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The northern hemisphere experienced an abrupt cold event ~ 8200 years ago (the 8.2 ka event) that was triggered by the release of meltwater into the Labrador Sea, and resulting in a weakening of the poleward oceanic heat transport. Although this event has been considered a possible analogue for future ocean circulation changes due to the projected Greenland Ice Sheet (GIS) melting, large uncertainties in the amount and rate of freshwater released during the 8.2 ka event make such a comparison difficult. In this study, we compare sea surface temperatures and oxygen isotope ratios from 28 isotope-enabled model simulations with 35 paleoproxy records to constrain the meltwater released during the 8.2 ka event. Our results suggest that a combination of 5.3 m of meltwater in sea level rise equivalent (SLR) released over a thousand years, with a short intensification over ~ 130 years (an additional 2.2 m of equivalent SLR) due to routing of the Canadian river discharge, best reproduces the proxy anomalies. Our estimate is of the same order of magnitude as projected future GIS melting rates under the high emission scenario RCP8.5.

Rapid changes in ocean circulation and climate have been observed in marine-sediment and ice cores over the last glacial period and deglaciation, highlighting the non-linear character of the climate system and underlining the possibility of rapid climate shifts in response to anthropogenic greenhouse gas forcing. To date, these rapid changes in climate and ocean circulation are still not fully explained. One obstacle hindering progress in our understanding of the interactions between past ocean circulation and climate changes is the difficulty of accurately dating marine cores. Here, we present a set of 92 marine sediment cores from the Atlantic Ocean for which we have established age-depth models that are consistent with the Greenland GICC05 ice core chronology, and computed the associated dating uncertainties, using a new deposition modeling technique. This is the first set of consistently dated marine sediment cores enabling paleoclimate scientists to evaluate leads/lags between circulation and climate changes over vast regions of the Atlantic Ocean. Moreover, this data set is of direct use in paleoclimate modeling studies.

Varying levels of boreal summer insolation and associated Earth system feedbacks led to differing climate and ice-sheet states during late-Quaternary interglaciations. In particular, Marine Isotope Stage (MIS) 11 was an exceptionally long interglaciation and potentially had a global mean sea level 6 to 13 metres above the present level around 410,000 to 400,000 years ago, implying substantial mass loss from the Greenland ice sheet (GIS). There are, however, no model simulations and only limited proxy data to constrain the magnitude of the GIS response to climate change during this 'super interglacial', thus confounding efforts to assess climate/ice-sheet threshold behaviour and associated sea-level rise. Here we show that the south GIS was drastically smaller during MIS 11 than it is now, with only a small residual ice dome over southernmost Greenland. We use the strontium-neodymium-lead isotopic composition of proglacial sediment discharged from south Greenland to constrain the provenance of terrigenous silt deposited on the Eirik Drift, a sedimentary deposit off the south Greenland margin. We identify a major reduction in sediment input derived from south Greenland's Precambrian bedrock terranes, probably reflecting the cessation of subglacial erosion and sediment transport as a result of near-complete deglaciation of south Greenland. Comparison with ice-sheet configurations from numerical models suggests that the GIS lost about 4.5 to 6 metres of sea-level-equivalent volume during MIS 11. This is evidence for late-Quaternary GIS collapse after it crossed a climate/ice-sheet stability threshold that may have been no more than several degrees above pre-industrial temperatures.

The KCNH voltage-dependent potassium channels (ether-à-go-go, EAG; EAG-related gene, ERG; EAG-like channels, ELK) are important regulators of cellular excitability and have key roles in diseases such as cardiac long QT syndrome type 2 (LQT2), epilepsy, schizophrenia and cancer. The intracellular domains of KCNH channels are structurally distinct from other voltage-gated channels. The amino-terminal region contains an eag domain, which is composed of a Per-Arnt-Sim (PAS) domain and a PAS-cap domain, whereas the carboxy-terminal region contains a cyclic nucleotide-binding homology domain (CNBHD), which is connected to the pore through a C-linker domain. Many disease-causing mutations localize to these specialized intracellular domains, which underlie the unique gating and regulation of KCNH channels. It has been suggested that the eag domain may regulate the channel by interacting with either the S4-S5 linker or the CNBHD. Here we present a 2 Å resolution crystal structure of the eag domain-CNBHD complex of the mouse EAG1 (also known as KCNH1) channel. It displays extensive interactions between the eag domain and the CNBHD, indicating that the regulatory mechanism of the eag domain primarily involves the CNBHD. Notably, the structure reveals that a number of LQT2 mutations at homologous positions in human ERG, in addition to cancer-associated mutations in EAG channels, localize to the eag domain-CNBHD interface. Furthermore, mutations at the interface produced marked effects on channel gating, demonstrating the important physiological role of the eag domain-CNBHD interaction. Our structure of the eag domain-CNBHD complex of mouse EAG1 provides unique insights into the physiological and pathophysiological mechanisms of KCNH channels.

According to the Milankovitch theory, changes in summer insolation in the high-latitude Northern Hemisphere caused glacial cycles through their impact on ice-sheet mass balance. Statistical analyses of long climate records supported this theory, but they also posed a substantial challenge by showing that changes in Southern Hemisphere climate were in phase with or led those in the north. Although an orbitally forced Northern Hemisphere signal may have been transmitted to the Southern Hemisphere, insolation forcing can also directly influence local Southern Hemisphere climate, potentially intensified by sea-ice feedback, suggesting that the hemispheres may have responded independently to different aspects of orbital forcing. Signal processing of climate records cannot distinguish between these conditions, however, because the proposed insolation forcings share essentially identical variability. Here we use transient simulations with a coupled atmosphere-ocean general circulation model to identify the impacts of forcing from changes in orbits, atmospheric CO(2) concentration, ice sheets and the Atlantic meridional overturning circulation (AMOC) on hemispheric temperatures during the first half of the last deglaciation (22-14.3 kyr BP). Although based on a single model, our transient simulation with only orbital changes supports the Milankovitch theory in showing that the last deglaciation was initiated by rising insolation during spring and summer in the mid-latitude to high-latitude Northern Hemisphere and by terrestrial snow-albedo feedback. The simulation with all forcings best reproduces the timing and magnitude of surface temperature evolution in the Southern Hemisphere in deglacial proxy records. AMOC changes associated with an orbitally induced retreat of Northern Hemisphere ice sheets is the most plausible explanation for the early Southern Hemisphere deglacial warming and its lead over Northern Hemisphere temperature; the ensuing rise in atmospheric CO(2) concentration provided the critical feedback on global deglaciation.

The KCNH family of ion channels, comprising ether-à-go-go (EAG), EAG-related gene (ERG), and EAG-like (ELK) K(+)-channel subfamilies, is crucial for repolarization of the cardiac action potential, regulation of neuronal excitability and proliferation of tumour cells. The carboxy-terminal region of KCNH channels contains a cyclic-nucleotide-binding homology domain (CNBHD) and C-linker that couples the CNBHD to the pore. The C-linker/CNBHD is essential for proper function and trafficking of ion channels in the KCNH family. However, despite the importance of the C-linker/CNBHD for the function of KCNH channels, the structural basis of ion-channel regulation by the C-linker/CNBHD is unknown. Here we report the crystal structure of the C-linker/CNBHD of zebrafish ELK channels at 2.2-Å resolution. Although the overall structure of the C-linker/CNBHD of ELK channels is similar to the cyclic-nucleotide-binding domain (CNBD) structure of the related hyperpolarization-activated cyclic-nucleotide-modulated (HCN) channels, there are marked differences. Unlike the CNBD of HCN, the CNBHD of ELK displays a negatively charged electrostatic profile that explains the lack of binding and regulation of KCNH channels by cyclic nucleotides. Instead of cyclic nucleotide, the binding pocket is occupied by a short β-strand. Mutations of the β-strand shift the voltage dependence of activation to more depolarized voltages, implicating the β-strand as an intrinsic ligand for the CNBHD of ELK channels. In both ELK and HCN channels the C-linker is the site of virtually all of the intersubunit interactions in the C-terminal region. However, in the zebrafish ELK structure there is a reorientation in the C-linker so that the subunits form dimers instead of tetramers, as observed in HCN channels. These results provide a structural framework for understanding the regulation of ion channels in the KCNH family by the C-linker/CNBHD and may guide the design of specific drugs.