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Marine phytoplankton have a crucial role in the modulation of marine-based food webs.sup.1, fishery yields.sup.2 and the global drawdown of atmospheric carbon dioxide.sup.3. However, owing to sparse measurements before satellite monitoring in the twenty-first century, the long-term response of planktonic stocks to climate forcing is unknown. Here, using a continuous, multi-century record of subarctic Atlantic marine productivity, we show that a marked 10 [plus or minus] 7% decline in net primary productivity has occurred across this highly productive ocean basin over the past two centuries. We support this conclusion by the application of a marine-productivity proxy, established using the signal of the planktonic-derived aerosol methanesulfonic acid, which is commonly identified across an array of Greenlandic ice cores. Using contemporaneous satellite-era observations, we demonstrate the use of this signal as a robust and high-resolution proxy for past variations in spatially integrated marine productivity. We show that the initiation of declining subarctic Atlantic productivity broadly coincides with the onset of Arctic surface warming.sup.4, and that productivity strongly covaries with regional sea-surface temperatures and basin-wide gyre circulation strength over recent decades. Taken together, our results suggest that the decline in industrial-era productivity may be evidence of the predicted.sup.5 collapse of northern Atlantic planktonic stocks in response to a weakened Atlantic Meridional Overturning Circulation.sup.6-8. Continued weakening of this Atlantic Meridional Overturning Circulation, as projected for the twenty-first century.sup.9,10, may therefore result in further productivity declines across this globally relevant region. A continuous, multi-century record of subarctic Atlantic marine productivity shows that a marked decline in net primary productivity has occurred across the subarctic Atlantic basin over the past two centuries., Author(s): Matthew B. Osman [sup.1] , Sarah B. Das [sup.2] , Luke D. Trusel [sup.3] , Matthew J. Evans [sup.4] , Hubertus Fischer [sup.5] , Mackenzie M. Grieman [sup.6] , [...]

The Greenland ice sheet (GrIS) is a growing contributor to global sea-level rise.sup.1, with recent ice mass loss dominated by surface meltwater runoff.sup.2,3. Satellite observations reveal positive trends in GrIS surface melt extent.sup.4, but melt variability, intensity and runoff remain uncertain before the satellite era. Here we present the first continuous, multi-century and observationally constrained record of GrIS surface melt intensity and runoff, revealing that the magnitude of recent GrIS melting is exceptional over at least the last 350 years. We develop this record through stratigraphic analysis of central west Greenland ice cores, and demonstrate that measurements of refrozen melt layers in percolation zone ice cores can be used to quantifiably, and reproducibly, reconstruct past melt rates. We show significant (P < 0.01) and spatially extensive correlations between these ice-core-derived melt records and modelled melt rates.sup.5,6 and satellite-derived melt duration.sup.4 across Greenland more broadly, enabling the reconstruction of past ice-sheet-scale surface melt intensity and runoff. We find that the initiation of increases in GrIS melting closely follow the onset of industrial-era Arctic warming in the mid-1800s, but that the magnitude of GrIS melting has only recently emerged beyond the range of natural variability. Owing to a nonlinear response of surface melting to increasing summer air temperatures, continued atmospheric warming will lead to rapid increases in GrIS runoff and sea-level contributions.Ice-core-derived melt records reveal that atmospheric warming has recently intensified Greenland ice-sheet surface melt and runoff to levels that are exceptional over at least the last 350 years., Author(s): Luke D. Trusel [sup.1] [sup.2] , Sarah B. Das [sup.2] , Matthew B. Osman [sup.3] , Matthew J. Evans [sup.4] , Ben E. Smith [sup.5] , Xavier Fettweis [sup.6] [...]

BackgroundSalmonella enterica serovar Typhimurium (S. Typhimurium) is a Gram-negative pathogen that must successfully adapt to the broad fluctuations in the concentration of dissolved dioxygen encountered in the host. In Escherichia coli, ArcA (Aerobic Respiratory Control) helps the cells to sense and respond to the presence of dioxygen. The global role of ArcA in E. coli is well characterized; however, little is known about its role in anaerobically grown S. Typhimurium.ResultsWe compared the transcriptional profiles of the virulent wild-type (WT) strain (ATCC 14028s) and its isogenic arcA mutant grown under anaerobic conditions. We found that ArcA directly or indirectly regulates 392 genes (8.5% of the genome); of these, 138 genes are poorly characterized. Regulation by ArcA in S. Typhimurium is similar, but distinct from that in E. coli. Thus, genes/operons involved in core metabolic pathways (e.g., succinyl-CoA, fatty acid degradation, cytochrome oxidase complexes, flagellar biosynthesis, motility, and chemotaxis) were regulated similarly in the two organisms. However, genes/operons present in both organisms, but regulated differently by ArcA in S. Typhimurium included those coding for ethanolamine utilization, lactate transport and metabolism, and succinate dehydrogenases. Salmonella-specific genes/operons regulated by ArcA included those required for propanediol utilization, flagellar genes (mcpAC, cheV), Gifsy-1 prophage genes, and three SPI-3 genes (mgtBC, slsA, STM3784). In agreement with our microarray data, the arcA mutant was non-motile, lacked flagella, and was as virulent in mice as the WT. Additionally, we identified a set of 120 genes whose regulation was shared with the anaerobic redox regulator, Fnr.Conclusion(s)We have identified the ArcA regulon in anaerobically grown S. Typhimurium. Our results demonstrated that in S. Typhimurium, ArcA serves as a transcriptional regulator coordinating cellular metabolism, flagella biosynthesis, and motility. Furthermore, ArcA and Fnr share in the regulation of 120 S. Typhimurium genes.

The multi-step process of hepatitis C virus (HCV) entry is facilitated by various host factors, including epidermal growth factor receptor (EGFR) and the tight junction proteins claudin-1 (CLDN1) and occludin (OCLN), which are thought to function at later stages of the HCV entry process. Using single particle imaging of HCV infection of polarized hepatoma spheroids, we observed that EGFR performs multiple functions in HCV entry, both phosphorylation-dependent and -independent. We previously observed, and in this study confirmed, that EGFR is not required for HCV migration to the tight junction. EGFR is required for the recruitment of clathrin to HCV in a phosphorylation-independent manner. EGFR phosphorylation is required for virion internalization at a stage following the recruitment of clathrin. HCV entry activates the RAF-MEK-ERK signaling pathway downstream of EGFR phosphorylation. This signaling pathway regulates the sorting and maturation of internalized HCV into APPL1- and EEA1-associated early endosomes, which form the site of virion uncoating. The tight junction proteins, CLDN1 and OCLN, function at two distinct stages of HCV entry. Despite its appreciated function as a "late receptor" in HCV entry, CLDN1 is required for efficient HCV virion accumulation at the tight junction. Huh-7.5 cells lacking CLDN1 accumulate HCV virions primarily at the initial basolateral surface. OCLN is required for the late stages of virion internalization. This study produced further insight into the unusually complex HCV endocytic process. Author summary: Hepatitis C virus (HCV) is a hepatotropic RNA virus. An estimated 58 million people are chronically infected with HCV, while HCV-associated hepatocellular carcinoma and cirrhosis accounted for 290, 000 deaths in 2019. HCV entry into hepatocytes is highly complex with distinct stages and multiple host cofactors. Perturbing the interaction of HCV with entry host factors is potential strategy for therapeutic and vaccine-based anti-HCV approaches. However, the precise functions of most of the host factors in HCV entry are not fully appreciated. Moreover, studies of entry using polarized cell culture that physiologically resembles hepatocytes in vivo are limited. In this paper, we evaluate the roles of three entry factors in polarized hepatoma spheroids: epidermal growth factor receptor (EGFR) and tight junction proteins claudin-1 (CLDN1) and occludin (OCLN). We observe that EGFR performs multiple functions to regulate HCV internalization and trafficking to endosomes. The process involves EGFR phosphorylation-dependent and -independent roles and downstream RAF-MEK-ERK signaling pathway. We also show that CLDN1 and OCLN, despite both localizing at the tight junction, function at two distinct stages of HCV entry. CLDN1 is required for the accumulation of HCV virions at the tight junction from the basolateral membrane, while OCLN regulates HCV internalization. These findings provide insights into the mechanism of HCV entry and highlight potential interventional strategies. [ABSTRACT FROM AUTHOR]