Characteristics, distribution and morphogenesis of subtidal microbial systems in Shark Bay, Australia

The distribution, nature and extent of microbial deposits in Hamelin Pool, Shark Bay have been investigated and mapped with emphasis on the occurrence, external morphologies, internal fabrics, constructional mechanisms, microbial communities, growth rates and sediment associations in the intertidal and previously little researched subtidal zone. Detailed georeferenced substrate mapping revealed extensive subtidal microbial deposits occupying approximately 300 km2 of the total Holocene 1400 km2 area of Hamelin Pool. The Microbial Pavement covers 227 km2 of the subtidal substrate that together with columnar structures reveals a subtidal microbial habitat which occupies an area 10 times larger than the area of the intertidal deposits. Microbial carbonate is composed of aragonite (80–98%) that reveals high positive values of δ13C (+4.46 to +5.88) and δ18O (+3.06 to +3.88) as a characteristic of the highly evaporative environment with extensive microbial activity. Oldest dated heads are 1915 and 1680 14C years BP, and the overall system was deposited in two stages; the first between 2000 and 1200 and the last from 900 years BP to the present. Slow growth rates vary from less than 0.1 mm/year to 0.5 mm/year. Different internal fabrics were constructed according to their position in relation to the littoral zone by distinct microbial communities, and lateral fabric relations have been established.Evidence of shallowing upward fabric sequences of microbial origin reflects relative falling sea levels during the late Holocene and is likely useful in ancient environmental interpretation. A sequence of events and mechanisms are described emphasizing differences between the stromatolitic, thrombolitic and cryptomicrobial deposits in Shark Bay. The new substrate map and depositional history for this distinctive and peculiar microbial habitat establish the significance of subtidal structures and emphasize the geoscientific importance of Hamelin Pool, especially with respect to early life studies and ancient analogues for understanding microbial activity, deposit characteristics, fenestral fabrics and distribution

Confined molecular liquids : how close to the bulk properties

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Immunity-related GTPase induces lipophagy to prevent excess hepatic lipid accumulation.

BACKGROUND & AIMS: Currently, only a few genetic variants explain the heritability of fatty liver disease. Quantitative trait loci (QTL) analysis of mouse strains has identified the susceptibility locus Ltg/NZO (liver triglycerides from New Zealand obese [NZO] alleles) on chromosome 18 as associating with increased hepatic triglycerides. Herein, we aimed to identify genomic variants responsible for this association.; METHODS: Recombinant congenic mice carrying 5.3 Mbp of Ltg/NZO were fed a high-fat diet and characterized for liver fat. Bioinformatic analysis, mRNA profiles and electrophoretic mobility shift assays were performed to identify genes responsible for the Ltg/NZO phenotype. Candidate genes were manipulated invivo by injecting specific microRNAs into C57BL/6 mice. Pulldown coupled with mass spectrometry-based proteomics and immunoprecipitation were performed to identify interaction partners of IFGGA2.; RESULTS: Through positional cloning, we identified 2 immunity-related GTPases (Ifgga2, Ifgga4) that prevent hepatic lipid storage. Expression of both murine genes and the human orthologue IRGM was significantly lower in fatty livers. Accordingly, liver-specific suppression of either Ifgga2 or Ifgga4 led to a 3-4-fold greater increase in hepatic fat content. In the liver of low-fat diet-fed mice, IFGGA2 localized to endosomes/lysosomes, while on a high-fat diet it associated with lipid droplets. Pulldown experiments and proteomics identified the lipase ATGL as a binding partner of IFGGA2 which was confirmed by co-immunoprecipitation. Both proteins partially co-localized with the autophagic marker LC3B. Ifgga2 suppression in hepatocytes reduced the amount of LC3B-II, whereas overexpression of Ifgga2 increased the association of LC3B with lipid droplets and decreased triglyceride storage.; CONCLUSION: IFGGA2 interacts with ATGL and protects against hepatic steatosis, most likely by enhancing the binding of LC3B to lipid droplets.; LAY SUMMARY: The genetic basis of non-alcoholic fatty liver disease remains incompletely defined. Herein, we identified members of the immunity-related GTPase family in mice and humans that act as regulators of hepatic fat accumulation, with links to autophagy. Overexpression of the gene Ifgga2 was shown to reduce hepatic lipid storage and could be a therapeutic target for the treatment of fatty liver disease. Copyright © 2020 European Association for the Study of the Liver. All rights reserved