Tuning Phase Composition of TiO₂ by Sn⁴⁺ Doping for Efficient Photocatalytic Hydrogen Generation

The anatase–rutile mixed-phase photocatalysts have attracted extensive research interest because of the superior activity compared to their single phase counterparts. In this study, doping of Sn⁴⁺ ions into the lattice of TiO₂ facilitates the phase transformation from anatase to rutile at a lower temperature while maintaining the same crystal sizes compared to the conventional annealling approach. The mass ratios between anatase and rutile phases can be easily manipulated by varying the Sn-dopant content. Characterization results reveal that the Sn⁴⁺ ions entered into the lattice of TiO₂ by substituting some of the Ti⁴⁺ ions and distributed evenly in the matrix of TiO₂. The substitution induced the distortion of the lattice structure, which realized the phase transformation from anatase to rutile at a lower temperature and the close-contact phase junctions were consequently formed between anatase and rutile, accounting for the efficient charge separations. The mixed-phase catalysts prepared by doping Sn⁴⁺ ions into the TiO₂ exhibit superior activity for photocatalytic hydrogen generation in the presence of Au nanoparticles, relatively to their counterparts prepared by the conventional annealling at higher temperatures. The band allignment between anatase and rutile phases is established based on the valence band X-ray photoelectron spectra and diffuse reflectance spectra to understand the spatial charge separation process at the heterojunction between the two phases. The study provides a new route for the synthesis of mixed-phase TiO₂ catalysts for photocatalytic applications and advances the understanding on the enhanced photocatalytic properties of anatase–rutile mixtures

Exploring the Origin of Enhanced Activity and Reaction Pathway for Photocatalytic H₂ Production on Au/B-TiO₂ Catalysts

Gold-embedded boron-doped TiO₂ (Au/B-TiO₂) photocatalysts were synthesized by a sol–gel hydrothermal method. The TEM images display that the gold nanoparticles were embedded into the B-TiO₂ framework. Hydrogen evolution under light irradiation showed that doping of boron into TiO₂ enhanced the photocatalytic activity. A further remarkable improvement of the activity was observed over the Au/B-TiO₂. Evidenced by B 1s XPS and ¹¹B MAS NMR spectra, the embedment of Au nanoparticles contributes to the formation of more interstitial boron species in B-TiO₂. In turn, it gives rise to surface or near-surface states facilitating the embedment of Au nanoparticles, as demonstrated by the Au 4f XPS spectra, which indicates the strong interaction between gold and the B-TiO₂ framework. This specific synergy significantly contributes to the enhancement of photocatalytic activity. For the first time, the isotopic tracer studies using a gas chromatograph isotope ratio mass spectrometer along with a series of control experiments reveal that the produced hydrogen originated mainly from water rather than methanol, whereas the direct oxidation of methanol did not lead to hydrogen generation. Acting as a sacrificial reagent, methanol could be oxidized to formaldehyde by protons/water under oxygen-free conditions

Table_2_NtbHLH49, a jasmonate-regulated transcription factor, negatively regulates tobacco responses to Phytophthora nicotianae.xls

Tobacco black shank caused by Phytophthora nicotianae is a devastating disease that causes huge losses to tobacco production across the world. Investigating the regulatory mechanism of tobacco resistance to P. nicotianae is of great importance for tobacco resistance breeding. The jasmonate (JA) signaling pathway plays a pivotal role in modulating plant pathogen resistance, but the mechanism underlying JA-mediated tobacco resistance to P. nicotianae remains largely unclear. This work explored the P. nicotianae responses of common tobacco cultivar TN90 using plants with RNAi-mediated silencing of NtCOI1 (encoding the perception protein of JA signal), and identified genes involved in this process by comparative transcriptome analyses. Interestingly, the majority of the differentially expressed bHLH transcription factor genes, whose homologs are correlated with JA-signaling, encode AtBPE-like regulators and were up-regulated in NtCOI1-RI plants, implying a negative role in regulating tobacco response to P. nicotianae. A subsequent study on NtbHLH49, a member of this group, showed that it’s negatively regulated by JA treatment or P. nicotianae infection, and its protein was localized to the nucleus. Furthermore, overexpression of NtbHLH49 decreased tobacco resistance to P. nicotianae, while knockdown of its expression increased the resistance. Manipulation of NtbHLH49 expression also altered the expression of a set of pathogen resistance genes. This study identified a set of genes correlated with JA-mediated tobacco response to P. nicotianae, and revealed the function of AtBPE-like regulator NtbHLH49 in regulating tobacco resistance to this pathogen, providing insights into the JA-mediated tobacco responses to P. nicotianae.</p

Table_3_NtbHLH49, a jasmonate-regulated transcription factor, negatively regulates tobacco responses to Phytophthora nicotianae.docx

Tobacco black shank caused by Phytophthora nicotianae is a devastating disease that causes huge losses to tobacco production across the world. Investigating the regulatory mechanism of tobacco resistance to P. nicotianae is of great importance for tobacco resistance breeding. The jasmonate (JA) signaling pathway plays a pivotal role in modulating plant pathogen resistance, but the mechanism underlying JA-mediated tobacco resistance to P. nicotianae remains largely unclear. This work explored the P. nicotianae responses of common tobacco cultivar TN90 using plants with RNAi-mediated silencing of NtCOI1 (encoding the perception protein of JA signal), and identified genes involved in this process by comparative transcriptome analyses. Interestingly, the majority of the differentially expressed bHLH transcription factor genes, whose homologs are correlated with JA-signaling, encode AtBPE-like regulators and were up-regulated in NtCOI1-RI plants, implying a negative role in regulating tobacco response to P. nicotianae. A subsequent study on NtbHLH49, a member of this group, showed that it’s negatively regulated by JA treatment or P. nicotianae infection, and its protein was localized to the nucleus. Furthermore, overexpression of NtbHLH49 decreased tobacco resistance to P. nicotianae, while knockdown of its expression increased the resistance. Manipulation of NtbHLH49 expression also altered the expression of a set of pathogen resistance genes. This study identified a set of genes correlated with JA-mediated tobacco response to P. nicotianae, and revealed the function of AtBPE-like regulator NtbHLH49 in regulating tobacco resistance to this pathogen, providing insights into the JA-mediated tobacco responses to P. nicotianae.</p

DataSheet_1_NtbHLH49, a jasmonate-regulated transcription factor, negatively regulates tobacco responses to Phytophthora nicotianae.docx

Tobacco black shank caused by Phytophthora nicotianae is a devastating disease that causes huge losses to tobacco production across the world. Investigating the regulatory mechanism of tobacco resistance to P. nicotianae is of great importance for tobacco resistance breeding. The jasmonate (JA) signaling pathway plays a pivotal role in modulating plant pathogen resistance, but the mechanism underlying JA-mediated tobacco resistance to P. nicotianae remains largely unclear. This work explored the P. nicotianae responses of common tobacco cultivar TN90 using plants with RNAi-mediated silencing of NtCOI1 (encoding the perception protein of JA signal), and identified genes involved in this process by comparative transcriptome analyses. Interestingly, the majority of the differentially expressed bHLH transcription factor genes, whose homologs are correlated with JA-signaling, encode AtBPE-like regulators and were up-regulated in NtCOI1-RI plants, implying a negative role in regulating tobacco response to P. nicotianae. A subsequent study on NtbHLH49, a member of this group, showed that it’s negatively regulated by JA treatment or P. nicotianae infection, and its protein was localized to the nucleus. Furthermore, overexpression of NtbHLH49 decreased tobacco resistance to P. nicotianae, while knockdown of its expression increased the resistance. Manipulation of NtbHLH49 expression also altered the expression of a set of pathogen resistance genes. This study identified a set of genes correlated with JA-mediated tobacco response to P. nicotianae, and revealed the function of AtBPE-like regulator NtbHLH49 in regulating tobacco resistance to this pathogen, providing insights into the JA-mediated tobacco responses to P. nicotianae.</p

Sensitization of Pt/TiO₂ Using Plasmonic Au Nanoparticles for Hydrogen Evolution under Visible-Light Irradiation

Au nanoparticles with different sizes (10, 20, 30, and 50 nm) were synthesized using a seed-assisted approach and anchored onto Pt/TiO₂ employing 3-mercaptopropionic acid as the organic linker. The sizes of the Au nanoparticles were controlled within a narrow range so that the size-dependent surface plasmonic resonance effect on sensitizing Pt/TiO₂ can be thoroughly studied. We found that 20 nm Au nanoparticles (Au₂₀) gave the best performance in sensitizing Pt/TiO₂ to generate H₂ under visible-light illumination. Photoelectrochemical measurements indicated that Au₂₀-Pt/TiO₂ exhibited the most efficient “hot” electrons separation among the studied catalysts, correlating well with the photocatalytic activity. The superior performance of Au-supported Pt/TiO₂ (Au₂₀-Pt/TiO₂) compared with Au anchored to TiO₂ (Au₂₀/TiO₂) revealed the important role of Pt as a cocatalyst for proton reduction. To elucidate how the visible-light excited hot electrons in Au nanoparticles involved in the proton-reduction reaction process, Au₂₀/TiO₂ was irradiated by visible light (λ > 420 nm) with the presence of Pt precursor (H₂PtCl₆) in a methanol aqueous solution under deaerated condition. Energy-dispersive X-ray spectroscopy mapping analysis on the recovered sample showed that Pt ions could be reduced on the surfaces of both Au nanoparticles and TiO₂ support. This observation indicated that the generated hot electrons on Au nanoparticles were injected into the TiO₂ conduction band, which were then subsequently transferred to Pt nanoparticles where proton reduction proceeded. Besides, the excited hot electrons could also participate in the proton reduction on Au nanoparticles surface

Table_1_NtbHLH49, a jasmonate-regulated transcription factor, negatively regulates tobacco responses to Phytophthora nicotianae.docx

Tobacco black shank caused by Phytophthora nicotianae is a devastating disease that causes huge losses to tobacco production across the world. Investigating the regulatory mechanism of tobacco resistance to P. nicotianae is of great importance for tobacco resistance breeding. The jasmonate (JA) signaling pathway plays a pivotal role in modulating plant pathogen resistance, but the mechanism underlying JA-mediated tobacco resistance to P. nicotianae remains largely unclear. This work explored the P. nicotianae responses of common tobacco cultivar TN90 using plants with RNAi-mediated silencing of NtCOI1 (encoding the perception protein of JA signal), and identified genes involved in this process by comparative transcriptome analyses. Interestingly, the majority of the differentially expressed bHLH transcription factor genes, whose homologs are correlated with JA-signaling, encode AtBPE-like regulators and were up-regulated in NtCOI1-RI plants, implying a negative role in regulating tobacco response to P. nicotianae. A subsequent study on NtbHLH49, a member of this group, showed that it’s negatively regulated by JA treatment or P. nicotianae infection, and its protein was localized to the nucleus. Furthermore, overexpression of NtbHLH49 decreased tobacco resistance to P. nicotianae, while knockdown of its expression increased the resistance. Manipulation of NtbHLH49 expression also altered the expression of a set of pathogen resistance genes. This study identified a set of genes correlated with JA-mediated tobacco response to P. nicotianae, and revealed the function of AtBPE-like regulator NtbHLH49 in regulating tobacco resistance to this pathogen, providing insights into the JA-mediated tobacco responses to P. nicotianae.</p

Table_4_NtbHLH49, a jasmonate-regulated transcription factor, negatively regulates tobacco responses to Phytophthora nicotianae.xls

Tobacco black shank caused by Phytophthora nicotianae is a devastating disease that causes huge losses to tobacco production across the world. Investigating the regulatory mechanism of tobacco resistance to P. nicotianae is of great importance for tobacco resistance breeding. The jasmonate (JA) signaling pathway plays a pivotal role in modulating plant pathogen resistance, but the mechanism underlying JA-mediated tobacco resistance to P. nicotianae remains largely unclear. This work explored the P. nicotianae responses of common tobacco cultivar TN90 using plants with RNAi-mediated silencing of NtCOI1 (encoding the perception protein of JA signal), and identified genes involved in this process by comparative transcriptome analyses. Interestingly, the majority of the differentially expressed bHLH transcription factor genes, whose homologs are correlated with JA-signaling, encode AtBPE-like regulators and were up-regulated in NtCOI1-RI plants, implying a negative role in regulating tobacco response to P. nicotianae. A subsequent study on NtbHLH49, a member of this group, showed that it’s negatively regulated by JA treatment or P. nicotianae infection, and its protein was localized to the nucleus. Furthermore, overexpression of NtbHLH49 decreased tobacco resistance to P. nicotianae, while knockdown of its expression increased the resistance. Manipulation of NtbHLH49 expression also altered the expression of a set of pathogen resistance genes. This study identified a set of genes correlated with JA-mediated tobacco response to P. nicotianae, and revealed the function of AtBPE-like regulator NtbHLH49 in regulating tobacco resistance to this pathogen, providing insights into the JA-mediated tobacco responses to P. nicotianae.</p

Supplement Number 1

Figures of XRD, resistivity, current induced switching sequence and spin Hall conductivit

Analysis of the Promoted Activity and Molecular Mechanism of Hydrogen Production over Fine Au–Pt Alloyed TiO₂ Photocatalysts

Fine metal nanoparticles (2–3 nm; Au, Pt, and alloyed Au–Pt) with a narrow size distribution were deposited on active TiO₂ through a facile chemical reduction method. Compared to the bare TiO₂, a remarkable enhancement of up to 10-fold for photocatalytic hydrogen evolution was achieved on the alloyed nanocomposites. By using core level and valence band XPS analysis, two electronic properties are shown to contribute to the promoted photocatalytic activity: stronger metal–support interaction between the alloyed structures and TiO₂ and higher electron population on the Au–Pt/TiO₂ photocatalysts in comparison with the bare TiO₂. Moreover, an improved charge separation over TiO₂ using Au–Pt nanoparticles was clearly evidenced by the significant increase of photocurrent responses obtained from the photoelectrochemical measurements. For the first time, in situ ¹³C and ¹H NMR spectroscopy was applied to monitor the gas–liquid–solid photocatalytic reactions under real working conditions. Via a two-electron oxidation pathway, the surface-adsorbed methanol was first oxidized to formaldehyde, followed by spontaneous hydrolysis and methanolysis to methanediol and methoxymethanol, rather than methyl formate and formic acid that have been previously reported in gaseous CH₃OH photocatalysis. The in situ monitoring also revealed that deposition of metal NPs would not alter the reaction pathways while making the reaction faster compared to the bare TiO₂