A 700-year paleoecological record of boreal ecosystem responses to climatic variation from Alaska

Recent observations and model simulations have highlighted the sensitivity of the forest - tundra ecotone to climatic forcing. In contrast, paleoecological studies have not provided evidence of tree-line fluctuations in response to Holocene climatic changes in Alaska, suggesting that the forest - tundra boundary in certain areas may be relatively stable at multicentennial to millennial time scales. We conducted a multiproxy study of sediment cores from an Alaskan lake near the altitudinal limits of key boreal-forest species. Paleoecological data were compared with independent climatic reconstructions to assess ecosystem responses of the forest - tundra boundary to Little Ice Age (LIA) climatic. uctuations. Pollen, diatom, charcoal, macrofossil, and magnetic analyses provide the first continuous record of vegetation -. re - climate interactions at decadal to centennial time scales during the past 700 years from southern Alaska. Boreal-forest diebacks characterized by declines of Picea mariana, P. glauca, and tree Betula occurred during the LIA ( AD 1500 - 1800), whereas shrubs ( Alnus viridis, Betula glandulosa/nana) and herbaceous taxa (Epilobium, Aconitum) expanded. Marked increases in charcoal abundance and changes in magnetic properties suggest increases in. re importance and soil erosion during the same period. In addition, the conspicuous reduction or disappearance of certain aquatic ( e. g., Isoetes, Nuphar, Pediastrum) and wetland ( Sphagnum) plants and major shifts in diatom assemblages suggest pronounced lake-level. uctuations and rapid ecosystem reorganization in response to LIA climatic deterioration. Our results imply that temperature shifts of 1 - 2 degrees C, when accompanied by major changes in moisture balance, can greatly alter high-altitudinal terrestrial, wetland, and aquatic ecosystems, including conversion between boreal-forest tree line and tundra. The climatic and ecosystem variations in our study area appear to be coherent with changes in solar irradiance, suggesting that changes in solar activity contributed to the environmental instability of the past 700 years.

The annexins: spatial and temporal coordination of signaling events during cellular stress

Annexins are a family of structurally related, Ca2+-sensitive proteins that bind to negatively charged phospholipids and establish specific interactions with other lipids and lipid microdomains. They are present in all eukaryotic cells and share a common folding motif, the "annexin core", which incorporates Ca2+- and membrane-binding sites. Annexins participate in a variety of intracellular processes, ranging from the regulation of membrane dynamics to cell migration, proliferation, and apoptosis. Here we focus on the role of annexins in cellular signaling during stress. A chronic stress response triggers the activation of different intracellular pathways, resulting in profound changes in Ca2+ and pH homeostasis and the production of lipid second messengers. We review the latest data on how these changes are sensed by the annexins, which have the ability to simultaneously interact with specific lipid and protein moieties at the plasma membrane, contributing to stress adaptation via regulation of various signaling pathways.

Apoptotic cell death in the lactating mammary gland is enhanced by a folding variant of alpha-lactalbumin

Apoptosis is essential to eliminate secretory epithelial cells during the involution of the mammary gland. The environmental regulation of this process is however, poorly understood. This study tested the effect of HAMLET (human alpha-lactalbumin made lethal to tumor cells) on mammary cells. Plastic pellets containing HAMLET were implanted into the fourth inguinal mammary gland of lactating mice for 3 days. Exposure of mammary tissue to HAMLET resulted in morphological changes typical for apoptosis and in a stimulation of caspase-3 activity in alveolar epithelial cells near the HAMLET pellets but not more distant to the pellet or in contralateral glands. The effect was specific for HAMLET and no effects were observed when mammary glands were exposed to native a-lactalbumin or fatty acid alone. HAMLET also induced cell death in vitro in a mouse mammary epithelial cell line. The results suggest that HAMLET can mediate apoptotic cell death in mammary gland tissue.