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Abstract In recent decades, the Barents Sea has warmed more than twice as fast as the rest of the Arctic in winter, but the exact causes behind this amplified warming remain unclear. In this study, we quantify the wintertime Barents Sea warming (BSW, for near-surface air temperature) with an average linear trend of 1.74 °C decade −1 and an interdecadal change around 2003 based on a surface energy budget analysis using the ERA5 reanalysis dataset from 1979–2019. Our analysis suggests that the interdecadal change in the wintertime near-surface air temperature is dominated by enhanced clear-sky downward longwave radiation (CDLW) associated with increased total column water vapor. Furthermore, it is found that a mode of atmospheric variability over the North Atlantic region known as the Barents oscillation (BO) strongly contributed to the BSW with a stepwise jump in 2003. Since 2003, the BO turned into a strengthened and positive phase, characteristic of anomalous high pressure over the North Atlantic and South of the Barents Sea, which promoted two branches of heat and moisture transport from southern Greenland along the Norwegian Sea and from the Eurasian continent to the Barents Sea. This enhanced the water vapor convergence over the Barents Sea, resulting in BSW through enhanced CDLW. Our results highlight the atmospheric circulation related to the BO as an emerging driver of the wintertime BSW through enhanced meridional atmospheric heat and moisture transport over the North Atlantic Ocean. 

Toll/Toll-like receptors (TLRs) are key regulators of the innate immune system in both invertebrates and vertebrates. However, while mammalian TLRs directly recognize pathogen-associated molecular patterns, the insect Toll pathway is thought to be primarily activated by binding Spätzle cytokines that are processed from inactive precursors in response to microbial infection. Phylogenetic and structural data generated in this study supported earlier results showing that Toll9 members differ from other insect Tolls by clustering with the mammalian TLR4 group, which recognizes lipopolysaccharide (LPS) through interaction with myeloid differentiation-2 (MD-2)–like proteins. Functional experiments showed that BmToll9 from the silkmothBombyx morialso recognized LPS through interaction with two MD-2–like proteins, previously named BmEsr16 and BmPP, that we refer to in this study as BmMD-2A and BmMD-2B, respectively. A chimeric BmToll9–TLR4 receptor consisting of the BmToll9 ectodomain and mouse TLR4 transmembrane and Toll/interleukin-1 (TIR) domains also activated LPS-induced release of inflammatory factors in murine cells but only in the presence of BmMD-2A or BmMD-2B. Overall, our results indicate that BmToll9 is a pattern recognition receptor for LPS that shares conserved features with the mammalian TLR4–MD-2–LPS pathway. 

Abstract This study investigates the stratospheric response to Arctic sea ice loss and subsequent near-surface impacts by analyzing 200-member coupled experiments using the Whole Atmosphere Community Climate Model version 6 (WACCM6) with preindustrial, present-day, and future sea ice conditions specified following the protocol of the Polar Amplification Model Intercomparison Project. The stratospheric polar vortex weakens significantly in response to the prescribed sea ice loss, with a larger response to greater ice loss (i.e., future minus preindustrial) than to smaller ice loss (i.e., future minus present-day). Following the weakening of the stratospheric circulation in early boreal winter, the coupled stratosphere–troposphere response to ice loss strengthens in late winter and early spring, projecting onto a negative North Atlantic Oscillation–like pattern in the lower troposphere. To investigate whether the stratospheric response to sea ice loss and subsequent surface impacts depend on the background oceanic state, ensemble members are initialized by a combination of varying phases of Atlantic multidecadal variability (AMV) and interdecadal Pacific variability (IPV). Different AMV and IPV states combined, indeed, can modulate the stratosphere–troposphere responses to sea ice loss, particularly in the North Atlantic sector. Similar experiments with another climate model show that, although strong sea ice forcing also leads to tighter stratosphere–troposphere coupling than weak sea ice forcing, the timing of the response differs from that in WACCM6. Our findings suggest that Arctic sea ice loss can affect the stratospheric circulation and subsequent tropospheric variability on seasonal time scales, but modulation by the background oceanic state and model dependence need to be taken into account. Significance StatementThis study uses new-generation climate models to better understand the impacts of Arctic sea ice loss on the surface climate in the midlatitudes, including North America, Europe, and Siberia. We focus on the stratosphere–troposphere pathway, which involves the weakening of stratospheric winds and its downward coupling into the troposphere. Our results show that Arctic sea ice loss can affect the surface climate in the midlatitudes via the stratosphere–troposphere pathway, and highlight the modulations from background mean oceanic states as well as model dependence.