RESUMEN
Electrochemically converting nitrate (NO3 -) into ammonia (NH3) has emerged as an alternative strategy for NH3 production and effluent treatment. Nevertheless, the electroreduction of dilute NO3 - is still challenging due to the competitive adsorption between various aqueous species and NO3 -, and unfavorable water dissociation providing *H. Herein, a new tandem strategy is proposed to boost the electrochemical nitrate reduction reaction (NO3RR) performance of Cu nanoparticles supported on single Fe atoms dispersed N-doped carbon (Cu@Fe1-NC) at dilute NO3 - concentrations (≤100 ppm NO3 --N). The optimized Cu@Fe1-NC presents a FENH3 of 97.7% at -0.4 V versus RHE, and a significant NH3 yield of 1953.9 mmol h-1 gCu -1 at 100 ppm NO3 --N, a record-high activity for dilute NO3RR. The metal/carbon heterojunctions in Cu@Fe1-NC enable a spontaneous electron transfer from Cu to carbon substrate, resulting in electron-deficient Cu. As a result, the electron-deficient Cu facilitates the adsorption of NO3 - compared with the pristine Cu. The adjacent atomic Fe sites efficiently promote water dissociation, providing abundant *H for the hydrogenation of *NOx e at Cu sites. The synergistic effects between Cu and single Fe atom sites simultaneously decrease the energy barrier for NO3 - adsorption and hydrogenation, thereby enhancing the overall activity of NO3 - reduction.
RESUMEN
LINC00116 encodes a microprotein first identified as Mitoregulin (MTLN), where it was reported to localize to the inner membrane of mitochondria to regulate fatty acid oxidation and oxidative phosphorylation. These initial discoveries were followed by reports with differing findings about its molecular functions and submitochondrial localization. To clarify the apparent discrepancies, we constructed multiple orthogonal methods of determining the localization of MTLN, including split GFP-based reporters that enable efficient and reliable topology analyses for microproteins. These methods unequivocally demonstrate MTLN primarily localizes to the outer membrane of mitochondria, where it interacts with enzymes of fatty acid metabolism including CPT1B and CYB5B. Loss of MTLN causes the accumulation of very long-chain fatty acids (VLCFAs), especially docosahexaenoic acid (DHA). Intriguingly, loss of MTLN protects mice against western diet/fructose-induced insulin-resistance, suggests a protective effect of VLCFAs in this context. MTLN thus serves as an attractive target to control the catabolism of VLCFAs.
RESUMEN
Chitin deacetylase (CDA) can hydrolyze the acetamido group of chitin polymers and its deacetylated derivatives to produce chitosan, an industrially important biopolymer. Compared with traditional chemical methods, biocatalysis by CDA is more environment-friendly and easy to control. However, most reported CDA-producing microbial strains show low CDA producing capabilities. Thus, the enhancement of CDA production has always been a challenge. In this study, we report co-culture fermentation to significantly promote the CDA production of Rhodococcus equi CGMCC14861 chitin deacetylase (ReCDA). Due to co-culture fermentation with Staphylococcus sp. MC7, ReCDA yield increased to 21.74 times that of pure culture of R. equi. Additionally, the enhancement was demonstrated to be cell-independent by adding cell-free extracts and the filtrate obtained by 10 kDa ultrafiltration of Staphylococcus sp. MC7. By preliminary characterization, we found extracellular, thermosensitive signal substances produced by Staphylococcus that were less than 10 kDa. We investigated the mechanism of promotion of ReCDA production by transcriptomic analysis. The data showed that 328 genes were upregulated and 1,258 genes were downregulated. The transcription level of the gene encoding ReCDA increased 2.3-fold. These findings provide new insights into the research of co-culture fermentation for the production of CDA and quorum sensing regulation.