Over-expression of an electron transport protein OmcS provides sufficient NADH for d-lactate production in cyanobacterium

Background An efficient supply of reducing equivalent is essential for chemicals production by engineered microbes. In phototrophic microbes, the NADPH generated from photosynthesis is the dominant form of reducing equivalent. However, most dehydrogenases prefer to utilize NADH as a cofactor. Thus, sufficient NADH supply is crucial to produce dehydrogenase-derived chemicals in cyanobacteria. Photosynthetic electron is the sole energy source and excess electrons are wasted in the light reactions of photosynthesis. Results Here we propose a novel strategy to direct the electrons to generate more ATP from light reactions to provide sufficient NADH for lactate production. To this end, we introduced an electron transport protein-encoding gene omcS into cyanobacterium Synechococcus elongatus UTEX 2973 and demonstrated that the introduced OmcS directs excess electrons from plastoquinone (PQ) to photosystem I (PSI) to stimulate cyclic electron transfer (CET). As a result, an approximately 30% increased intracellular ATP, 60% increased intracellular NADH concentrations and up to 60% increased biomass production with fourfold increased d-lactate production were achieved. Comparative transcriptome analysis showed upregulation of proteins involved in linear electron transfer (LET), CET, and downregulation of proteins involved in respiratory electron transfer (RET), giving hints to understand the increased levels of ATP and NADH. Conclusions This strategy provides a novel orthologous way to improve photosynthesis via enhancing CET and supply sufficient NADH for the photosynthetic production of chemicals.

Redox induced S-S bond cleavage of 2,2′-dithiobisbenzothiazole - leading to a [2Ru-2S] core analogous to [2Fe-2S] Cluster

Facile reduction of 2,2-dithiobisbenzothiazole by the mediation of metal-to-ligand charge transfer or by internal reducing equivalent was demonstrated. It led to varying binding modes of thiolates (1, 2, ) in...

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

The generation of reducing equivalent NADPH via glucose-6-phosphate dehydrogenase (G6PD) is critical for the maintenance of redox homeostasis and reductive biosynthesis in cells. NADPH also plays key roles in cellular processes mediated by redox signaling. Insufficient G6PD activity predisposes cells to growth retardation and demise. Severely lacking G6PD impairs embryonic development and delays organismal growth. Altered G6PD activity is associated with pathophysiology, such as autophagy, insulin resistance, infection, inflammation, as well as diabetes and hypertension. Aberrant activation of G6PD leads to enhanced cell proliferation and adaptation in many types of cancers. The present review aims to update the existing knowledge concerning G6PD and emphasizes how G6PD modulates redox signaling and affects cell survival and demise, particularly in diseases such as cancer. Exploiting G6PD as a potential drug target against cancer is also discussed.

Plugging in microbial metabolism for industrial applications

The ability of electric microbes to electrically interact with electrodes is opening up a number of possibilities with industrial applications. Microbes are able to utilise the electrode as an electron source to reduce CO2 for the production of organic compounds directly or produce H2 as a reducing equivalent for partner microbes for the production of commodity chemicals. Electrodes can also allow redox unbalanced fermentation processes to occur through the addition or subtraction of reducing equivalents that remove bottle necks in these pathways. Electrodes are also providing a physical refuge for electric microbes to maintain anaerobic fermenter stability. It can be expected that the role for electric microbes will continued to be expanded as part of industrial applications in the future.