Reevaluation of mid-Pliocene North Atlantic sea surface temperatures

Multiproxy temperature estimation requires careful attention to biological, chemical, physical, temporal, and calibration differences of each proxy and paleothermometry method. We evaluated mid-Pliocene sea surface temperature (SST) estimates from multiple proxies at Deep Sea Drilling Project Holes 552A, 609B, 607, and 606, transecting the North Atlantic Drift. SST estimates derived from faunal assemblages, foraminifer Mg/Ca, and alkenone unsaturation indices showed strong agreement at Holes 552A, 607, and 606 once differences in calibration, depth, and seasonality were addressed. Abundant extinct species and/or an unrecognized productivity signal in the faunal assemblage at Hole 609B resulted in exaggerated faunal-based SST estimates but did not affect alkenone-derived or Mg/Ca-derived estimates. Multiproxy mid-Pliocene North Atlantic SST estimates corroborate previous studies documenting high-latitude mid-Pliocene warmth and refine previous faunal-based estimates affected by environmental factors other than temperature. Multiproxy investigations will aid SST estimation in high-latitude areas sensitive to climate change and currently underrepresented in SST reconstructions. Copyright 2008 by the American Geophysical Union.

Ligand-induced overexpression of a constitutively active beta2-adrenergic receptor: pharmacological creation of a phenotype in transgenic mice.

Transgenic overexpression (40- to 100-fold) of the wild-type human beta2-adrenergic receptor in the hearts of mice leads to a marked increase in cardiac contractility, which is apparently due to the low level of spontaneous (i.e., agonist-independent) activity inherent in the receptor. Here we report that transgenic mice expressing a mutated constitutively active form of the receptor (CAM) show no such phenotype, owing to its modest expression (3-fold above endogenous cardiac beta-adrenergic receptor levels). Surprisingly, treatment of the animals with a variety of beta-adrenergic receptor ligands leads to a 50-fold increase in CAM beta2-adrenergic receptor expression, by stabilizing the CAM beta2-adrenergic receptor protein. Receptor up-regulation leads in turn to marked increases in adenylate cyclase activity, atrial tension determined in vitro, and indices of cardiac contractility determined in vivo. These results illustrate a novel mechanism for regulating physiological responses, i.e., ligand-induced stabilization of a constitutively active but inherently unstable protein.