The first realization of a tunable band-gap in monolayer WS2(1-x) Se2x is demonstrated. The tuning of the bandgap exhibits a strong dependence of S and Se content, as proven by PL spectroscopy. Because of its remarkable electronic structure, monolayer WS2(1-x) Se2x exhibits novel electrochemical catalytic activity and offers long-term electrocatalytic stability for the hydrogen evolution reaction.

Piwi-piRNA (Piwi-interacting RNA) ribonucleoproteins (piRNPs) enforce retrotransposon silencing, a function critical for preserving the genome integrity of germ cells. The molecular functions of most of the factors that have been genetically implicated in primary piRNA biogenesis are still elusive. Here we show that MOV10L1 exhibits 5 ′ -to-3 ′ directional RNA-unwinding activity in vitro and that a point mutation that abolishes this activity causes a failure in primary piRNA biogenesis in vivo. We demonstrate that MOV10L1 selectively binds piRNA precursor transcripts and is essential for the generation of intermediate piRNA processing fragments that are subsequently loaded to Piwi proteins. Multiple analyses suggest an intimate coupling of piRNA precursor processing with elements of local secondary structures such as G quadruplexes. Our results support a model in which MOV10L1 RNA helicase activity promotes unwinding and funneling of the single-stranded piRNA precursor transcripts to the endonuclease that catalyzes the first cleavage step of piRNA processing.

Most cases of neonatal Escherichia coli meningitis develop as a result of hematogenous spread, but it is not clear how circulating E. coli crosses the blood-brain barrier. In an attempt to identify E. coli structures contributing to invasion into the central nervous system (CNS), TnphoA mutagenesis was performed with an invasive CSF isolate of E. coli K1 strain RS218 (O18:K1:H7), and TnphoA mutants were examined for their noninvasive capability in brain microvascular endothelial cells (BMEC). The noninvasive mutants exhibited the invasive ability of <1% of the parent strain. One of the noninvasive mutants (10A-23) with a single TnphoA insertion and no changes in phenotypic characteristics was found to be significantly less invasive into the CNS in the newborn rat model of hematogenous E. coli meningitis. The TnphoA inserts with flanking sequences were cloned and sequenced. A novel open reading frame (8.2 kDa) was identified. Open reading frame analysis indicated that the 8.2-kDa protein (Ibe10) contained multiple transmembrane domains. ibe10 was cloned into an expression vector, pQE30, and the purified Ibe10 was shown to inhibit invasion of BMEC by strain RS218. These findings indicate that ibe10 is one of the E. coli genes involved in the invasion of BMEC in vitro and in vivo.

Recently two-dimensional layered semiconductors with promising electronic and optical properties have opened up a new way for applications in atomically thin electronics and optoelectronics. Here we report a large-area growth of monolayer WSe2 directly on SiO2/Si substrates by a chemical vapor deposition (CVD) method under atmospheric pressure. A sub-cooling step was demonstrated to have a key role in achieving this large-area growth. The monolayer configuration of the as-grown WSe2 was proven by spherical-aberration-corrected high resolution scanning transmission electron microscopy (HRSTEM), atomic force microscopy (AFM), Raman spectroscopy and photoluminescence (PL) spectroscopy. P-type behavior of as-grown monolayer WSe2 with a mobility of ∼0.2 cm(2) V(-1) s(-1) and a carrier concentration of 1.11 × 10(18) cm(-3) was confirmed using back-gated field effect transistor (FET) devices. This large-area growth directly on a SiO2/Si substrate provides a new way to meet the industrial manufacturing requirements.

"Band gap engineering" in two-dimensional (2D) materials plays an important role in tailoring their physical and chemical properties. The tuning of the band gap is typically achieved by controlling the composition of the semiconductor alloys. However, large-area preparation of 2D alloys remains a major challenge. Here, we report the large-area synthesis of high-quality monolayered MoS2(1-x)Se2x with a size coverage of hundreds of microns using a chemical vapor deposition method. The photoluminescence (PL) spectroscopy results confirm the tunable band gap in MoS2(1-x)Se2x, which is modulated by varying the Se content. Atomic-scale analysis was performed and the chemical composition was characterized using high-resolution scanning transmission electron microscopy and X-ray photoemission spectroscopy. With the introduction of Se into monolayered MoS2, it leads to enhanced catalytic activity in an electrochemical reaction for hydrogen generation, compared to monolayered MoS2 and MoSe2. It is promising as a potential alternative to expensive noble metals.

Nanostructured molybdenum disulfide (MoS2) has emerged as a promising catalytic alternative to the widely used Pt in the hydrogen evolution reaction from water because it is inexpensive and earth-abundant. The central prerequisite in realizing its potential is to enhance the surface activities by increasing the concentration of metallic edge sites. However, MoS2 thermodynamics favors the presence of a two-dimensional basal plane, and therefore, the one-dimensional edge sites surrounding the basal plane are very limited. Herein, we report the first synthesis of single-crystal MoS2 nanobelts with the top surface fully covered by edge sites. The nanobelt structure comprises parallel stacked atomic layers with the basal plane vertical to the substrate, and these layer edges form the top surface of the nanobelt. The surface is highly active: it optically quenches all of the indirect band gap excitons and chemically leads to a high electrocatalytic hydrogen evolution efficiency (a low onset overpotential of 170 mV for an electrocatalytic current density of 20 mA/cm(2) and a Tafel slope of 70 mV/decade).

The physiological role of Escherichia coli azoreductase AzoR was studied. It was found that AzoR was capable of reducing several benzo-, naphtho-, and anthraquinone compounds, which were better substrates for AzoR than the model azo substrate methyl red. The ⌬azoR mutant displayed reduced viability when exposed to electrophilic quinones, which are capable of depleting cellular reduced glutathione (GSH). Externally added GSH can partially restore the impaired growth of the ⌬azoR mutant caused by 2-methylhydroquinone. The transcription of azoR was induced by electrophiles, including 2-methylhydroquinone, catechol, menadione, and diamide. A transcription start point was identified 44 bp upstream from the translation start point. These data indicated that AzoR is a quinone reductase providing resistance to thiol-specific stress caused by electrophilic quinones.

Escherichia coli K1 is the most common gram-negative organism causing neonatal meningitis, but the mechanism by whichE. coli K1 crosses the blood-brain barrier is incompletely understood. We have previously described the cloning and molecular characterization of a determinant, ibeA (also called ibe10), from the chromosome of an invasive cerebrospinal fluid isolate of E. coli K1 strain RS218 (O18:K1:H7). Here we report the identification of another chromosomal locus, ibeB, which allows RS218 to invade brain microvascular endothelial cells (BMEC). The noninvasive TnphoA mutant 7A-33 exhibited <1% the invasive ability of the parent strain in vitro in BMEC and was significantly less invasive in the central nervous system in the newborn rat model of hematogenousE. coli meningitis than the parent strain. The TnphoA insert with flanking sequences was cloned and sequenced. A 1,383-nucleotide open reading frame (ORF) encoding a 50-kDa protein was identified and termed ibeB. This ORF was found to be 97% identical to a gene encoding a 50-kDa hypothetical protein (p77211) and located in the 13-min region of the E. coli K-12 genome. However, no homology was observed between ibeB and other known invasion genes when DNA and protein databases in GenBank were searched. Like the TnphoA insertion mutant 7A-33, an isogenic ibeBdeletion mutant (IB7D5) was unable to invade BMEC. A 7.0-kb locus containing ibeB was isolated from a LambdaGEM-12 genomic library of E. coli RS218 and subcloned into a pBluescript KS vector (pKS7-7B). pKS7-7B was capable of completely restoring the BMEC invasion of the noninvasive TnphoA mutant 7A-33 and the ibeB deletion mutant IB7D5 to the level of the parent strain. More importantly, the ibeB deletion mutant IB7D5 was fully complemented by pFN476 carrying the ibeB ORF (pFN7C), indicating thatibeB is required for E. coli K1 invasion of BMEC. Taken together, these findings indicate that severalE. coli determinants, including ibeA andibeB, contribute to crossing of the blood-brain barrier.