Description: Melting of coastal glaciers at the West Antarctic Peninsula (WAP) causes shorter winter sea ice duration, intensified ice scouring, sediment erosion and surface freshening in summer, which alters coastal productivity and feeding conditions for the benthos. The soft shell clam Laternula elliptica is a fast growing and abundant filter feeder in coastal Antarctica and a key element for bentho-pelagic carbon recycling. Our aim was to assess the cellular growth and maintenance capacity of small and large clams during natural winter food shortage (seasonal sampling) and in response to experimental starvation exposure. We measured tissue specific proliferation rates and the expression of cell cycling genes and the iron binding protein Le-ferritin in freshly collected specimens in spring (Nov 2008) and at the end of summer (March 2009). For the experimental approach, we focused on 14 cell cycling and metabolic genes using the same animal size groups. Mantle tissue of young bivalves was the only tissue showing accelerated proliferation in summer (1.7 % of cells dividing per day in March) compared to 0.4% dividing cells in animals collected in November. In mantel, siphon and adductor muscle proliferation rates were higher in younger compared to older indiciduals. At transcript level, Le-cyclin D was upregulated in digestive gland of older animals collected in spring (Nov) compared to March indicating enhanced cell proliferation. Likewise, during experimental starvation Le-cyclin D expression increased in large clam digestive gland, whereas Le-cyclin D and the autophagic factor beclin1 decreased in digestive gland of smaller starved clams. The paper corroborates earlier findings of size and age dependent differences in the metabolic response and gene expression patterns in L. elliptica under energetic deprivation. Age structure of shallow water populations can potentially change due to differences in cellular response between young and old animals as environmental stress levels increase.

Description: Intertidal blue mussels, Mytilus edulis, experience hypoxia reoxygenation during tidal emersion and resubmersion cycles, and this is often suggested to represent a major stress for the animals, especially for their respiratory tissues, the gills. We exposed mussels to experimental short and prolonged anoxia and subsequent reoxygenation and analyzed the respiratory response in excised gill tissue and the effects of treatment on reactive oxygen species (mainly ROS: superoxide anion, O2•- and hydrogen peroxide, H2O2), formation using live imaging techniques and confocal microscopy. Our aim was to understand if this “natural stress” would indeed produce oxidative damage and whether antioxidant defenses are induced under anoxia, to prevent oxidative damage during reoxygenation. Exposure to declining pO2 in the respiration chamber caused an increase of gill metabolic rate between 21 and 10 kPa, a pO2 range in which whole animal respiration is reported to be oxyregulating. Exposure of the animals to severe anoxia caused an onset of anaerobiosis (succinate accumulation) and shifted high and low critical pc values (pc1: onset of oxyregulation in gills, pc2: switch from oxyregulation to oxyconformity) to higher pO2. Concentrations of both ROS decreased strongly during anoxic exposure of the mussels and increased upon reoxygenation. This ROS burst induced lipid peroxidation in the mantle, but neither were protein carbonyl levels increased (oxidative damage in the protein fraction), nor did the tissue glutathione concentration change in the gills. Further, analysis of apoptosis markers indicated no induction of cell death in the gills. To our knowledge, this is the first paper that directly measures ROS formation during anoxia reoxygenation in mussels. We conclude that hypoxia tolerant intertidal mussels do not suffer major oxidative stress in gill and mantle tissues under these experimental conditions. Keywords: blue mussel, oxidative stress, reoxygenation, live imaging