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mate system, leading to increased global mean temperatures (i.e. global warming) of approximately 0.7°C, a trend that will continue and fluctuate over a broad range (1−4°C) towards the end of the century (IPCC 2014 ABSTRACT: Coastal upwelling regions already constitute hot spots of ocean acidification as naturally acidified waters are brought to the surface. This effect could be exacerbated by ocean acidification and warming, both caused by rising concentrations of atmospheric CO 2 . Along the Chilean coast, upwelling supports highly productive fisheries and aquaculture activities. However, during recent years, there has been a documented decline in the national production of the native scallop Argopecten purpuratus. We assessed the combined effects of temperature and pCO 2 -driven ocean acidification on the growth rates and shell characteristics of this species farmed under the natural influence of upwelling waters occurring in northern Chile (30°S, Tongoy Bay). The experimental scenario representing current conditions (14°C, pH ~8.0) were typical of natural values recorded in Tongoy Bay, whilst conditions representing the low pH scenario were typical of an adjacent upwelling area (pH ~7.6). Shell thickness, weight, and biomass were reduced under low pH (pH ~7.7) and increased temperature (18°C) conditions. At ambient temperature (14°C) and low pH, scallops showed increased shell dissolution and low growth rates. However, elevated temperatures ameliorated the impacts of low pH, as evidenced by growth rates in both pH treatments at the higher temperature treatment that were not significantly different from the control treatment. The impact of low pH at current temperature on scallop growth suggests that the upwelling could increase the time required for scallops to reach marketable size. Mortality of farmed scallops is discussed in relation to our observations of multiple environmental stressors in this upwelling-influenced area.

After removal of the fast N-type inactivation gate, voltage-sensitive Shaker (Shaker IR) K channels are still able to inactivate, albeit slowly, upon sustained depolarization. The classical mechanism proposed for the slow inactivation observed in cell-free membrane patches—the so called C inactivation—is a constriction of the external mouth of the channel pore that prevents K+ ion conduction. This constriction is antagonized by the external application of the pore blocker tetraethylammonium (TEA). In contrast to C inactivation, here we show that, when recorded in whole Xenopus oocytes, slow inactivation kinetics in Shaker IR K channels is poorly dependent on external TEA but severely delayed by internal TEA. Based on the antagonism with internally or externally added TEA, we used a two-pulse protocol to show that half of the channels inactivate by way of a gate sensitive to internal TEA. Such gate had a recovery time course in the tens of milliseconds range when the interpulse voltage was −90 mV, whereas C-inactivated channels took several seconds to recover. Internal TEA also reduced gating charge conversion associated to slow inactivation, suggesting that the closing of the internal TEA-sensitive inactivation gate could be associated with a significant amount of charge exchange of this type. We interpreted our data assuming that binding of internal TEA antagonized with U-type inactivation (Klemic, K.G., G.E. Kirsch, and S.W. Jones. 2001. Biophys. J. 81:814–826). Our results are consistent with a direct steric interference of internal TEA with an internally located slow inactivation gate as a “foot in the door” mechanism, implying a significant functional overlap between the gate of the internal TEA-sensitive slow inactivation and the primary activation gate. But, because U-type inactivation is reduced by channel opening, trapping the channel in the open conformation by TEA would also yield to an allosteric delay of slow inactivation. These results provide a framework to explain why constitutively C-inactivated channels exhibit gating charge conversion, and why mutations at the internal exit of the pore, such as those associated to episodic ataxia type I in hKv1.1, cause severe changes in inactivation kinetics.