Description: Frank, K. T., Leggett, W. C., Petrie, B., Fisher, J. A. D., Shackell, N. L., and Taggart, C. T. 2013. Pelagic fish outbreak in the Northwest Atlantic - reality or illusion? – ICES Journal of Marine Science, 70: . The collapse of Northwest Atlantic groundfish in the early 1990s yielded a "natural experiment" within which to explore responses of ecosystems to a major perturbation. The "Pelagic Outburst" hypothesis was developed to explain an up to 900% increase in the abundance of small-bodied forage fishes and macroinvertebrates following this collapse and a subsequent trophic cascade extending across four trophic levels. Recently, this theory has been challenged and an alternative "Suprabenthic Habitat Occupation" (SHO) hypothesis has been advanced; it proposes the prey outburst associated with the forage fish component was an illusion created by changes in the vertical distribution of small pelagic fishes after the cod collapse in favour of a more bottom-oriented distribution that increased their vulnerability to bottom trawls. We evaluated the SHO hypothesis as it applied to the relationship between changes in the biomass of cod and the vertical distribution of herring and sand lance, the major small pelagic species of the Scotian Shelf ecosystem off eastern Nova Scotia. Contrary to predictions of the SHO hypothesis our initial conclusion that a pelagic outburst occurred in that ecosystem was confirmed and we found no evidence of a predator effect on vertical distributions of these species. We also explored the acoustic survey design and execution that generated the data that form the cornerstone of the SHO hypothesis, and the coherence between the behaviour depicted in these data and catch rates in the surface-oriented purse-seine fishery for herring operating at the time of these surveys. In combination, the results of our re-analysis of the population dynamics and behaviour of herring on the eastern Scotian Shelf, lead us to conclude that the SHO hypothesis, at least as it relates to the post-cod collapse dynamics of the affected Northwest Atlantic ecosystems, is not supported.

Description: Synchronous variations in the abundance of geographically distinct marine fish populations are known to occur across spatial scales on the order of 1,000 km and greater. The prevailing assumption is that this large-scale coherent variability is a response to coupled atmosphere–ocean dynamics, commonly represented by climate indexes, such as the...

Description: Epidermal growth factor receptor (EGFR) expression and signaling can induce cellular protection after intestinal inflammation. l -Glutamine (GLN) is known to prevent apoptosis after intestinal injury by activating MAPK and phosphatidylinositol 3-kinase (PI3-K)/Akt pathways. However, the role of EGFR expression and signaling in GLN-mediated cellular protection in intestinal epithelial-6 (IEC-6) cells after heat stress (HS) is unknown. To address the role of EGFR in GLN-mediated protection, IEC-6 cells were treated with GLN in the presence or absence of EGFR small interfering RNA, the EGFR tyrosine kinase inhibitor AG1478, the ERK1/2 inhibitor PD98059, the p38MAPK inhibitor SB203580, or the PI3-K/Akt inhibitor LY294002 under basal and HS conditions. GLN-mediated cell survival was measured using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Phosphorylated and/or total levels of EGFR, cleaved caspase-3, poly(ADP-ribose) polymerase-1, ERK1/2, p38MAPK, and Akt were assessed by Western blotting. We showed that HS induced a decrease in total, cytoplasmic, and nuclear EGFR levels in IEC-6 cells, which was prevented by GLN supplementation, leading to attenuated apoptosis via EGFR small interfering RNA. Furthermore, the protective effect of GLN was lessened by AG1478, PD98059, and LY294002 but was not affected by SB203580. AG1478 attenuated GLN-mediated increases in ERK1/2 and decreases in p38MAPK phosphorylation. However, AG1478 had no effect on GLN-mediated augmentations in Akt phosphorylation. In summary, EGFR expression was important in the protective mechanism of GLN, as well as GLN-mediated activation of EGFR tyrosine kinase activity. GLN-mediated EGFR signaling activated ERK1/2 and decreased p38MAPK signaling. However, GLN-mediated Akt phosphorylation after HS seems to be independent of EGFR signaling.

Description: Unlike many temperate marine species that alter spatial or depth distributions in response to environmental change, tilefish ( Lopholatilus chamaeleonticeps ) has such specific habitat requirements that off the coast of New England, USA, it is restricted to the normally warm-water, upper continental shelf slope, where it excavates and occupies burrows. In 1882, tens of millions of adult tilefish died suddenly following the intrusion of lethally cold Subarctic water into the tilefish habitat. Here we show that the same climate driver implicated in the 1882 event (the North Atlantic Oscillation: NAO) has also affected commercial tilefish landings throughout most of the 20th century by altering slope water temperatures and likely the tilefish's reproductive success. We also show that this temperature–landings relationship broke down in the 1970s coincident with dramatically increased exploitation. Reconstructions of decadal to millennial scale variations in slope water temperatures explain why no mass mortality occurred following the 2010 negative NAO anomaly, despite being similar in magnitude to the NAO anomaly that preceded the 1882 event.