Bioregeneration of spent mercury bearing sulfur-impregnated activated carbon adsorbent.

Among various adsorbents studied, sulfur-impregnated activated carbon is one of the most promising adsorbents for mercury removal from flue gas. However, a large amount of spent activated carbons containing high content of mercury are generated after adsorption. To make the adsorption a more viable option, the regeneration and reuse of the spent activated carbon should be considered. The purpose of this study is to develop a novel technique for bioregeneration of sulfur-impregnated activated carbons after adsorption of mercury from flue gases by sulfur-oxidizing bacteria. The optimal operating parameters for this bioregeneration process were studied using central composite design (CCD) and response surface methodology (RSM). Results showed that the sulfur oxidation rate was increased with increasing activated carbon dosage. Furthermore, the increase of inoculum size only caused a slight increase of sulfur oxidation rate in the bioregeneration. The maximum mercury removal efficiency of more than 50% was obtained at 10% (w/v) activated carbon dosage and 20% (v/v) inoculum size. After the bioregeneration process, Brunauer-Emmett-Teller (BET) surface area and micropore volume of spent activated carbon increased due to the bio-oxidation of mercury bearing sulfur on the surface of activated carbons.

Combined Interactions of Plant Homeodomain and Chromodomain Regulate NuA4 Activity at DNA Double-Strand Breaks.

DNA double-strand breaks (DSBs) represent one of the most threatening lesions to the integrity of genomes. In yeast Saccharomyces cerevisiae, NuA4, a histone acetylation complex, is recruited to DSBs, wherein it acetylates histones H2A and H4, presumably relaxing the chromatin and allowing access to repair proteins. Two subunits of NuA4, Yng2 and Eaf3, can interact in vitro with methylated H3K4 and H3K36 via their plant homeodomain (PHD) and chromodomain. However, the roles of the two domains and how they interact in a combinatorial fashion are still poorly characterized. In this study, we generated mutations in the PHD and chromodomain that disrupt their interaction with methylated H3K4 and H3K36. We demonstrate that the combined mutations in both the PHD and chromodomain impair the NuA4 recruitment, reduce H4K12 acetylation at the DSB site, and confer sensitivity to bleomycin that induces DSBs. In addition, the double mutant cells are defective in DSB repair as judged by Southern blot and exhibit prolonged activation of phospho-S129 of H2A. Cells harboring the H3K4R, H3K4R, K36R, or set1Δ set2Δ mutant that disrupts H3K4 and H3K36 methylation also show very similar phenotypes to the PHD and chromodomain double mutant. Our results suggest that multivalent interactions between the PHD, chromodomain, and methylated H3K4 and H3K36 act in a combinatorial manner to recruit NuA4 and regulate the NuA4 activity at the DSB site.