the concentration of Cu(II) superoxo species measured by CO temperature-programmed reduction and O 2 temperatureprogrammed desorption. The reaction mechanism for ammonia catalytic oxidation on Cu(II) superoxo species has also been discussed on the basis of in situ IR and temperature-programmed surface reaction studies. The tailored synthesis and identification of active sites lay the basis for the understanding of the structure−catalysis relationship and future catalyst design for NH 3 elimination through selective oxidation.

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HighlightGene duplication has led to the existence of a large HAP gene family. In this study, three HAP genes were identified that regulate flowering in rice in addition to the previously reported Ghd8/OsHAP3H.

N-acyl homoserine lactones (AHLs) act as quorum sensing signals that regulate cell-density dependent behaviors in many gram-negative bacteria, in particular those important for plant-microbe interactions. AHLs can also be recognized by plants, and this may influence their interactions with bacteria. Here we tested whether the exposure to AHLs affects the nodule-forming symbiosis between legume hosts and rhizobia. We treated roots of the model legume, Medicago truncatula, with a range of AHLs either from its specific symbiont, Sinorhizobium meliloti, or from the potential pathogens, Pseudomonas aeruginosa and Agrobacterium vitis. We found increased numbers of nodules formed on root systems treated with the S. meliloti-specific AHL, 3-oxo-C14-homoserine lactone, at a concentration of 1 μM, while the other AHLs did not result in significant changes to nodule numbers. We did not find any evidence for altered nodule invasion by the rhizobia. Quantification of flavonoids that could act as nod gene inducers in S. meliloti did not show any correlation with increased nodule numbers. The effects of AHLs were specific for an increase in nodule numbers, but not lateral root numbers or root length. Increased nodule numbers following 3-oxo-C14-homoserine lactone treatment were under control of autoregulation of nodulation and were still observed in the autoregulation mutant, sunn4 (super numeric nodules4). However, increases in nodule numbers by 3-oxo-C14-homoserine lactone were not found in the ethylene-insensitive sickle mutant. A comparison between M. truncatula with M. sativa (alfalfa) and Trifolium repens (white clover) showed that the observed effects of AHLs on nodule numbers were specific to M. truncatula, despite M. sativa nodulating with the same symbiont. We conclude that plant perception of the S. meliloti-specific 3-oxo-C14-homoserine lactone influences nodule numbers in M. truncatula via an ethylene-dependent, but autoregulation-independent mechanism.