Emergence of non-centrosymmetric topological insulating phase in BiTeI under pressure

The spin-orbit interaction affects the electronic structure of solids in various ways. Topological insulators are one example where the spin-orbit interaction leads the bulk bands to have a non-trivial topology, observable as gapless surface or edge states. Another example is the Rashba effect, which lifts the electron-spin degeneracy as a consequence of spin-orbit interaction under broken inversion symmetry. It is of particular importance to know how these two effects, i.e. the non-trivial topology of electronic states and Rashba spin splitting, interplay with each other. Here we show, through sophisticated first-principles calculations, that BiTeI, a giant bulk Rashba semiconductor, turns into a topological insulator under a reasonable pressure. This material is shown to exhibit several unique features such as, a highly pressure-tunable giant Rashba spin splitting, an unusual pressure-induced quantum phase transition, and more importantly the formation of strikingly different Dirac surface states at opposite sides of the material.Comment: 5 figures are include

A heterotrimeric G protein of the Gi family is required for cAMP-triggered trafficking of aquaporin 2 in kidney epithelial cells.

Vasopressin is the key regulator of water homeostasis in vertebrates. Central to its antidiuretic action in mammals is the redistribution of the water channel aquaporin 2 (AQP2) from intracellular vesicles to the apical membrane of kidney epithelial cells, an event initiated by an increase in cAMP and activation of protein kinase A. The subsequent steps of the signaling cascade are not known. To identify proteins involved in the AQP2 shuttle we exploited a recently developed cell line (CD8) derived from the rabbit cortical collecting duct and stably transfected with rat AQP2 cDNA, Treatment of CD8 cells with pertussis toxin (PTX) inhibited both the vasopressin-induced increase in water permeability and the redistribution of AQP2 from an intracellular compartment to the apical membrane. ADP-ribosylation studies revealed the presence of at least two major PTX substrates, Correspondingly, two a: subunits of PTX-sensitive G proteins, G alpha(i2), and G alpha(i3), were identified by Western blotting. Introduction of a synthetic peptide corresponding to the C terminus of the G(i3) alpha subunit into permeabilized CD8 cells efficiently inhibited the cAMP-induced AQP2 translocation; a peptide corresponding to the a subunits of G(i1/2) was much less potent. Thus a member of the G(i) family, most likely G(i3), is involved in the cAMP-triggered targeting of AQP2-bearing vesicles to the apical membrane of kidney epithelial cells

Coordinated oscillations in cortical actin and Ca2+ correlate with cycles of vesicle secretion

The actin cortex both facilitates and hinders exocytosis of secretory granules. How cells consolidate these two opposing roles was not well understood. Here we show that antigen activation of mast cells induces oscillations in Ca2+ and PI(4,5)P2 lipids that in turn drive cyclic recruitment of N-WASP and cortical actin oscillations. Experimental and computational analysis argues that vesicle fusion correlates with the observed actin and Ca2+ oscillations. A vesicle secretion cycle starts with the capture of vesicles by actin when cortical F-actin is high, followed by vesicle passage through the cortex when F-actin levels are low, and vesicle fusion with the plasma membrane when Ca2+ levels subsequently increase. Thus, cells employ oscillating levels of Ca2+, PI(4,5)P2 and cortical F-actin to increase secretion efficiency, explaining how the actin cortex can function as a carrier as well as barrier for vesicle secretion