Anaerobic spp. degrade sulfoquinovose via a bifurcated 6-deoxy-6-sulfofructose transketolase/transaldolase pathway to both C- and C-sulfonate intermediates.

Plant-produced sulfoquinovose (SQ, 6-deoxy-6-sulfoglucose) is one of the most abundant sulfur-containing compounds in nature and its bacterial degradation plays an important role in the biogeochemical sulfur and carbon cycles and in all habitats where SQ is produced and degraded, particularly in gut microbiomes. Here, we report the enrichment and characterization of a strictly anaerobic SQ-degrading bacterial consortium that produces the C-sulfonate isethionate (ISE) as the major product but also the C-sulfonate 2,3-dihydroxypropanesulfonate (DHPS), with concomitant production of acetate and hydrogen (H). In the second step, the ISE was degraded completely to hydrogen sulfide (HS) when an additional electron donor (external H) was supplied to the consortium.

Protein kinase 2 of the giant sarcomeric protein UNC-89 regulates mitochondrial morphology and function.

UNC-89 is a giant sarcomeric M-line protein required for sarcomere organization and optimal muscle function. UNC-89 contains two protein kinase domains, PK1 and PK2, separated by an elastic region. Here we show that PK2 is a canonical kinase expected to be catalytically active.

Metformin hydrolase is a recently evolved nickel-dependent heteromeric ureohydrolase.

The anti-diabetic drug metformin is one of the most widely prescribed medicines in the world. Together with its degradation product guanylurea, it is a major pharmaceutical pollutant in wastewater treatment plants and surface waters. An operon comprising two genes of the ureohydrolase family in Pseudomonas and Aminobacter species has recently been implicated in metformin degradation.

Liver receptor homolog-1 (NR5A2) orchestrates hepatic inflammation and TNF-induced cell death.

The nuclear receptor liver receptor homolog-1 (LRH-1) has been shown to promote apoptosis resistance in various tissues and disease contexts; however, its role in liver cell death remains unexplored. Hepatocyte-specific deletion of LRH-1 causes mild steatosis and inflammation but unexpectedly shields female mice from tumor necrosis factor (TNF)-induced hepatocyte apoptosis and associated hepatitis. LRH-1-deficient hepatocytes show markedly attenuated estrogen receptor alpha and elevated nuclear factor κB (NF-κB) activity, while LRH-1 overexpression inhibits NF-κB activity.

AMP-dependent phosphite dehydrogenase, a phosphorylating enzyme in dissimilatory phosphite oxidation.

Oxidation of phosphite (HPO) to phosphate (HPO) releases electrons at a very low redox potential (E= -690 mV) which renders phosphite an excellent electron donor for microbial energy metabolism. To date, two pure cultures of strictly anaerobic bacteria have been isolated that run their energy metabolism on the basis of phosphite oxidation, the Gram-negative (DSM 13687) and the Gram-positive (DSM 112739). Here, we describe the key enzyme for dissimilatory phosphite oxidation in these bacteria.