Nonpolar Cells Research Articles

Performance optimization of solar cells using non-polar, semi-polar and polar InGaN/GaN multiple quantum wells alongside AlGaN blocking layers

This paper reports opto-electronic properties and photo-voltaic performances of non-polar, semi-polar and polar solar cells employing InGaN/GaN multiple quantum wells (MQWs) with and without using AlGaN material as electron and hole blocking layers. In addition, the investigation is conducted for a number of QWs, e. g., 3, 5, 7, and 10. The performance of such devices is evaluated in terms of current density–voltage characteristics, power–voltage characteristics, fill factor, and power conversion efficiency. Our TCAD simulation results show that the InGaN/GaN solar cell featuring non-polar crystal structure, seven QWs alongside AlGaN blocking layers turns out to be the optimised device exhibiting open circuit voltage (Voc) of 1.08 V, short circuit current density (Jsc) of − 7.64 mA/cm2 and power conversion efficiency (η) of 5.36% among all other solar cells. The optimized device exhibits a considerably high value of η compared to earlier findings of nitride based solar cells. Hence our present design for InGaN/GaN MQW solar cells could provide an encouraging guideline for design and development of solar cells utilizing III–V nitride semiconductors in near future.

PTEN dephosphorylates Abi1 to promote epithelial morphogenesis.

The tumor suppressor PTEN is essential for early development. Its lipid phosphatase activity converts PIP3 to PIP2 and antagonizes the PI3K-Akt pathway. In this study, we demonstrate that PTEN's protein phosphatase activity is required for epiblast epithelial differentiation and polarization. This is accomplished by reconstitution of PTEN-null embryoid bodies with PTEN mutants that lack only PTEN's lipid phosphatase activity or both PTEN's lipid and protein phosphatase activities. Phosphotyrosine antibody immunoprecipitation and mass spectrometry were used to identify Abi1, a core component of the WASP-family verprolin homologous protein (WAVE) regulatory complex (WRC), as a new PTEN substrate. We demonstrate that PTEN dephosphorylation of Abi1 at Y213 and S216 results in Abi1 degradation through the calpain pathway. This leads to down-regulation of the WRC and reorganization of the actin cytoskeleton. The latter is critical to the transformation of nonpolar pluripotent stem cells into the polarized epiblast epithelium. Our findings establish a link between PTEN and WAVE-Arp2/3-regulated actin cytoskeletal dynamics in epithelial morphogenesis.

Effect of light wavelengths on the non-polar InGaN-based thin film solar cells performances using one-dimensional modeling

Abstract In the present contribution, we determine the effect of light wavelength variation on the performances of the non-polar InGaN-based solar cells in order to find the optimum light wavelength that yields a high efficiency. The calculations are performed using a one-dimensional SCAPS-1D tool (One-Dimensional Solar Cell Capacitance Simulator). The simulation has been carried out by lighting through a n-In0.3Ga0.7As layer. An efficiency of 12.24% with the fill-factor FF = 51.35%, open-circuit voltage VOC = 0.72 V and short-circuit current density JSC = 32.80 mA/cm2 is obtained under AM1.5G illumination. The quantum efficiency characteristic displays a maximum value of more than 90% in the visible range using AM1.5G illumination. Moreover, our results show that with increasing light wavelengths from the blue light (around 450 nm) to the end of the red light (around 700 nm), the efficiency increases from 13.76% to above of 20%. The short-circuit current density is also increased from 37.33 mA/cm2 to 53.81 mA/cm2 with increasing light wavelengths from 450 nm to 700 nm. However, the variation of the light wavelength seems to have only a small influence on the open-circuit voltage and fill-factor. The present study provides information about the properties of the materials used in the cell structure of efficient InGaN solar cells.

Nonpolar and semipolar InGaN/GaN multiple-quantum-well solar cells with improved carrier collection efficiency

We demonstrate the nonpolar and semipolar InGaN/GaN multiple-quantum-well (MQW) solar cells grown on the nonpolar m-plane and semipolar (202¯1) plane bulk GaN substrates. The optical properties and photovoltaic performance of the nonpolar and semipolar InGaN solar cells were systematically studied, and the results were compared to the conventional polar c-plane devices. The absorption spectra, current density–voltage (J–V) characteristics, external quantum efficiency (EQE), and internal quantum efficiency (IQE) were measured for nonpolar m-plane, semipolar (202¯1) plane, and polar c-plane InGaN/GaN MQW solar cells. Nonpolar m-plane InGaN/GaN MQW solar cells showed the best performance across all devices, with a high open-circuit voltage of 2.32 V, a low bandgap-voltage offset of 0.59 V, and the highest EQE and IQE. In contrast, the polar c-plane device showed the lowest EQE despite the highest absorption spectra. This huge difference is attributed to the better carrier transport and collection on nonpolar m-plane devices due to the reduced polarization effects, which were further confirmed by bias-dependent EQE measurements and energy band diagram simulations. This study demonstrates the high potential of nonpolar and semipolar InGaN solar cells and can serve as guidance for the future design and fabrication of high efficiency III-nitride solar cells.

Polarity-dependent effect of humidity on the resistive switching characteristics of nonpolar devices

The roles of moisture in resistive switching (RS) devices are closely related to the RS mechanism. In principle, the nonpolar RS promises symmetric behaviors independent of the polarities of operating voltages. However, the effect of humidity on the RS characteristics of Pt/TiO2−x/Pt nonpolar cells is confirmed to be polarity-dependent. The positive electroforming threshold voltage decreases when humidity increases, whereas the negative one is unaffected. This asymmetric phenomenon can be attributed to the polarity-associated rule of current varying with humidity before electroforming. The voltage distribution in the device and then the electroforming threshold voltage are modified.

Integrin and dystroglycan compensate each other to mediate laminin-dependent basement membrane assembly and epiblast polarization

During early embryogenesis, endodermal γ1-laminin expression is required for basement membrane (BM) assembly, promoting conversion of non-polar pluripotent cells into polarized epiblast. The influence of laminin-111 (Lm111) and its integrin and dystroglycan (DG) receptors on epiblast in embryoid bodies (EBs), a model for differentiation of the embryonic plate, was further investigated. Lm111 added to the medium of EBs initiated conversion of inner nonpolar cell to the polarized epiblast epithelium with an exterior-to-central basal-to-apical orientation. Microinjection of Lm111 into EB interiors resulted in an interior BM with complete inversion of cell polarity. Lm111 assembled a BM on integrin-β1 null EBs with induction of polarization at reduced efficiency. β-Integrin compensation was not detected in these nulls with integrin adaptor proteins failing to assemble. A dimer of laminin LG domains 4–5 (LZE3) engineered to strongly bind to α-dystroglycan almost completely inhibited laminin accumulation on integrin β1-null EBs, reducing BM and ablating cell polarization. When Lm111 was incubated with integrin-β1/dystroglycan double-knockout EBs, laminin failed to accumulate on the EBs, the EBs did not differentiate, and the EBs underwent apoptosis. Collectively the findings support the hypotheses that the locus of laminin cell surface assembly can determine the axis of epithelial polarity. This requires integrin- and/or dystroglycan-dependent binding to laminin LG domains with the highest efficiency achieved when both receptors are present. Finally, EBs that cannot assemble a matrix undergo apoptosis.

Structural and optical study of core–shell InGaN layers of nanorod arrays with multiple stacks of InGaN/GaN superlattices for absorption of longer solar spectrum

We report on the material and optical properties of core–shell InGaN layers grown on GaN nanorod arrays. The core–shell InGaN layers were well grown on polarization-reduced surfaces such as semipolar pyramids and nonpolar sidewalls. In addition, to compensate the biaxial strain between GaN and InGaN layers, we grew interlayers underneath a thick InGaN layer. Here, the interlayers were composed of multiple superlattice structures. We could observe that the indium composition of core–shell InGaN structures increased with the number of interlayers. This indicates that the absorption energy band of InGaN alloys can be better matched to the spectral irradiance of the solar spectrum in nature. We also implemented a simulation of Ga-polar and nonpolar InGaN-based solar cells based on the indium composition obtained from the experiments. The result showed that nonpolar InGaN solar cells had a much higher efficiency than Ga-polar InGaN solar cells with the same thickness of the absorption layer.

Novel Vein Patterns in Arabidopsis Induced by Small Molecules.

The critical role of veins in transporting water, nutrients, and signals suggests that some key regulators of vein formation may be genetically redundant and, thus, undetectable by forward genetic screens. To identify such regulators, we screened more than 5000 structurally diverse small molecules for compounds that alter Arabidopsis (Arabidopsis thaliana) leaf vein patterns. Many compound-induced phenotypes were observed, including vein networks with an open reticulum; decreased or increased vein number and thickness; and misaligned, misshapen, or nonpolar vascular cells. Further characterization of several individual active compounds suggests that their targets include hormone cross talk, hormone-dependent transcription, and PIN-FORMED trafficking.

The role of microtubules in electrotaxis of rat Walker carcinosarcoma WC256 cells.

The endogenous electric field may provide an important signal for directional cell migration during cancer metastasis but the mechanism of cell electrotaxis is poorly understood. It was postulated that microtubules play a central role in the polarization and directional migration of several types of cells. In this paper we investigated the role of microtubules in electrotaxis of rat Walker carcinosarcoma WC256 cells. We found that colchicine-stimulated disassembly of microtubules caused the formation of blebs instead of lamellipodia at the front of about 45% of cells. Most of the remaining cells contracted and became rounded or transformed into non-polar cells. Depolymerization of microtubules in both subpopulations of cells reduced the directionality of cell migration to about 50% of the control, but bleb- forming cells migrated much more efficiently than lamellipodia-forming cells. The analysis of microtubules architecture in the presence of an endogenous electric field showed that there is no relationship between the direction of migration and the polarization of microtubules. These results suggest that microtubules are not indispensable for electrotaxis of WC256 cells, however they may improve the directionality of cell migration.

Fine-tuning of cortical progenitor proliferation by thalamic afferents.

During cerebral cortical cortex neurogenesis two major types of progenitors generate a variety of morphologically and functionally diverse projection neurons destined for the different cortical layers in non-gyrified mice. Radial glia cells (RGCs) undergo mitosis in the cortical ventricular zone and exhibit an apical-basal cell polarity, whereas non-polar intermediate progenitor cells (IPCs) divide basally in the subventricular zone (Franco and Muller, 2013; Taverna et al., 2014). The contribution of these cortical progenitor subtypes to particular cortical layers remains debated. Several lines of evidence suggest that IPCs give rise to the majority of cortical neurons, while only 10–20 % are directly generated by apical progenitors (Franco and Muller, 2013). The generation of excitatory cortical neurons follows a temporal order with deep layer neurons born first and upper layers are generated successively during later stages of neurogenesis. Furthermore, the symmetry of mitotic division is instructive for the prospective fate of daughter cells and thus for their laminar destination (Taverna et al., 2014). Various intrinsic and extrinsic cues have been identified that regulate the division mode and cell fate of cortical precursors. In addition to intra-cortical control of cortical neurogenesis such as paracrine interactions between progenitor cells (North et al., 2009) and feedback signaling from post-mitotic neurons of the cortical plate (Seuntjens et al., 2009), extra-cortical signals exerting control over cortical proliferation are increasingly attracting attention. These include factors from the cortico-spinal fluid (Lehtinen and Walsh, 2011) or invading glutamatergic neurons (Teissier et al., 2012). However, the impact of invading thalamo-cortical axons on cortical neurogenesis and layer formation remains largely unknown. Previous in vitro studies suggested that thalamic fibres regulate cell cycle properties and division mode by releasing soluble factors (Dehay et al., 2001). In turn, our data show a contact-mediated extra-cortical regulation of cortical neurogenesis by invading thalamic afferents (Figure 1) (Gerstmann et al., 2015).

Polarity-Dependent Distribution of Angiomotin Localizes Hippo Signaling in Preimplantation Embryos

In preimplantation mouse embryos, the first cell fate specification to the trophectoderm or inner cell mass occurs by the early blastocyst stage. The cell fate is controlled by cell position-dependent Hippo signaling, although the mechanisms underlying position-dependent Hippo signaling are unknown. We show that a combination of cell polarity and cell-cell adhesion establishes position-dependent Hippo signaling, where the outer and inner cells are polar and nonpolar, respectively. The junction-associated proteins angiomotin (Amot) and angiomotin-like 2 (Amotl2) are essential for Hippo pathway activation and appropriate cell fate specification. In the nonpolar inner cells, Amot localizes to adherens junctions (AJs), and cell-cell adhesion activates the Hippo pathway. In the outer cells, the cell polarity sequesters Amot from basolateral AJs to apical domains, thereby suppressing Hippo signaling. The N-terminal domain of Amot is required for actin binding, Nf2/Merlin-mediated association with the E-cadherin complex, and interaction with Lats protein kinase. In AJs, S176 in the N-terminal domain of Amot is phosphorylated by Lats, which inhibits the actin-binding activity, thereby stabilizing the Amot-Lats interaction to activate the Hippo pathway. We propose that the phosphorylation of S176 in Amot is a critical step for activation of the Hippo pathway in AJs and that cell polarity disconnects the Hippo pathway from cell-cell adhesion by sequestering Amot from AJs. This mechanism converts positional information into differential Hippo signaling, thereby leading to differential cell fates.

Modeling For High Efficiency GaN/InGaN Solar Cell

GaN/InGaN heterostructure contains a unique property of piezoelectric polarization charges at the interface due to different thermal expansion coefficients. In this paper, we report a simple mathematical model for Ga-face GaN/InGaN heterostructure solar cell. The results obtained from the given model indicates that the piezoelectric polarization charges at the interface of Ga-face GaN/InGaN heterostructure improves the efficiency of a single GaN/InGaN heterostructure photovoltaic solar cell in comparison to the non-polar solar cells by 45% for AM 1.5. This structure can also provide a fundamental solar cell unit for developing very high efficiency MQW solar cell and a MJ solar cell using Ga-face GaN/InGaN structure.

Overexpression of claudin‐5 but not claudin‐3 induces formation of trans‐interaction–dependent multilamellar bodies

Tight junctions (TJs) regulate paracellular barriers and claudins (Cld) form the backbone of TJ strands. To elucidate the molecular mechanism of claudin polymer formation, TJs were reconstituted by claudin transfection of TJ-free HEK293 cells. Therewith, typical TJ stands can be found at cell-cell contacts. In addition, overexpression of Cld5-YFP induces formation of huge intracellular multilamellar bodies. In contrast, Cld3 does not induce similar structures. Inhibition of trans-interaction of Cld5 by Y148A substitution diminished formation of multilamellar bodies. These results demonstrate claudin subtype-specific oligomerization. Cld3 and Cld5 localize to the plasma membrane differentially. Phosphorylation at T207 of Cld5 was suggested to participate in regulation of Cld5 internalization. However, prevention of potential phosphorylation by T207A substitution did not increase Cld5 amount in the plasma membrane of transfected cells. Taken together, if carefully evaluated, transfection of claudin constructs in nonpolar cells is a powerful strategy to improve understanding of subcellular targeting and assembly of TJ proteins.

Simulation of Nonpolar p-GaN/i-N/n-GaN Solar Cells

It is well known that nitride-based devices suffer the polarization effects. A promising way to overcome the polarization effects is growth in a direction perpendicular to thec-axis (nonpolar direction). Nonpolar devices do not suffer polarization charge, and then they have a chance to achieve the high solar efficiency. The understanding of the solar performance of non-polar InGaN-based solar cells will be interesting. For a pin non-polar solar cell with GaN p- and n-cladding layers, the conduction band offset (or barrier height, ) between an intrinsic layer and n-GaN layer is an important issue correlating to the efficiency and fill factor. The efficiency and fill factor will be seriously degraded due to sufficiently high barrier height. To reduce a high barrier height, some graded layers with an energy bandgap between the energy bandgap of n-GaN and InxGa1−xN intrinsic layer can be inserted to the interface of n-GaN and InxGa1-xN layers. From simulation, it indicates that the insertion of graded layer is an effective method to lower energy barrier when there exists a high energy band offset in non-polar nitride devices.

A Novel Gene Inactivation System Reveals Altered Periplasmic Flagellar Orientation in aBorrelia burgdorferi fliLMutant

Motility and chemotaxis are essential components of pathogenesis for many infectious bacteria, including Borrelia burgdorferi, the causative agent of Lyme disease. Motility and chemotaxis genes comprise 5 to 6% of the genome of B. burgdorferi, yet the functions of most of those genes remain uncharacterized, mainly due to the paucity of a nonpolar gene inactivation system. In this communication, we describe the development of a novel gene inactivation methodology to target B. burgdorferi fliL, a putative periplasmic flagellar gene located in a large motility operon and transcribed by RNA polymerase containing σ(70). Although the morphology of nonpolar fliL mutant cells was indistinguishable from that of wild-type cells, the mutant exhibited a defective-motility phenotype. Cryo-electron tomography (cryo-ET) of intact organisms revealed that the periplasmic flagella in the fliL mutant were frequently tilted toward the cell pole instead of their normal orientation toward the cell body. These defects were corrected when the mutant was complemented in cis. Moreover, a comparative analysis of flagellar motors from the wild type and the mutant provides the first structural evidence that FliL is localized between the stator and rotor. Our results suggest that FliL is likely involved in coordinating or regulating the orientation of periplasmic flagella in B. burgdorferi.

21-P020 The apical–basal polarity kinase aPKC functions as a nuclear determinant and regulates cell proliferation and fate during Xenopus neurogenesis

During neurogenesis in Xenopus, apico-basally polarized superficial and non-polar deep cells take-up differential fates – only deep cells become primary neurons while superficial cells stay as progenitors for later wave(s) of neurogenesis. The polarity of the superficial cells is defined by the antagonistic interactions between apically localized atypical protein kinase C (aPKC) and basolateral Lethal Giant Larvae (Lgl). It is unknown whether the proteins affecting polarity of cells also affect their fate, and if so, then how membrane polarity information is transmitted to the nucleus is also not known. We show that over-expression of a constitutively active, membrane-tethered form of aPKC (aPKC-CAAX) suppresses primary neurogenesis, and promotes cell proliferation and superficial fate. Unexpectedly, these effects can be accounted for by a nuclear fraction of aPKC-CAAX, pointing towards shuttling of aPKC from membrane to the nucleus. Conversely, antagonising apical aPKC by Lgl2 over-expression causes depolarization and internalization of superficial cells; these internalized superficial cells form ectopic neurons when supplemented with a proneural factor like X-ngnr-1. These findings suggest that aPKC itself is a nuclear determinant, affecting mainly cell proliferation; and in the right environment, loss of aPKC is also permissive for a change in cell fate.

The apicobasal polarity kinase aPKC functions as a nuclear determinant and regulates cell proliferation and fate duringXenopusprimary neurogenesis

During neurogenesis in Xenopus, apicobasally polarised superficial and non-polar deep cells take up different fates: deep cells become primary neurons while superficial cells stay as progenitors. It is not known whether the proteins that affect cell polarity also affect cell fate and how membrane polarity information may be transmitted to the nucleus. Here, we examine the role of the polarity components, apically enriched aPKC and basolateral Lgl2, in primary neurogenesis. We report that a membrane-tethered form of aPKC (aPKC-CAAX) suppresses primary neurogenesis and promotes cell proliferation. Unexpectedly, both endogenous aPKC and aPKC-CAAX show some nuclear localisation. A constitutively active aPKC fused to a nuclear localisation signal has the same phenotypic effect as aPKC-CAAX in that it suppresses neurogenesis and enhances proliferation. Conversely, inhibiting endogenous aPKC with a dominant-negative form that is restricted to the nucleus enhances primary neurogenesis. These observations suggest that aPKC has a function in the nucleus that is important for cell fate specification during primary neurogenesis. In a complementary experiment, overexpressing basolateral Lgl2 causes depolarisation and internalisation of superficial cells, which form ectopic neurons when supplemented with a proneural factor. These findings suggest that both aPKC and Lgl2 affect cell fate, but that aPKC is a nuclear determinant itself that might shuttle from the membrane to the nucleus to control cell proliferation and fate; loss of epithelial cell polarity by Lgl2 overexpression changes the position of the cells and is permissive for a change in cell fate.

Sodium transport across the isolated epithelium of sheep omasum is influenced by luminal ammonia.

Ammonia is a physiological fermentation product in the forestomachs and is absorbed from the rumen and omasum. Cellular uptake of ammonia affects the intracellular pH of polar and non-polar cells. The effect of the uptake on the pH of the cytosol depends on the predominant form of ammonia. NH(3) uptake and its intracellular protonation tend to alkalinize the cytoplasm, whereas the uptake of NH(4)(+) acidifies the cytoplasm by reversing this reaction. Consequently, the absorption of ammonia across the omasal epithelium could cause a change of the intracellular pH and pH-dependent transport mechanisms like Na/H exchange. Because no information is available about the form of ammonia absorbed in the omasum and, hence, possible modulation of Na transport by ammonia, the effect of increasing luminal ammonia concentrations (0, 5, 15 and 30 mmol/l) on Na transport were studied. In epithelia of hay-fed animals, ammonia linearly inhibited Na transport in a dose-dependent manner, at a luminal pH of 7.40, but not at a pH of 6.40. Ammonia did not influence Na transport in epithelia of concentrate-fed animals. Because luminal ammonia did not consistently change the short circuit current or tissue conductance absorption of ammonia as NH(4)(+) appears to be unlikely. The predominant form of ammonia absorbed in the omasum is probably NH(3), which is protonated in the cytosol. The reduced availability of protons may be the cause of inhibition of Na transport via Na/H exchange.

Effect of ammonia on Na+ transport across isolated rumen epithelium of sheep is diet dependent.

The cellular uptake of ammonia affects the intracellular pH (pHi) of polar and non-polar cells. A predominant uptake of NH3 and its intracellular protonation tend to alkalinise the cytoplasm, whereas a predominant uptake of NH4(+) acidifies the cytoplasm by reversing this reaction. Hence, the well-known absorption of ammonia across the rumen epithelium probably causes a change in the pHi. The magnitude and direction of this change in pHi (acid or alkaline) depends on the relative transport rates of NH3 and NH4(+). Consequently, the intracellular availability of protons will influence the activity of the Na(+)-H(+) exchanger, which could affect transepithelial Na(+) transport. The aim of the present study has been to test this possible interaction between ruminal ammonia concentrations and Na(+) transport. The term ammonia is used to designate the sum of the protonated (NH4(+)) and unprotonated (NH3) forms. Isolated ruminal epithelium of sheep was investigated by using the Ussing-chamber technique in vitro. The present results indicate that ammonia inhibits Na(+) transport across the rumen epithelium of hay-fed sheep, probably by binding intracellular protons and thus inhibiting Na(+)-H(+) exchange. By contrast, ammonia stimulates Na(+) transport in concentrate-fed and urea-fed sheep, which develop an adaptation mechanism in the form of an increased metabolism of ammonia in the rumen mucosa and/or an increased permeability of rumen epithelium to the charged ammonium ion (NH4(+)). Intracellular dissociation of NH4(+) increases the availability of protons, which stimulate Na(+)-H(+) exchange. This positive effect of ruminal ammonia on Na(+) absorption may significantly contribute to the regulation of osmotic pressure of the ruminal fluid, because intraruminal ammonia concentrations up to 40 mmol/l have been reported.

Asymmetric localization of flotillins/reggies in preassembled platforms confers inherent polarity to hematopoietic cells.

Hematopoietic cells have long been defined as round, nonpolar cells that show uniform distribution of cell surface-associated molecules. However, recent analyses of the immunological synapse and the importance of lipid microdomains in signaling have shed new light on the aspect of lymphocyte polarization during the activation processes, but none of the molecules implicated so far in either the activation process or the microdomain residency are known to have a preferential localization in nonactivated cells. Chemical crosslinking and fluorescence resonance energy transfer methods have allowed the visualization of certain glycosylphosphatidylinositol-anchored proteins in lipid rafts but so far no microdomain resident protein has been shown to exist as visible stable platforms in the membrane. We report here that two lipid microdomain resident proteins, flotillins/reggies, form preassembled platforms in hematopoietic cells. These platforms recruit signaling molecules upon activation through lipid rafts. The preassembled platforms significantly differ from the canonical cholesterol-dependent "lipid rafts," as they are resistant to cholesterol-disrupting agents. Most evidence for the functional relevance of microdomains in living cells remains indirect. Using laser scanning confocal microscopy, we show that these proteins exist as stable, microscopically patent domains localizing asymmetrically to one pole of the cell. We present evidence that the asymmetric concentration of these microdomain resident proteins is built up during cytokinesis.