Shallow seismicity and the classification of structures in the Lau back-arc basin

Back‐arc basins open in response to subduction processes, which cause extension in the upper plate, usually along trench‐parallel spreading axes. However, global seismic databases reveal that the majority of seismic events in the Lau Basin occur along transcurrent (strike‐slip) rather than extensional faults. To better characterize active deformation in this region we compared Centroid Moment Tensors (CMTs), calculated for large (Mw >5), shallow (<30 km) seismic events to the orientations of seafloor lineaments mapped throughout the Lau Basin. Ship‐based multibeam was combined with vertical gravity gradient data to provide comprehensive coverage to create the lineament map. By comparing the possible focal planes of the CMTs to the orientations of the lineaments, the most likely fault plane solutions were selected, thus classifying the faults and establishing the nature of the highly variable stress regimes in the basin. We resolved the strike, dip and dip direction of 308 faults, and classified 258 additional structures by fault type. The analysis highlights a stress regime that is dominated by a combination of left‐lateral and right‐lateral strike‐slip faults, large‐scale transcurrent motion along rigid crustal‐scale fault zones, and non‐rigid diffuse deformation along pre‐existing seafloor structures, with extension mainly limited to the tips of propagating rifts and spreading centers. By resolving many of the uncertain motions on the mapped lineaments of the Lau Basin, the CMT analysis addresses a number of questions concerning basin‐scale stress regimes and microplate development, complementing GPS measurements and providing a more complete picture of the complexities of back‐arc basin development

Microbial regulation of hexokinase 2 links mitochondrial metabolism and cell death in colitis.

Hexokinases (HK) catalyze the first step of glycolysis limiting its pace. HK2 is highly expressed in gut epithelium, contributes to immune responses, and is upregulated during inflammation. We examined the microbial regulation of HK2 and its impact on inflammation using mice lacking HK2 in intestinal epithelial cells (Hk2ΔIEC). Hk2ΔIEC mice were less susceptible to acute colitis. Analyzing the epithelial transcriptome from Hk2ΔIEC mice during colitis and using HK2-deficient intestinal organoids and Caco-2 cells revealed reduced mitochondrial respiration and epithelial cell death in the absence of HK2. The microbiota strongly regulated HK2 expression and activity. The microbially derived short-chain fatty acid (SCFA) butyrate repressed HK2 expression via histone deacetylase 8 (HDAC8) and reduced mitochondrial respiration in wild-type but not in HK2-deficient Caco-2 cells. Butyrate supplementation protected wild-type but not Hk2ΔIEC mice from colitis. Our findings define a mechanism how butyrate promotes intestinal homeostasis and suggest targeted HK2-inhibition as therapeutic avenue for inflammation