Food of Lake Trout in Lake Superior

Stomachs were examined from 1,492 lake trout and 83 siscowets collected from Lake Superior. Data are given on the food of lake trout of legal size (17 inches or longer) by year, season, and depth of water, and on the relation between food and size among smaller lake trout.Fish contributed 96.7 to 99.9 per cent of the total volume of food in the annual samples. Ciscoes (Coregonus spp.) were most common (52.2 to 87.5 per cent of the volume) in 1950 to 1953 and American smelt ranked first (65.6 per cent of the volume) in 1963. Cottids were in 8.9 to 12.3 per cent of the stomachs in 1950 to 1953 but in only 4.3 per cent in 1963. Insects ranked second to fish in occurrence (9.6 per cent for the combined samples) and crustaceans followed at 3.9 per cent.The greatest seasonal changes in the food of lake trout were among fish caught at 35 fathoms and shallower. The occurrence of Coregonus increased from 34.6 per cent in February‐March to 71.1 per cent in October‐December. Smelt were in 76.9 per cent of the stomachs in February‐March but in only 2.2 per cent in October‐December. Cottids, Mysis relicta, and insects were most common in the July‐September collections.Lake trout taken at depths greater than 35 fathoms had eaten a higher percentage of Cottidae and Coregonus than had those captured in shallower water. Smelt, ninespine sticklebacks, Mysis, and insects were more frequent in stomachs of lake trout from less than 35 fathoms.Crustaceans comprised more than 70 per cent of the total volume of food for 4.0‐ to 7.9‐inch lake trout but their importance decreased as the lake trout grew larger. Pontoporeia affinis was the most common in the stomachs of 4.0‐ to 6.9‐inch lake trout and Mysis held first rank at 7.0 to 12.9 inches. Ostracods were important only to 4.0‐ to 4.9‐inch lake trout. As the lake trout became larger, the importance of fish grew from 4.4‐per cent occurrence at 5.0 to 5.9 inches to 93.9 per cent at 16.0 to 16.9 inches. Smelt were most commonly eaten by undersize (less than 17 inches) lake trout.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141203/1/tafs0169.pd

Rapid submarine melting driven by subglacial discharge, LeConte Glacier, Alaska

We show that subglacial freshwater discharge is the principal process driving high rates of submarine melting at tidewater glaciers.We show that subglacial freshwater discharge is the principal process driving high rates of submarine melting at tidewater glaciers. This buoyant discharge draws in warm seawater, entraining it in a turbulent upwelling flow along the submarine face that melts glacier ice. To capture the effects of subglacial discharge on submarine melting, we conducted 4 days of hydrographic transects during late summer 2012 at LeConte Glacier, Alaska. A major rainstorm allowed us to document the influence of large changes in subglacial discharge. We found strong submarine melt fluxes that increased from 9.1 ± 1.0 to 16.8 ± 1.3 m d1 (ice face equivalent frontal ablation) as a result of the rainstorm. With projected continued global warming and increased glacial runoff, our results highlight the direct impact that increases in subglacial discharge will have on tidewater outlet systems. These effects must be considered when modeling glacier response to future warming and increased runoff.This work was funded by a grant from the Gordon and Betty Moore Foundation grant GBMF2627 to M.T. and M.F. Additional support for J.M.A. was provided by NSF grant ANT0944193. The manuscript was greatly improved by comments from two anonymous re- viewers. We thank Captain Scott Hursey for vessel support and safely navi- gating us through icebergs. J. Elliot provided the orthorectified World View image in Figure 1c.Ye

SLO-2 Is Cytoprotective and Contributes to Mitochondrial Potassium Transport

Mitochondrial potassium channels are important mediators of cell protection against stress. The mitochondrial large-conductance “big” K+ channel (mBK) mediates the evolutionarily-conserved process of anesthetic preconditioning (APC), wherein exposure to volatile anesthetics initiates protection against ischemic injury. Despite the role of the mBK in cardioprotection, the molecular identity of the channel remains unknown. We investigated the attributes of the mBK using C. elegans and mouse genetic models coupled with measurements of mitochondrial K+ transport and APC. The canonical Ca2+-activated BK (or “maxi-K”) channel SLO1 was dispensable for both mitochondrial K+ transport and APC in both organisms. Instead, we found that the related but physiologically-distinct K+ channel SLO2 was required, and that SLO2-dependent mitochondrial K+ transport was triggered directly by volatile anesthetics. In addition, a SLO2 channel activator mimicked the protective effects of volatile anesthetics. These findings suggest that SLO2 contributes to protection from hypoxic injury by increasing the permeability of the mitochondrial inner membrane to K+