Tunable Single-Photon Emission with Wafer-Scale Plasmonic Array

Bright, scalable, and deterministic single-photon emission (SPE) is essential for quantum optics, nanophotonics, and optical information systems. Recently, SPE from hexagonal boron nitride (h-BN) has attracted intense interest because it is optically active and stable at room temperature. Here, we demonstrate a tunable quantum emitter array in h-BN at room temperature by integrating a wafer-scale plasmonic array. The transient voltage electrophoretic deposition (EPD) reaction is developed to effectively enhance the filling of single-crystal nanometals in the designed patterns without aggregation, which ensures the fabricated array for tunable performances of these single-photon emitters. An enhancement of ∼500% of the SPE intensity of the h-BN emitter array is observed with a radiative quantum efficiency of up to 20% and a saturated count rate of more than 4.5 × 106 counts/s. These results suggest the integrated h-BN-plasmonic array as a promising platform for scalable and controllable SPE photonics at room temperature

An Evolved RNA Recognition Motif That Suppresses HIV‑1 Tat/TAR-Dependent Transcription

Potent and selective recognition and modulation of disease-relevant RNAs remain a daunting challenge. We previously examined the utility of the U1A N-terminal RNA recognition motif as a scaffold for tailoring new RNA hairpin recognition and showed that as few as one or two mutations can result in moderate affinity (low μM dissociation constant) for the human immunodeficiency virus (HIV) trans-activation response element (TAR) RNA, an RNA hairpin controlling transcription of the human immunodeficiency virus (HIV) genome. Here, we use yeast display and saturation mutagenesis of established RNA-binding regions in U1A to identify new synthetic proteins that potently and selectively bind TAR RNA. Our best candidate has truly altered, not simply broadened, RNA-binding selectivity; it binds TAR with subnanomolar affinity (apparent dissociation constant of ∼0.5 nM) but does not appreciably bind the original U1A RNA target (U1hpII). It specifically recognizes the TAR RNA hairpin in the context of the HIV-1 5′-untranslated region, inhibits the interaction between TAR RNA and an HIV trans-activator of transcription (Tat)-derived peptide, and suppresses Tat/TAR-dependent transcription. Proteins described in this work are among the tightest TAR RNA-binding reagents–small molecule, nucleic acid, or protein–reported to date and thus have potential utility as therapeutics and basic research tools. Moreover, our findings demonstrate how a naturally occurring RNA recognition motif can be dramatically resurfaced through mutation, leading to potent and selective recognitionand modulationof disease-relevant RNA

Overexpression of Delta can rescue the defected wing margin in deprived <i>dBCAS2</i> fly.

<p>The coexpression of <i>dBCAS2</i>^<i>dsRNA</i> and <i>Dl</i> fly was generated under the control of <i>C96-GAL4</i>. (A) Control adult wing (<i>C96>+</i>). (B) Overexpression of <i>Delta</i> (<i>C96>Dl</i>). Arrow: sparse bristles; arrowhead: shortened wing vein. (C) The deformation of wing margin in (<i>C96>dBCAS2</i>^<i>dsRNA</i>). Arrowhead: sparse bristles; arrow: notched margin. (D) Overexpression of <i>Delta</i> with <i>dBCAS2</i>^<i>dsRNA</i> (<i>C96 >dBCAS2</i>^<i>dsRNA</i>, <i>Dl</i>). Scale bar, 0.5 mm.</p

BCAS2 does not regulate the transcription initiation of <i>Delta</i> but is involved in <i>Delta</i> pre-mRNA splicing.

<p>(A) Control of <i>Dl-lacZ</i> (red) in the <i>en</i>><i>GFP</i> wing disc stained with anti-β-gal antibody. (B) <i>en</i>><i>GFP</i>, <i>dBCAS2</i>^<i>dsRNA</i>. In the <i>dBCAS2</i>-depleted posterior compartment, marked by GFP, the expression of <i>Dl-lacZ</i> (red) gives a signal of similar strength as the normal anterior compartment. The expression of GFP and β-galactosidase were merged and displayed in the right panel. Images were taken by confocal microscopy, scale bar, 50 μm. (C). RNA expression of β-galactosidase. RNAs were extracted from wing discs of third instar larvae and subjected to RT-PCR to confirm the RNA expression of β-galactosidase driven by <i>Dl</i> promoter in <i>Act>dBCAS2</i>^<i>dsRNA</i> (lane 2) compared with the control (lane 1). The internal control, <i>rp49</i>. (D) Schematic diagram of primer design for detecting the intron-containing precursor mRNA (upper) and mRNA of <i>Delta</i> (lower). Primers, exons and introns are denoted with arrowheads, boxes and lines, respectively. (E) Coexpression of <i>dBCAS2</i> and <i>dBCAS2</i>^<i>dsRNA</i> in larvae can rescue the phenotypes of mRNA decrease and pre-mRNA accumulation caused by <i>dBCAS2</i>^<i>dsRNA</i>. The pre-mRNA and mRNA of <i>Delta</i> were analyzed by quantitative RT-PCR and described in the Materials and Methods. Each genotype was under the control of <i>Act5c-GAL4</i> driver. White bar: <i>Act5c>+;</i> black bar: <i>Act5c>dBCAS2</i>^<i>dsRNA</i>; gray bar: <i>Act5c>dBCAS2</i>^<i>dsRNA</i>, <i>dBCAS2</i>. Data are shown as means and SD relative to the controls from three independent experiments. The P-values was measured by the Student’s t-test. *<i>p</i><0.05, **<i>p</i><0.01.</p

BCAS2 Regulates Delta-Notch Signaling Activity through <i>Delta</i> Pre-mRNA Splicing in <i>Drosophila</i> Wing Development

<div><p>Previously, we showed that BCAS2 is essential for <i>Drosophila</i> viability and functions in pre-mRNA splicing. In this study, we provide strong evidence that BCAS2 regulates the activity of Delta-Notch signaling via <i>Delta</i> pre-mRNA splicing. Depletion of <i>dBCAS2</i> reduces <i>Delta</i> mRNA expression and leads to accumulation of <i>Delta</i> pre-mRNA, resulting in diminished transcriptions of Delta-Notch signaling target genes, such as <i>cut</i> and <i>E(spl)m8</i>. Furthermore, ectopic expression of human <i>BCAS2</i> (<i>hBCAS2</i>) and <i>Drosophila BCAS2</i> (<i>dBCAS2</i>) in a <i>dBCAS2</i>-deprived fly can rescue <i>dBCAS2</i> depletion-induced wing damage to the normal phenotypes. These rescued phenotypes are correlated with the restoration of <i>Delta</i> pre-mRNA splicing, which affects Delta-Notch signaling activity. Additionally, overexpression of <i>Delta</i> can rescue the wing deformation by deprivation of <i>dBCAS2</i>; and the depletion of <i>dBCAS2</i> can restore the aberrant eye associated with <i>Delta</i>-overexpressing retinas; providing supporting evidence for the regulation of Delta-Notch signaling by dBCAS2. Taken together, dBCAS2 participates in <i>Delta</i> pre-mRNA splicing that affects the regulation of Delta-Notch signaling in <i>Drosophila</i> wing development.</p></div

BCAS2 is involved in the regulation of Delta-Notch signaling.

<p>(A, B) Depletion of <i>dBCAS2</i>, driven by the wing margin <i>C96-GAL4</i> driver, generates a phenotype similar to reduction of Delta-Notch signaling activity. (A) Control wing (<i>C96</i>>+). (B) <i>dBCAS2</i>-depleted wing (<i>C96</i>><i>dBCAS2</i>^<i>dsRNA</i>). Arrow, loss of margin bristles; arrow head, wing notching. Scale bar, 0.5 mm. (C to M) Depletion of dBCAS2 decreases the activity of Delta-Notch signaling that can be restored by dBCAS2. The late third instar larval wing discs were driven under the control of <i>engrailed-GAL4</i> and immunostained with the indicated antibodies. (C, F, I, L) Control (<i>en</i>><i>GFP</i>); (D, G, J, M) <i>dBCAS2</i>-depletion (<i>en</i>><i>GFP</i>, <i>dBCAS2</i>^<i>dsRNA</i>); (E, H, K) Coexpression of <i>dBCAS2</i> with <i>dBCAS2</i>^<i>dsRNA</i> (<i>en</i>><i>GFP</i>, <i>dBCAS2</i>^<i>dsRNA</i>, <i>dBCAS2</i>). (C, D, E) Anti-Delta antibody. The normal pattern of Delta (red) can be seen in the cells of presumptive veins and on either side of the D/V boundary; (F, G, H) Anti-NICD antibody. The Notch expression can be observed in the presumptive intervein territories; (I, J, K) Anti-Cut antibody. The Cut expression is located in the stripe of D/V boundary; and (L, M) E(spl)m8-lacZ. <i>LacZ</i> reporter of <i>E(splm8)</i>, a Delta-Notch signaling target gene is expressed along the D/V boundary. Left of the panel: red stain with the indicated antigen expression in the anterior and posterior compartments. Right of the panel: the merged images reveal the simultaneous expression of the protein of interest (red) and GFP fluorescence (green) in the posterior. Images were taken by confocal microscopy, scale bar, 50 μm.</p

13% Efficiency Hybrid Organic/Silicon-Nanowire Heterojunction Solar Cell <i>via</i> Interface Engineering

Interface carrier recombination currently hinders the performance of hybrid organic–silicon heterojunction solar cells for high-efficiency low-cost photovoltaics. Here, we introduce an intermediate 1,1-bis[(di-4-tolylamino)phenyl]cyclohexane (TAPC) layer into hybrid heterojunction solar cells based on silicon nanowires (SiNWs) and conjugate polymer poly(3,4-ethylenedioxy-thiophene):poly(styrenesulfonate) (PEDOT:PSS). The highest power conversion efficiency reaches a record 13.01%, which is largely ascribed to the modified organic surface morphology and suppressed saturation current that boost the open-circuit voltage and fill factor. We show that the insertion of TAPC increases the minority carrier lifetime because of an energy offset at the heterojunction interface. Furthermore, X-ray photoemission spectroscopy reveals that TAPC can effectively block the strong oxidation reaction occurring between PEDOT:PSS and silicon, which improves the device characteristics and assurances for reliability. These learnings point toward future directions for versatile interface engineering techniques for the attainment of highly efficient hybrid photovoltaics