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The domain morphology in the growth of transition-metal dichalcogenides (TMDCs) is mostly triangular but rarely dendritic. Here, we report a robust chemical vapor deposition method to fabricate atomic-thin 2H-phase MoS2 dendrites on several single-crystalline substrates with different lattice structures, such as rutile-TiO2(001), SrTiO3(001), and sapphire(0001). It is found that by tuning the concentration of Mo adatoms, the morphology of MoS2 domains on these substrates evolves from tridentate dendrites at a low Mo concentration to semicompact fractal domains at an intermediate Mo concentration, and to a compact triangular shape at a high Mo concentration. First-principles calculations reveal that the edge diffusion barrier of Mo is comparable to the attachment barrier, inhibiting fast Mo atom diffusion along the edge. Kinetics Monte Carlo simulations with varying Mo concentrations well reproduce the experimental results. Our combined experimental and theoretical analyses evidently show that the growth of MoS2 dendritic domains at a low Mo concentration is a nonequilibrium process, which is dominated by the kinetics of Mo adatoms. Our study presents an effective route to control the morphology of TMDCs by simply tuning the transition-metal adatom concentration.

2D crystalline MoS2 flakes with the dendritic shape have been controllably fabricated on a sapphire (0 0 0 1) substrate for catalytic applications in the hydrogen evolution reaction (HER) using atmospheric pressure chemical vapor deposition (CVD). The proposed growth process was controlled by separately setting the temperature of two precursors and heating MoO3 for 15 min in advance compared with the sulfur source. Then, under a sulfur-rich condition, the desired dendritic MoS2 monolayer flakes were obtained and exhibited a threefold symmetric feature. The individual branch of MoS2 dendrites was distinguished to be consisted of tiny triangular structures sequentially arranged by the corner to the bottom along the specific crystalline orientations. The shape evolution from the dendritic to the compact triangular morphology was further observed strongly depending on their regions located on the substrate along the carrier gas flow. The mechanism underlying the entire evolution process was discussed in relation to the CVD growth parameters, such as the sulfur-to-metal (S/M) flux ration, the introduction time of sulfur and the substrate symmetry. By carefully tailoring the growth condition, the large scale MoS2 dendrites monolayer flakes were obtained on sapphire substrate, which was strictly transferred on the Au foil to detect the photo-electrocatalytic properties. The photo-electrocatalytic HER of the thus dendritic MoS2 crystalline flakes and the compact triangular structures with different domain edge lengths in the same unit area were analytically compared. The lowered Tafel slope and the large exchange current density of the high-porous edge-exposed MoS2 dendrites in HER demonstrated that they are a promising HER catalyst.

Foot-and-mouth disease virus (FMDV) protein 2C is one of the most highly conserved viral proteins among the serotypes of FMDV. However, its effect on host cell response is not very clear. In our previous report, we showed that FMDV protein 2C interacts with cellular protein N-myc and STAT interactor (Nmi), inducing moderate apoptosis in cells. Here, we show that transfection of HEK293T cells with pEGFP-N1-2C or pEGFP-N1-Nmi induces activation of type I interferon promoters, leading to delayed vesicular stomatitis virus (VSV) growth. Using immunoprecipitation and confocal microscopy assays, we found that interferon-induced protein IFP35 interacts with Nmi. Knockdown of IFP35 expression by siRNA abolished pEGFP-N1-2C and pEGFP-N1-Nmi-induced activation of type I interferon promoters and restored VSV growth, suggesting that IFP35 plays a critical role in the type I interferon response induced by FMDV protein 2C. These findings may help to further understand cell responses to FMDV infection.