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The Advanced Technology Large Aperture Space Telescope (ATLAST) team identified five key technology areas to enable candidate architectures for a future large-aperture ultraviolet/optical/infrared (LUVOIR) space observatory envisioned by the NASA Astrophysics 30-year roadmap, "Enduring Quests, Daring Visions." The science goals of ATLAST address a broad range of astrophysical questions from early galaxy and star formation to the processes that contributed to the formation of life on Earth, combining general astrophysics with direct-imaging and spectroscopy of habitable exoplanets. The key technology areas are internal coronagraphs, starshades (or external occulters), ultra-stable large-aperture telescope systems, detectors, and mirror coatings. For each technology area, we define best estimates of required capabilities, current state-of-the-art performance, and current technology readiness level (TRL), thus identifying the current technology gap. We also report on current, planned, or recommended efforts to develop each technology to TRL 5.

The activation of the Na+-H+ exchanger 1 (NHE1) and extracellular-signal regulated kinase (ERK) phosphorylation in Chinese hamster lung fibroblasts (CCL39) was characterized in response to the specific alpha1-adrenergic agonist, phenylephrine (PE). Addition of 100 micromol PE/L increased the steady-state intracellular pH (pHi) by 0.16 +/- 0.03 pH units, as well as increasing the phosphorylation of ERK. The response of NHE1 to PE in CCL39 cells was determined by the use of specific antagonists. Use of 2 specific chemical inhibitors of phosphoinositide-specific phospholipase C (PLC) reduced the ability of PE to activate either the exchanger or ERK. Studies were conducted in PLCbeta-deficient cell lines derived from parental CCL39 cells. NHE1 activity in both mutant cell lines was increased in response to phorbal esters or lysophosphatidic acid, whereas the addition of PE only caused a minimal change in either pHi or ERK phosphorylation. These results, combined with reconstitution experiments with exogenously expressed PLCbeta1, PLCbeta2, or PLCbeta3, revealed that stimulation of NHE1 activity by PE in CCL39 cells is a PLCbeta1-coupled event. Furthermore, the data indicate that alpha1-adrenergic signaling of PLCbeta is upstream of ERK activation. These data demonstrate that PLCbeta1 is primarily involved in the activation of NHE1 in CCL39 fibroblasts.