Measurement of junctional tension in epithelial cells at the onset of primitive streak formation in the chick embryo via non-destructive optical manipulation

Directional cell intercalations of epithelial cells during gastrulation has in several organisms been shown to be associated with a planar cell polarity in the organisation of the actin-myosin cytoskeleton and is postulated to reflect directional tension that drives oriented cell intercalations. We have characterised and applied a recently introduced non-destructive optical manipulation technique to measure the tension in individual epithelial cell junctions of cells in various locations and orientations in the epiblast of chick embryos in the early stages of primitive streak formation. Junctional tension of mesendoderm precursors in the epiblast is higher in junctions oriented in the direction of intercalation than in junctions oriented perpendicular to the direction of intercalation and higher than in junctions of other cells in the epiblast. The kinetic data are fitted best with a simple visco-elastic Maxwell model and we find that junctional tension and to a lesser extent viscoelastic relaxation time are dependent on myosin activity

Heart of glass anchors Rasip1 at endothelial cell-cell junctions to support vascular integrity.

Heart of Glass (HEG1), a transmembrane receptor, and Rasip1, an endothelial-specific Rap1-binding protein, are both essential for cardiovascular development. Here we performed a proteomic screen for novel HEG1 interactors and report that HEG1 binds directly to Rasip1. Rasip1 localizes to forming endothelial cell (EC) cell-cell junctions and silencing HEG1 prevents this localization. Conversely, mitochondria-targeted HEG1 relocalizes Rasip1 to mitochondria in cells. The Rasip1-binding site in HEG1 contains a 9 residue sequence, deletion of which abrogates HEG1's ability to recruit Rasip1. HEG1 binds to a central region of Rasip1 and deletion of this domain eliminates Rasip1's ability to bind HEG1, to translocate to EC junctions, to inhibit ROCK activity, and to maintain EC junctional integrity. These studies establish that the binding of HEG1 to Rasip1 mediates Rap1-dependent recruitment of Rasip1 to and stabilization of EC cell-cell junctions

Performance analysis of AlGaAs/GaAs tunnel junctions for ultra-high concentration photovoltaics

An n(++)-GaAs/p(++)-AlGaAs tunnel junction with a peak current density of 10 100Acm(-2) is developed. This device is a tunnel junction for multijunction solar cells, grown lattice-matched on standard GaAs or Ge substrates, with the highest peak current density ever reported. The voltage drop for a current density equivalent to the operation of the multijunction solar cell up to 10 000 suns is below 5 mV. Trap-assisted tunnelling is proposed to be behind this performance, which cannot be justified by simple band-to-band tunnelling. The metal-organic vapour-phase epitaxy growth conditions, which are in the limits of the transport-limited regime, and the heavy tellurium doping levels are the proposed origins of the defects enabling trap-assisted tunnelling. The hypothesis of trap-assisted tunnelling is supported by the observed annealing behaviour of the tunnel junctions, which cannot be explained in terms of dopant diffusion or passivation. For the integration of these tunnel junctions into a triple-junction solar cell, AlGaAs barrier layers are introduced to suppress the formation of parasitic junctions, but this is found to significantly degrade the performance of the tunnel junctions. However, the annealed tunnel junctions with barrier layers still exhibit a peak current density higher than 2500Acm(-2) and a voltage drop at 10 000 suns of around 20 mV, which are excellent properties for tunnel junctions and mean they can serve as low-loss interconnections in multijunction solar cells working at ultra-high concentrations

Depinning of kinks in a Josephson-junction ratchet array

We have measured the depinning of trapped kinks in a ratchet potential using a fabricated circular array of Josephson junctions. Our ratchet system consists of a parallel array of junctions with alternating cell inductances and junctions areas. We have compared this ratchet array with other circular arrays. We find experimentally and numerically that the depinning current depends on the direction of the applied current in our ratchet ring. We also find other properties of the depinning current versus applied field, such as a long period and a lack of reflection symmetry, which we can explain analytically.Comment: to be published in PR

Genetically engineered cardiac pacemaker: stem cells transfected with HCN2 gene and myocytes - a model

Artificial biological pacemakers were developed and tested in canine ventricles. Next steps will require obtaining oscillations sensitive to external regulations, and robust with respect to long term drifts of expression levels of pacemaker currents and gap junctions. We introduce mathematical models intended to be used in parallel with the experiments. The models describe human mesenchymal stem cells ({\it hMSC}) transfected with HCN2 genes and connected to myocytes. They are intended to mimic experiments with oscillation induction in a cell pair, in cell culture and in the cardiac tissue. We give examples of oscillations in a cell pair, in a 1 dim cell culture, and oscillation dependence on number of pacemaker channels per cell and number of gap junctions. The models permit to mimic experiments with levels of gene expressions not achieved yet, and to predict if the work to achieve this levels will significantly increase the quality of oscillations. This give arguments for selecting the directions of the experimental work

The structural organization and protein composition of lens fiber junctions.

The structural organization and protein composition of lens fiber junctions isolated from adult bovine and calf lenses were studied using combined electron microscopy, immunolocalization with monoclonal and polyclonal anti-MIP and anti-MP70 (two putative gap junction-forming proteins), and freeze-fracture and label-fracture methods. The major intrinsic protein of lens plasma membranes (MIP) was localized in single membranes and in an extensive network of junctions having flat and undulating surface topologies. In wavy junctions, polyclonal and monoclonal anti-MIPs labeled only the cytoplasmic surface of the convex membrane of the junction. Label-fracture experiments demonstrated that the convex membrane contained MIP arranged in tetragonal arrays 6-7 nm in unit cell dimension. The apposing concave membrane of the junction displayed fracture faces without intramembrane particles or pits. Therefore, wavy junctions are asymmetric structures composed of MIP crystals abutted against particle-free membranes. In thin junctions, anti-MIP labeled the cytoplasmic surfaces of both apposing membranes with varying degrees of asymmetry. In thin junctions, MIP was found organized in both small clusters and single membranes. These small clusters also abut against particle-free apposing membranes, probably in a staggered or checkerboard pattern. Thus, the structure of thin and wavy junctions differed only in the extent of crystallization of MIP, a property that can explain why this protein can produce two different antibody-labeling patterns. A conclusion of this study is that wavy and thin junctions do not contain coaxially aligned channels, and, in these junctions, MIP is unlikely to form gap junction-like channels. We suggest MIP may behave as an intercellular adhesion protein which can also act as a volume-regulating channel to collapse the lens extracellular space. Junctions constructed of MP70 have a wider overall thickness (18-20 nm) and are abundant in the cortical regions of the lens. A monoclonal antibody raised against this protein labeled these thicker junctions on the cytoplasmic surfaces of both apposing membranes. Thick junctions also contained isolated clusters of MIP inside the plaques of MP70. The role of thick junctions in lens physiology remains to be determined

A theoretical investigation of ferromagnetic tunnel junctions with 4-valued conductances

In considering a novel function in ferromagnetic tunnel junctions consisting of ferromagnet(FM)/barrier/FM junctions, we theoretically investigate multiple valued (or multi-level) cell property, which is in principle realized by sensing conductances of four states recorded with magnetization configurations of two FMs; that is, (up,up), (up,down), (down,up), (down,down). To obtain such 4-valued conductances, we propose FM1/spin-polarized barrier/FM2 junctions, where the FM1 and FM2 are different ferromagnets, and the barrier has spin dependence. The proposed idea is applied to the case of the barrier having localized spins. Assuming that all the localized spins are pinned parallel to magnetization axes of the FM1 and FM2, 4-valued conductances are explicitly obtained for the case of many localized spins. Furthermore, objectives for an ideal spin-polarized barrier are discussed.Comment: 9 pages, 3 figures, accepted for publication in J. Phys.: Condens. Matte

Improved silicon solar cells

Redistribution of phosphorus within the n-type layers of n-on-p silicon solar cells results in significant improvements in cell performance. Electrical current output is increased, reduction in current output due to radiation damage is lessened, and very shallow junctions are no longer needed

Tight junctions as regulators of tissue remodelling

Formation of tissue barriers by epithelial and endothelial cells requires neighbouring cells to interact via intercellular junctions, which includes tight junctions. Tight junctions form a semipermeable paracellular diffusion barrier and act as signalling hubs that guide cell behaviour and differentiation. Components of tight junctions are also expressed in cell types not forming tight junctions, such as cardiomyocytes, where they associate with facia adherens and/or gap junctions. This review will focus on tight junction proteins and their importance in tissue homeostasis and remodelling with a particular emphasis on what we have learned from animal models and human diseases