In Situ Hydrothermal Construction of Direct Solid-State Nano-Z-Scheme BiVO₄/Pyridine-Doped g‑C₃N₄ Photocatalyst with Efficient Visible-Light-Induced Photocatalytic Degradation of Phenol and Dyes

In the current study, a mediator-free solid-state BiVO₄/pyridine-doped g-C₃N₄ nano-Z-scheme photocatalytic system (BDCN) with superior visible-light absorption and optimized photocatalytic activity was constructed via an in situ hydrothermal method for the first time. The pyridine-doped g-C₃N₄ (DCN) nanosheets show strong absorbance in the visible-light region by pyridine doping, and the BiVO₄ (∼10 nm) nanoparticles are successfully in situ grown on the surface of DCN nanosheets by the controlled hydrothermal method. Under the irradiation of visible light (λ > 420 nm), the BiVO₄/DCN nanocomposite photocatalysts efficiently degrade phenol and methyl orange (MO) and display much higher photocatalytic activity than the individual DCN, bulk BiVO₄, or the simple physical mixture of DCN and BiVO₄. The greatly improved photocatalytic ability is attributed to the construction of the direct Z-scheme system in the BiVO₄/DCN nanocomposite free from any mediator, which leads to enhanced separation of photogenerated electron–hole pairs, as confirmed by the photocurrent analysis. The possible Z-scheme mechanism of the BiVO₄/DCN nanocomposite photocatalyst was investigated by transient time-resolved luminescence decay spectrum, active species trapping experiments, electron paramagnetic resonance (EPR) technology, and hydrogen evolution test

Electrically Tunable Bandgaps in Bilayer MoS₂

Artificial semiconductors with manufactured band structures have opened up many new applications in the field of optoelectronics. The emerging two-dimensional (2D) semiconductor materials, transition metal dichalcogenides (TMDs), cover a large range of bandgaps and have shown potential in high performance device applications. Interestingly, the ultrathin body and anisotropic material properties of the layered TMDs allow a wide range modification of their band structures by electric field, which is obviously desirable for many nanoelectronic and nanophotonic applications. Here, we demonstrate a continuous bandgap tuning in bilayer MoS₂ using a dual-gated field-effect transistor (FET) and photoluminescence (PL) spectroscopy. Density functional theory (DFT) is employed to calculate the field dependent band structures, attributing the widely tunable bandgap to an interlayer direct bandgap transition. This unique electric field controlled spontaneous bandgap modulation approaching the limit of semiconductor-to-metal transition can open up a new field of not yet existing applications

Eye discs predominantly mutant for ESCRT-II are overgrown and lose cellular architecture.

<p>All discs are labeled for phalloidin and were obtained with the <i>eyFlp</i>-<i>cell lethal</i> system. Scale bars represent 100 µm. (A) Control eye-antennal imaginal disc. (B–D) Eye-antennal imaginal discs predominantly mutant for <i>vps22</i> (B), <i>vps25</i> (C) and <i>vps36</i> (D). Genotypes: (A) <i>eyFlp</i> ; <i>FRT82B</i>/<i>FRT82B cl GMR</i>-<i>hid</i>. (B) <i>eyFlp</i> ; <i>FRT82B vps22^5F8-3</i>/<i>FRT82B cl GMR</i>-<i>hid</i>. (C) <i>eyFlp</i> ; <i>FRT42 vps25^N55</i>/<i>FRT42 cl GMR</i>-<i>hid</i>. (D) <i>eyFlp</i> ; <i>vps36^L5212 FRT80</i>/<i>GMR</i>-<i>hid cl FRT80</i>.</p

Accumulation of Notch and Delta proteins in clones of ESCRT-II mutants.

<p>(A,B,C) Areas of increased Ubiquitin (Ub) immunoreactivity frequently co-localize with areas containing accumulated levels of the Notch receptor (antibody against the extracellular domain of Notch, N[extra]) in ESCRT-II mutant tissue. GFP/Ubiquitin/N^extra (green/red/blue) co-labelings of (A) <i>vps22^5F8-3</i>, (B) <i>vps25^N55</i> and (C) <i>vps36^L5212</i> eye mosaics. Scale bars represent 50 µm. (A′,B′,C′) Ubiquitin/N^extra (red/blue) co-labeling of (A′) <i>vps22^5F8-3</i>, (B′) <i>vps25^N55</i> and (C′) <i>vps36^L5212</i> eye mosaics. (A″,B″,C″) Ubiquitin labeling of (A″) <i>vps22^5F8-3</i>, (B″) <i>vps25^N55</i> and (C″) <i>vps36^L5212</i> eye mosaics. (A′″,B′″,C′″) N^extra labeling of (A′″) <i>vps22^5F8-3</i>, (B′″) <i>vps25^N55</i> and (C′″) <i>vps36^L5212</i> eye mosaics. (D,E,F) Accumulation of Notch protein using an antibody detecting the intracellular domain of Notch, N[intra]). GFP/N^intra (green, red) co-labelings of (D) <i>vps22^5F8-3</i>, (E) <i>vps25^N55</i> and (F) <i>vps36^L5212</i> eye mosaics. Scale bars represent 100 µm (D′,E′,F′) N^intra (red) labeling of (D′) <i>vps22^5F8-3</i>, (E′) <i>vps25^N55</i> and (F′) <i>vps36^L5212</i> eye mosaics. (G,H,I) The Notch ligand Delta accumulates in clones of ESCRT-II mutants. GFP/Delta (green/magenta) co-labeling of (G) <i>vps22^5F8-3</i>, (H) <i>vps25^N55</i> and (I) <i>vps36^L5212</i> eye mosaics. Scale bars represent 100 µm (G′,H′,I′) Delta labeling of (G′) <i>vps22^5F8-3</i>, (H′) <i>vps25^N55</i> and (I′) <i>vps36^L5212</i> eye mosaics. Genotypes: (A,D,G) <i>eyFlp</i>; <i>FRT82B vps22^5F8-3/FRT82B P[ubi-GFP]</i>. (B,E,H) <i>eyFlp</i> ; <i>FRT42D vps25^N55/FRT42D P[ubi-GFP]</i>. (C,F,I) <i>eyFlp</i> ; <i>vps36^L5212 FRT2A/P[ubi-GFP] FRT2A</i>.</p

Mutant clones of ESCRT-II components display endosomal defects and accumulate ubiquitinated proteins.

<p>Shown are eye imaginal discs of 3rd instar larvae mosaic for ESCRT-II mutants. Mutant clones are marked by the absence of GFP. Mutant clones of ESCRT-II components show abnormal accumulation of the early endosomal marker Hrs and accumulation of ubiquitin-conjugated proteins as visualized by the FK1 antibody. Hrs and ubiquitin-conjugated proteins accumulate in foci which frequently co-localize. Scale bars represent 50 µm. (A,B,C) GFP/Hrs/FK1 (green/red/blue) co-labelings of (A) <i>vps22^5F8-3</i>, (B) <i>vps25^N55</i> and (C) <i>vps36^L5212</i> eye mosaics. (A′,B′,C′) Hrs/FK1 (red/blue) co-labelings of (A′) <i>vps22^5F8-3</i>, (B′) <i>vps25^N55</i> and (C′) <i>vps36^L5212</i> eye mosaics. (A″,B″,C″) Hrs labeling of (A″) <i>vps22^5F8-3</i>, (B″) <i>vps25^N55</i> and (C″) <i>vps36^L5212</i> eye mosaics. (A′″,B′″,C′″) FK1 labeling of (A′″) <i>vps22^5F8-3</i>, (B′″) <i>vps25^N55</i> and (C′″) <i>vps36^L5212</i> eye mosaics. Genotypes: (A) <i>eyFlp</i> ; <i>FRT82B vps22^5F8-3</i>/<i>FRT82B</i> P[<i>ubi-GFP</i>]. (B) <i>eyFlp</i>; <i>FRT42D vps25^N55</i>/<i>FRT42D</i> P[<i>ubi-GFP</i>]. (C) <i>eyFlp</i> ; <i>vps36^L5212 FRT2A</i>/P[<i>ubi-GFP</i>] <i>FRT2A</i>.</p

Proliferation phenotype of ESCRT-II mosaics.

<p>Non-autonomous regulation of proliferation in <i>vps22</i> and <i>vps25</i> eye mosaics as depicted by BrdU incorporation (red). Arrows in (B) and (C) point to areas of increased BrdU density next to mutant clones. Compared to control discs, <i>vps36</i> mutations do not affect the proliferation pattern significantly. The scale bar represents 50 µm. (A–D) GFP/BrdU (green/red) co-labelings of (A) control, (B) <i>vps22^5F8-3</i>, (C) <i>vps25^N55</i> and (D) <i>vps36^L5212</i> eye mosaics. (A′–D′) BrdU labeling of (A′) control, (B′) <i>vps22^5F8-3</i>, (C′) <i>vps25^N55</i> and (D′) <i>vps36^L5212</i> eye mosaics. Genotypes: (A) <i>eyFlp</i>; <i>FRT42B/FRT42B P[ubi-GFP]</i>. (B) <i>eyFlp</i>; <i>FRT82B vps22^5F8-3/FRT82B P[ubi-GFP]</i>. (C) <i>eyFlp</i>; <i>FRT42D vps25^N55/FRT42D P[ubi-GFP]</i>. (D) <i>eyFlp</i>; <i>vps36^L5212 FRT2A/P[ubi-GFP] FRT2A</i>.</p

Adult phenotypes of ESCRT-II mosaics.

<p><i>vps22</i> and <i>vps25</i> mosaics display strong overgrowth phenotypes of the adult eyes and heads, and the larval eye imaginal discs. In contrast, <i>vps36</i> mutants show no or only a mild proliferation phenotype and cause a roughening of the adult eye. (A–D) Side view of genetic eye mosaics of (A) control flies, (B) <i>vps22^5F8-3</i>, (C) <i>vps25^N55</i> and (D) <i>vps36^L5212</i> mutants. (E–H) Eye mosaics of (E) control (heterozygous <i>Notch</i>), (F) <i>vps22^5F8-3</i>, (G) <i>vps25^N55</i> and (H) <i>vps36^L5212</i> in heterozygous <i>Notch</i> (<i>N</i>) background. The Notch allele used is <i>N^264-39</i>. (I–L) Top view of genetic mosaics of (I) control flies, (J) <i>vps22^5F8-3</i>, (K) <i>vps25^N55</i> and (L) <i>vps36^L5212</i> mutants. (M–P) Head mosaics of (M) control (heterozygous <i>Notch</i>), (N) <i>vps22^5F8-3</i>, (O) <i>vps25^N55</i> and (P) <i>vps36^L5212</i> in heterozygous <i>Notch</i> (<i>N</i>) background. The Notch allele used is <i>N^264-39</i>. (Q–T) Size comparison of (Q) control, (R) <i>vps22^5F8-3</i>, (S) <i>vps25^N55</i> and (T) <i>vps36^L5212</i> mosaic eye imaginal discs. Green: GFP; red: BrdU labeling. The scale bars represent 100 µm. Genotypes: (A) <i>eyFlp</i> ; <i>FRT82B/FRT82B P[w⁺]</i>. (B,J) <i>eyFlp</i> ; <i>FRT82B vps22^5F8-3/FRT82B P[w⁺]</i>. (C,K) <i>eyFlp</i> ; <i>FRT42D vps25^N55/FRT42D P[w⁺]</i>. (D,L) <i>eyFlp</i> ; <i>vps36^L5212 FRT2A/P[w⁺] FRT2A</i>. (E,M) <i>N^264-39</i>/+. (F–H) and (N–P): same as (B–D) and (J–L) except they also carry <i>N^264-39</i> as heterozygous mutation. (Q–T) same as in corresponding panels A–D except they carry P[ubi-GFP] instead of P[w⁺].</p

Suppression of the <i>GMR-hid</i>-eye ablation phenotype by ESCRT-II mosaics.

<p>(A) Expression of the pro-apoptotic gene <i>hid</i> under control of the eye-specific <i>GMR</i> enhancer (<i>GMR-hid</i>) gives rise to a strong eye ablation phenotype due to excessive apoptosis. (B–D) <i>vps25^N55</i> (C) and <i>vps36^L5212</i> (D) eye mosaics are strong suppressors of the <i>GMR-hid</i>-induced eye ablation phenotype in adult flies. <i>vps22^5F8-3</i> mosaics (B) do not suppress the <i>GMR-hid</i>-eye ablation phenotype. Genotypes: (A) <i>eyFlp ; GMR-hid</i>; <i>FRT82B/FRT82B P[w⁺]</i>. (B) <i>eyFlp</i>; <i>GMR-hid</i>; <i>FRT82B vps22^5F8-3/FRT82B P[w⁺]</i>. (C) <i>GMR-hid eyFlp</i>; <i>FRT42D vps25^N55/FRT42D P[w⁺]</i>. (D) <i>eyFlp</i>; <i>GMR-hid</i>; <i>vps36^L5212 FRT2A/P[w⁺] FRT2A</i>.</p

Apoptosis phenotype of ESCRT-II mutants.

<p>Labeling of <i>vps22</i>, <i>vps25</i> and <i>vps36</i> eye-antennal imaginal discs with cleaved Caspase-3 antibody as apoptotic marker. Arrows in (A′), (B′) and (C′) point to one representative clone in each panel containing increased caspase-3 activity. (A–C) GFP/Caspase-3 (green/red) co-labelings of (A) <i>vps22^5F8-3</i>, (B) <i>vps25^N55</i> and (C) <i>vps36^L5212</i> eye mosaics. (A′–C′) Caspase-3 labeling (red) of (A′) <i>vps22^5F8-3</i>, (B′) <i>vps25^N55</i> and (C′) <i>vps36^L5212</i> eye mosaics. Genotypes: (A) <i>eyFlp</i> ; <i>FRT82B vps22^5F8-3/FRT82B P[ubi-GFP]</i>. (B) <i>eyFlp</i> ; <i>FRT42D vps25^N55/FRT42D P[ubi-GFP]</i>. (C) <i>eyFlp</i> ; <i>vps36^L5212 FRT2A/P[ubi-GFP] FRT2A</i>.</p

Notch activity in ESCRT-II mutants.

<p>Notch activity in ESCRT-II mutants was assessed using the reporter transgene <i>E</i>(<i>spl</i>)<i>m8 2.61</i>-<i>lacZ</i> and β-Gal immunohistochemistry. In wild-type discs, this reporter is turned on posterior to the morphogenetic furrow (see bar in A″). Note that in <i>vps22^5F8-3</i> and <i>vps25^N55</i> mutant clones located anterior to the morphogenetic furrow ectopic reporter activity is detectable (arrows in A″ and B″). <i>vps36^L5212</i> clones do not or only weakly (arrow) induce reporter activity (C″). Genotypes: (A) <i>eyFlp</i>; <i>E</i>(<i>spl</i>)<i>m8 2.61</i>-<i>lacZ</i> ; <i>FRT82B vps22^5F8-3/FRT82B P[w⁺]</i>. (B) <i>eyFlp</i> ; <i>FRT42D vps25^N55 E</i>(<i>spl</i>)<i>m8 2.61</i>-<i>lacZ/FRT42D E</i>(<i>spl</i>)<i>m8 2.61-lacZ</i>. (C) <i>eyFlp</i> ; <i>E</i>(<i>spl</i>)<i>m8 2.61</i>-<i>lacZ</i>; <i>vps36^L5212 FRT2A/P[w⁺] FRT2A</i>.</p