On Valence-Band Splitting in Layered MoS₂

As a representative two-dimensional semiconducting transition-metal dichalcogenide (TMD), the electronic structure in layered MoS₂ is a collective result of quantum confinement, interlayer interaction, and crystal symmetry. A prominent energy splitting in the valence band gives rise to many intriguing electronic, optical, and magnetic phenomena. Despite numerous studies, an experimental determination of valence-band splitting in few-layer MoS₂ is still lacking. Here, we show how the valence-band maximum (VBM) splits for one to five layers of MoS₂. Interlayer coupling is found to contribute significantly to phonon energy but weakly to VBM splitting in bilayers, due to a small interlayer hopping energy for holes. Hence, spin–orbit coupling is still predominant in the splitting. A temperature-independent VBM splitting, known for single-layer MoS₂, is, thus, observed for bilayers. However, a Bose–Einstein type of temperature dependence of VBM splitting prevails in three to five layers of MoS₂. In such few-layer MoS₂, interlayer coupling is enhanced with a reduced interlayer distance, but thermal expansion upon temperature increase tends to decouple adjacent layers and therefore decreases the splitting energy. Our findings that shed light on the distinctive behaviors about VBM splitting in layered MoS₂ may apply to other hexagonal TMDs as well. They will also be helpful in extending our understanding of the TMD electronic structure for potential applications in electronics and optoelectronics

Rad23b and Ddit3 expression determined by realtime-PCR. Data analysis was done using the 2^-ΔΔCT method for relative quantification.

<p>The expression data was normalized to blood sample in control group. (A) early effects; (B) delay effects. ^*<i>P</i><0.05 versus control.</p

Real-time PCR on MeDIP-enriched DNA^a.

a<p>The data were the mean ratios of the signals in the immunoprecipitated DNA <i>vs</i> input DNA.</p><p>* <i>P</i><0.05 versus control and acute exposure group.</p><p>NA, no amplification.</p

Functional and pathway analysis of the 811 genes with hypermethylated promoter identified by MeDIP-chip.

<p>Gene ontology (GO) analysis by three domains: Biological Process (A), Cellular Component (B) and Molecular Function (C). (D) KEGG Pathway analysis.</p

Genome-Wide Screen of DNA Methylation Changes Induced by Low Dose X-Ray Radiation in Mice

<div><p>Epigenetic mechanisms play a key role in non-targeted effects of radiation. The purpose of this study was to investigate global hypomethylation and promoter hypermethylation of particular genes induced by low dose radiation (LDR). Thirty male BALB/c mice were divided into 3 groups: control, acutely exposed (0.5Gy X-rays), and chronic exposure for 10 days (0.05Gy/d×10d). High-performance liquid chromatography (HPLC) and MeDIP-quantitative polymerase chain reaction (qPCR) were used to study methylation profiles. DNMT1 and MBD2 expression was determined by qPCR and western blot assays. Methylation and expression of Rad23b and Ddit3 were determined by bisulfate sequencing primers (BSP) and qPCR, respectively. The results show that LDR induced genomic hypomethylation in blood 2 h postirraditaion, but was not retained at 1-month. DNMT1 and MBD2 were downregulated in a tissue-specific manner but did not persist. Specific hypermethylation was observed for 811 regions in the group receiving chronic exposure, which covered almost all key biological processes as indicated by GO and KEGG pathway analysis. Eight hypermethylated genes (Rad23b, Tdg, Ccnd1, Ddit3, Llgl1, Rasl11a, Tbx2, Scl6a15) were verified by MeDIP-qPCR. Among them, Rad23b and Ddit3 gene displayed tissue-specific methylation and downregulation, which persisted for 1-month postirradiation. Thus, LDR induced global hypomethylation and tissue-specific promoter hypermethylation of particular genes. Promoter hypermethylation, rather than global hypomethylation, was relatively stable. Dysregulation of methylation might be correlated with down-regulation of DNMT1 and MBD2, but much better understanding the molecular mechanisms involved in this process will require further study.</p></div

Rad23b and Ddit3 methylation determined by BSP.

<p>Bisulfite treated DNA was amplified by PCR with BSP primers. PCR products were cloned into the pUC57 vector, and five clones selected and sequenced from each sample. Methylation level was defined as the ratio of methylated CpG sites in all clones. (A) Typical sequencing results; (B) early effects, tissues were collected 2 h postirradiation; (C) delay effects, 1 month postirradiation. ^*<i>P</i><0.05 versus control.</p

Effects of low dose X-rays on global methylation levels in mouse blood.

<p>Whole blood was sampled 2(dC and 5-mdC) detected by HPLC. Standard curve of dC(A) and 5mdC (B). DNA hydrolyzate compared with standard by liquid chromatography, early effects (C) and delay effects (D). Global methylation represented by 5-mdC(%), early effects (E) and delay effects (F). *<i>P</i><0.05 versus control. ^△<i>P</i>>0.05 versus control.</p

DNMT1 and MBD2 expression determined by realtime-PCR (A,B) and Western blot (C,D).

<p>Data are representative of at least 3 independent experiments. Early effects mean 2(A,C); Delay effects mean 1 month postirradiation (B,D). PBMC, peripheral blood mononuclear cell. 1, control; 2, acute exposed to 0.5 Gy; 3, chronic fractionated exposure. ^*<i>P</i><0.05 versus control.</p

Additional file 2: Figure S1. of Identification and expression profiling of microRNAs involved in the stigma exsertion under high-temperature stress in tomato

Nucleotide bias at each position of identified miRNAs. Y-axis: frequency of A/U/G/C; X-axis: position in miRNAs. Figure S2. Real-time quantitative PCR validation of nine heat-responsive miRNAs in stamen (a) and pistil (b), respectively. Y-axis shows the log2 ratio of miRNAs expression in HS versus CK. SnoU6 was used as the internal control. Each bar represents the mean ± SE of triplicated assays. Figure S3. Distribution of tRNAs, snoRNAs, and snRNAs in stamen and pistil libraries. Y-axis: frequency of each category of small RNAs. Figure S4. qRT-PCR analysis of the expression of SlLAC4 in stamen (a) and pistil (b) under heat-stress treatment. SlUbi3 was used as the internal control. Each bar represents the mean ± SE of triplicated assays. (ZIP 508 kb

Additional file 1: Table S1. of Identification and expression profiling of microRNAs involved in the stigma exsertion under high-temperature stress in tomato

Evaluation of the correction of the reduplicate biological samples. Table S2. Known miRNAs identified from stamen and pistil libraries. Table S3. Differentially expressed known and novel miRNAs between stamen and pistil CK-2d libraries. Table S4. Novel miRNAs identified from stamen and pistil libraries. Table S5. Differentially expressed miRNAs shared between stamen and pistil under heat stress condition. Table S6. Stamen specific differentially expressed miRNAs. Table S7. Pistil specific differentially expressed miRNAs. Table S8. Target genes of differentially expressed miRNAs in stamen. Table S9. Target genes of differentially expressed miRNAs in pistil. Table S10. List of primers used for qRT-PCR analysis. Table S11. List of primers used for RLM-5′ RACE analysis. (XLS 299 kb