Upwelling intensity modulates the fitness and physiological performance of coastal species: Implications for the aquaculture of the scallop Argopecten purpuratus in the Humboldt Current System.

Understanding how marine species cope with the natural environmental variability of their native habitats will provide significant information about their sensitivity to the potential environmental changes driven by climate change. In particular, marine species inhabiting upwelling ecosystems are experiencing low seawater temperatures, as well as, acidic and low oxygen conditions as a consequence of the nature of the deep upwelled waters. Our study is focused on one of the most important socio-economical resources of the Humboldt Current System (HCS): the scallop Argopecten purpuratus which has been historically subjected to intensive aquaculture in areas influenced by upwelling processes. Here, a long-term field experiment was performed to understand how tolerant and well-locally-adapted is A. purpuratus to upwelling conditions by studying a set of fitness, physiological, and biomineralogical traits. Stronger upwelling generated a minor water column stratification, with lower temperatures, pH, and oxygen conditions. On the contrary, as upwelling weakened, temperature, pH, and oxygen availability increased. Finally, upwelling intensity also determined the number, duration, and intensity of the cooling and de-oxygenation events occurring in A. purpuratus habitat, as well as, the food availability (chlorophyll-a concentration, Chl-a). Physiologically, A. purpuratus was able to cope with stressful environmental conditions imposed by higher upwelling intensities by enhancing its metabolic and calcification rates, as well, producing higher concentrations of the shell organic matter. These physiological changes impacted the total energy budget, which was highly dependent on Chl-a concentration, and revealed important traits trade-offs with significant fitness costs (higher mortalities emerged when longer and more intense upwelling events succeed). Our study increases the knowledge about the physiological performance and tolerance of this important resource to the ocean acidification and ocean-deoxygenation imposed by variable upwelling intensities, as well as, its potential vulnerability under future changing conditions driven by a potential upwelling intensification.

Slow inactivation in Shaker K channels is delayed by intracellular tetraethylammonium.

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.