Biomass changes and trophic amplification of plankton in a warmer ocean

Ocean warming can modify the ecophysiology and distribution of marine organisms, and relationships between species, with nonlinear interactions between ecosystem components potentially resulting in trophic amplification. Trophic amplification (or attenuation) describe the propagation of a hydroclimatic signal up the food web, causing magnification (or depression) of biomass values along one or more trophic pathways. We have employed 3‐D coupled physical‐biogeochemical models to explore ecosystem responses to climate change with a focus on trophic amplification. The response of phytoplankton and zooplankton to global climate‐change projections, carried out with the IPSL Earth System Model by the end of the century, is analysed at global and regional basis, including European seas (NE Atlantic, Barents Sea, Baltic Sea, Black Sea, Bay of Biscay, Adriatic Sea, Aegean Sea) and the Eastern Boundary Upwelling System (Benguela). Results indicate that globally and in Atlantic Margin and North Sea, increased ocean stratification causes primary production and zooplankton biomass to decrease in response to a warming climate, whilst in the Barents, Baltic and Black Seas, primary production and zooplankton biomass increase. Projected warming characterized by an increase in sea surface temperature of 2.29 ± 0.05 °C leads to a reduction in zooplankton and phytoplankton biomasses of 11% and 6%, respectively. This suggests negative amplification of climate driven modifications of trophic level biomass through bottom‐up control, leading to a reduced capacity of oceans to regulate climate through the biological carbon pump. Simulations suggest negative amplification is the dominant response across 47% of the ocean surface and prevails in the tropical oceans; whilst positive trophic amplification prevails in the Arctic and Antarctic oceans. Trophic attenuation is projected in temperate seas. Uncertainties in ocean plankton projections, associated to the use of single global and regional models, imply the need for caution when extending these considerations into higher trophic levels.     

The C-terminal transmembrane domain of human phospholipid scramblase 1 is essential for the protein flip-flop activity and Ca2+-binding

Human phospholipid scramblase 1 (SCR) is a 318 amino acid protein that was originally described as catalyzing phospholipid transbilayer (flip-flop) motion in plasma membranes in a Ca²⁺-dependent, ATP-independent way. Further studies have suggested an intranuclear role for this protein in addition. A putative transmembrane domain located at the C terminus (aa 291–309) has been related to the flip-flop catalysis. In order to clarify the role of the C-terminal region of SCR, a mutant was produced (SCRΔ) in which the last 28 amino acid residues were lacking, including the α-helix. SCRΔ had lost the scramblase activity and its affinity for Ca²⁺ was decreased by one order of magnitude. Fluorescence and IR spectroscopic studies revealed that the C-terminal region of SCR was essential for the proper folding of the protein. Moreover, it was found that Ca²⁺ exerted an overall destabilizing effect on SCR, which might facilitate its binding to membranes.     

GlialCAM,a CLC-2 Cl- Channel Subunit,Activates the Slow Gate of CLC Chloride Channels

GlialCAM, a glial cell adhesion molecule mutated in megalencephalic leukoencephalopathy with subcortical cysts, targets the CLC-2 Cl^- channel to cell contacts in glia and activates CLC-2 currents in vitro and in vivo. We found that GlialCAM clusters all CLC channels at cell contacts in vitro and thus studied GlialCAM interaction with CLC channels to investigate the mechanism of functional activation. GlialCAM slowed deactivation kinetics of CLC-Ka/barttin channels and increased CLC-0 currents opening the common gate and slowing its deactivation. No functional effect was seen for common gate deficient CLC-0 mutants. Similarly, GlialCAM targets the common gate deficient CLC-2 mutant E211V/H816A to cell contacts, without altering its function. Thus, GlialCAM is able to interact with all CLC channels tested, targeting them to cell junctions and activating them by stabilizing the open configuration of the common gate. These results are important to better understand the physiological role of GlialCAM/CLC-2 interaction.     

Weather effect on widely distributed seabirds through migration flyways: a case study with the Northern Gannet Morus bassanus in the Bay of Biscay

Capsule: Northern Gannet Morus bassanus counts obtained from a coastal monitoring network in northern Spain were highly determined by wind conditions.

Aims: To determine how external factors including weather conditions affect seabird counts in a land-based seabird monitoring project (Red de observación de Aves y Mamíferos marinos, RAM project; Seabird & Marine Mammal Observation Network).

Methods: Seabird counts were obtained from four study capes situated in the southeastern part of the Bay of Biscay in northern Spain. Counts were conducted on a monthly-basis for a period of 3 hours starting at dawn on each sampling day. Data used here were compiled over a 10-year period (2006–15).

Results: Northern Gannet numbers were chiefly influenced by meteorological conditions at a local spatial scale. Northwesterly winds were found to positively influence gannet abundance, whereas high relative humidity caused a decrease in abundance. Moreover, gannets were more abundant during the non-breeding period as compared to breeding period.

Conclusion: We recommend considering the effect of the wind and relative humidity on land-based seabird counts in the Bay of Biscay when handling data from the RAM protocol in order to avoid biases and misinterpretation of data. Since seabirds approach the coast during harsh weather conditions, the RAM protocol should be improved in order to better account for the distance at which the birds are seen.     

Microglial immune response is impaired against the neurotropic fungus Lomentospora prolificans

Lomentospora (Scedosporium) prolificans is an opportunistic pathogen capable of causing invasive infections in immunocompromised patients. The fungus is able to disseminate via the bloodstream finally arriving at the central nervous system producing neurological symptoms and, in many cases, patient death. In this context, microglial cells, which are the resident immune cells in the central nervous system, may play an important role in these infections. However, this aspect of anti‐L. prolificans immunity has been poorly researched to date. Thus, the interactions and activity of microglial cells against L. prolificans were analysed, and the results show that there was a remarkable impairment in their performance regarding phagocytosis, the development of oxidative burst, and in the production of pro‐inflammatory cytokines, compared with macrophages. Interestingly, L. prolificans displays great growth also when challenged with immune cells, even when inside them. We also proved that microglial phagocytosis of the fungus is highly dependent on mannose receptor and especially on dectin‐1. Taken together, these data provide evidence for an impaired microglial response against L. prolificans and contribute to understanding the pathobiology of its neurotropism.     

Food availability as a potential source of bias in the egg production method for copepods

The measurement of copepod adult female fecundity as an estimateof adult growth (production) rates has been an approach widelyused in both laboratory and field studies. Here we demonstratethat the basic assumption of this approach, i.e. that estimatedegg production during the incubation reflects the ‘insitu’ conditions, is not always legitimate and that itis temperature dependent. The enhancement of metabolic ratesinduced by high temperatures induces a more accented bias ofthe method. We also provide guidelines on how to conduct theincubations in order to obtain more reliable estimates.     

Sea-level dynamics and palaeoecological factors affecting trace fossil distribution in Eocene turbiditic deposits (Gorrondatxe section,N Spain)

Ichnological analysis of the upper Ypresian–lower Lutetian interval at the Gorrondatxe section (W Pyrenees, N Spain), reveals a relationship between sea-level dynamics and the eco-sedimentary factors influencing trace fossil assemblages. The 600 m thick section of deep-sea turbiditic deposits contains 41 ichnospecies belonging to 28 ichnogenera, which are typical of the Nereites ichnofacies, and mostly of the Paleodictyon ichnosubfacies, suggesting deposition in a basin plain to fan-fringe setting. The trace fossil diversity and abundance fluctuate, irrespective of turbidite frequency. These ichnological features are strongly affected by trophic level changes related partly to sea-level dynamics according to the sequence stratigraphic interpretations for the studied section. Temperature, oxygenation and substrate changes are also considered as relevant factors. Increased ichnodiversity, particularly among graphoglyptids, coincides with moderate oligotrophy and stable ecological conditions. Eutrophisation, lowered oxygenation and drop of temperature, typical of low sea level, can reduce ichnodiversity.     

Differential regulation of the JNK/AP-1 pathway by S-adenosylmethionine and methylthioadenosine in primary rat hepatocytes versus HuH7 hepatoma cells

S-adenosylmethionine (AdoMet) and 5'-methylthioadenosine (MTA) exert a protective action on apoptosis induced by okadaic acid in primary rat hepatocytes but not in human transformed HuH7 cells. In the present work, we analyzed the role played by the JNK/activator protein (AP)-1 pathway in this differential effect. Okadaic acid induced the phosphorylation of JNK and c-Jun and the binding activity of AP-1 in primary hepatocytes, and pretreatment with either AdoMet or MTA prevented those effects. In HuH7 cells, pretreatment with either AdoMet or MTA did not affect JNK and c-Jun activation or AP-1 binding induced by okadaic acid. In both cell types, p38 was activated by okadaic acid, but neither AdoMet nor MTA presented a significant effect on its activity. Therefore, the differential effect of both AdoMet and MTA on the JNK/AP-1 pathway could explain their antiapoptotic effect on primary hepatocytes and the lack of protection they show against okadaic acid-induced apoptosis in hepatoma cells.