Actin depolymerizing factor destrin governs cell migration in neural development during Xenopus embryogenesis.

The actin-based cytoskeleton is considered a fundamental driving force for cell differentiation and development. Destrin (Dstn), a member of the actin-depolymerizing factor family, regulates actin dynamics by treadmilling actin filaments and increasing globular actin pools. However, the specific developmental roles of dstn have yet to be fully elucidated. Here, we investigated the physiological functions of dstn during early embryonic development using Xenopus laevis as an experimental model organism. dstn is expressed in anterior neural tissue and neural plate during Xenopus embryogenesis. Depleting dstn promoted morphants with short body axes and small heads. Moreover, dstn inhibition extended the neural plate region, impairing cell migration and distribution during neurulation. In addition to the neural plate, dstn knockdown perturbed neural crest cell migration. Our data suggest new insights for understanding the roles of actin dynamics in embryonic neural development, simultaneously presenting a new challenge for studying the complex networks governing cell migration involving actin dynamics.

Mebendazole preferentially inhibits cilia formation and exerts anticancer activity by synergistically augmenting DNA damage.

The cilium is a microtubule-based organelle that plays a pivotal role in embryonic development and maintenance of physiological functions in the human body. In addition to their function as sensors that transduce diverse extracellular signals, including growth factors, fluid flow, and physical forces, cilia are intricately involved in cell cycle regulation and preservation of DNA integrity, as their formation and resorption dynamics are tightly linked to cell cycle progression. Recently, several studies have linked defects in specific ciliary proteins to the DNA damage response. However, it remains unclear whether and how primary cilia contribute to cancer development. Mebendazole (MBZ) is an anthelmintic drug with anticancer properties in some cancer cells. MBZ is continuously being tested for clinical studies, but the precise mechanism of its anticancer activities remains unknown. Here, using Xenopus laevis embryos as a model system, we discovered that MBZ significantly hinders cilia formation and induces DNA damage. Remarkably, primary cilium-bearing cancer cells exhibited heightened vulnerability to combined treatment with MBZ and conventional anticancer drugs. Our findings shed light on the specific influence of MBZ on cilia, rather than cytosolic microtubules, in triggering DNA damage, elucidating a previously unidentified mechanism underlying potential MBZ-mediated cancer therapy.

Unlocking the Potential of Porous Bi2Te3-Based Thermoelectrics Using Precise Interface Engineering through Atomic Layer Deposition.

Porous thermoelectric materials offer exciting prospects for improving the thermoelectric performance by significantly reducing the thermal conductivity. Nevertheless, porous structures are affected by issues, including restricted enhancements in performance attributed to decreased electronic conductivity and degraded mechanical strength. This study introduces an innovative strategy for overcoming these challenges using porous Bi0.4Sb1.6Te3 (BST) by combining porous structuring and interface engineering via atomic layer deposition (ALD). Porous BST powder was produced by selectively dissolving KCl in a milled mixture of BST and KCl; the interfaces were engineered by coating ZnO films through ALD. This novel architecture remarkably reduced the thermal conductivity owing to the presence of several nanopores and ZnO/BST heterointerfaces, promoting efficient phonon scattering. Additionally, the ZnO coating mitigated the high resistivity associated with the porous structure, resulting in an improved power factor. Consequently, the ZnO-coated porous BST demonstrated a remarkable enhancement in thermoelectric efficiency, with a maximum zT of approximately 1.53 in the temperature range of 333-353 K, and a zT of 1.44 at 298 K. Furthermore, this approach plays a significant role in enhancing the mechanical strength, effectively mitigating a critical limitation of porous structures. These findings open new avenues for the development of advanced porous thermoelectric materials and highlight their potential for precise interface engineering through the ALD.

Early life exposure to perfluorooctanesulfonate (PFOS) impacts vital biological processes in Xenopus laevis: Integrated morphometric and transcriptomic analyses.

Perfluorooctanesulfonate (PFOS) is a ubiquitous environmental pollutant associated with increasing health concerns and environmental hazards. Toxicological analyses of PFOS exposure are hampered by large interspecies variations and limited studies on the mechanistic details of PFOS-induced toxicity. We investigated the effects of PFOS exposure on Xenopus laevis embryos based on the reported developmental effects in zebrafish. X. laevis was selected to further our understanding of interspecies variation in response to PFOS, and we built upon previous studies by including transcriptomics and an assessment of ciliogenic effects. Midblastula-stage X. laevis embryos were exposed to PFOS using the frog embryo teratogenesis assay Xenopus (FETAX). Results showed teratogenic effects of PFOS in a time- and dose-dependent manner. The morphological abnormalities of skeleton deformities, a small head, and a miscoiled gut were associated with changes in gene expression evidenced by whole-mount in situ hybridization and transcriptomics. The transcriptomic profile of PFOS-exposed embryos indicated the perturbation in the expression of genes associated with cell death, and downregulation in adenosine triphosphate (ATP) biosynthesis. Moreover, we observed the effects of PFOS exposure on cilia development as a reduction in the number of multiciliated cells and changes in the directionality and velocity of the cilia-driven flow. Collectively, these data broaden the molecular understanding of PFOS-induced developmental effects, whereby ciliary dysfunction and disrupted ATP synthesis are implicated as the probable modes of action of embryotoxicity. Furthermore, our findings present a new challenge to understand the links between PFOS-induced developmental toxicity and vital biological processes.

Convergent differentiation of multiciliated cells.

Multiciliated cells (MCCs) are epithelial cells that control body fluid flow and contribute to the clearance of pathogenic microbes and other particles from the airways, egg transport in oviducts, and circulation of cerebrospinal fluid in the central nervous system. Although MCCs have shared functions to control fluid flow via coordinated motility of multiple ciliary structures, they are found in multiple mammalian tissues originating from distinct germ layers and differentiate via distinct developmental pathways. To understand the similarities and differences of MCCs in multiple tissues, we investigated single-cell transcriptome data of nasal epithelial cells, bronchial tubes, fallopian tubes, and ependymal cells in the subventricular zone from humans and mice by cross-species data integration. Expression of cilia-associated genes was indistinguishable between these MCCs, although cell populations had unique properties by the species and tissue, demonstrating that they share the same final differentiation status for ciliary functions. We further analyzed the final differentiation step of MCCs from their distinctive progenitors and confirmed their convergent gene set expression for ciliogenesis at the final step. These results may provide new insight into understanding ciliogenesis during the developmental process.

Nucleation and Layer Closure Behavior of Iridium Films Grown Using Atomic Layer Deposition.

Understanding the initial growth process during atomic layer deposition (ALD) is essential for various applications employing ultrathin films. This study investigated the initial growth of ALD Ir films using tricarbonyl-(1,2,3-η)-1,2,3-tri(tert-butyl)-cyclopropenyl-iridium and O2. Isolated Ir nanoparticles were formed on the oxide surfaces during the initial growth stage, and their density and size were significantly influenced by the growth temperature and substrate surface, which strongly affected the precursor adsorption and surface diffusion of the adatoms. Higher-density and smaller nanoparticles were formed at high temperatures and on the Al2O3 surface, forming a continuous Ir film with a smaller thickness, resulting in a very smooth surface. These findings suggest that the initial growth behavior of the Ir films affects their surface roughness and continuity and that a comprehensive understanding of this behavior is necessary for the formation of continuous ultrathin metal films.

A single-cell, time-resolved profiling of Xenopus mucociliary epithelium reveals nonhierarchical model of development.

The specialized cell types of the mucociliary epithelium (MCE) lining the respiratory tract enable continuous airway clearing, with its defects leading to chronic respiratory diseases. The molecular mechanisms driving cell fate acquisition and temporal specialization during mucociliary epithelial development remain largely unknown. Here, we profile the developing Xenopus MCE from pluripotent to mature stages by single-cell transcriptomics, identifying multipotent early epithelial progenitors that execute multilineage cues before specializing into late-stage ionocytes and goblet and basal cells. Combining in silico lineage inference, in situ hybridization, and single-cell multiplexed RNA imaging, we capture the initial bifurcation into early epithelial and multiciliated progenitors and chart cell type emergence and fate progression into specialized cell types. Comparative analysis of nine airway atlases reveals an evolutionary conserved transcriptional module in ciliated cells, whereas secretory and basal types execute distinct function-specific programs across vertebrates. We uncover a continuous nonhierarchical model of MCE development alongside a data resource for understanding respiratory biology.

Selective Dissolution-Derived Nanoporous Design of Impurity-Free Bi2 Te3 Alloys with High Thermoelectric Performance.

Thermoelectric technology, which has been receiving attention as a sustainable energy source, has limited applications because of its relatively low conversion efficiency. To broaden their application scope, thermoelectric materials require a high dimensionless figure of merit (ZT). Porous structuring of a thermoelectric material is a promising approach to enhance ZT by reducing its thermal conductivity. However, nanopores do not form in thermoelectric materials in a straightforward manner; impurities are also likely to be present in thermoelectric materials. Here, a simple but effective way to synthesize impurity-free nanoporous Bi0.4 Sb1.6 Te3 via the use of nanoporous raw powder, which is scalably formed by the selective dissolution of KCl after collision between Bi0.4 Sb1.6 Te3 and KCl powders, is proposed. This approach creates abundant nanopores, which effectively scatter phonons, thereby reducing the lattice thermal conductivity by 33% from 0.55 to 0.37 W m-1 K-1 . Benefitting from the optimized porous structure, porous Bi0.4 Sb1.6 Te3 achieves a high ZT of 1.41 in the temperature range of 333-373 K, and an excellent average ZT of 1.34 over a wide temperature range of 298-473 K. This study provides a facile and scalable method for developing high thermoelectric performance Bi2 Te3 -based alloys that can be further applied to other thermoelectric materials.

PCNB exposure during early embryogenic development induces developmental delay and teratogenicity by altering the gene expression in Xenopus laevis.

Pentachloronitrobenzene (PCNB) is an organochlorine fungicide commonly used to treat seeds against seedling infections and controlling snow mold on golf courses. PCNB has been demonstrated to be toxic to living organisms, including fish and several terrestrial organisms. However, only phenotypical deformities have been studied, and the effects of PCNB on early embryogenesis, where primary organogenesis occurs, have not been completely studied. In the current study, the developmental toxicity and teratogenicity of PCNB is evaluated by using frog embryo teratogenesis assay Xenopus (FETAX). Our results confirmed the teratogenic potential of PCNB revealing the teratogenic index of 1.29 during early embryogenesis. Morphological studies revealed tiny head, bent axis, reduced inter ocular distance, hyperpigmentation, and reduced total body lengths. Whole mount in situ hybridization and reverse transcriptase polymerase chain reaction were used to identify PCNB teratogenic effects at the gene level. The gene expression analyses revealed that PCNB was embryotoxic to the liver and heart of developing embryos. Additionally, to determine the most sensitive developmental stages to PCNB, embryos were exposed to the compound at various developmental stages, demonstrating that the most sensitive developmental stage to PCNB is primary organogenesis. Taken together, we infer that PCNB's teratogenic potential affects not just the phenotype of developing embryos but also the associated genes and involving the oxidative stress as a possible mechanism of toxicity, posing a hazard to normal embryonic growth. However, the mechanisms of teratogenesis require additional extensive investigation to be defined completely.

Ckb and Ybx2 interact with Ribc2 and are necessary for the ciliary beating of multi-cilia.

BACKGROUND: Motile cilia in a vertebrate are important to sustaining activities of life. Fluid flow on the apical surface of several tissues, including bronchial epithelium, ependymal epithelium, and fallopian tubules is generated by the ciliary beating of motile cilia. Multi-ciliated cells in ependymal tissue are responsible for the circulation of cerebrospinal fluid (CSF), which is essential for the development and homeostasis of the central nervous system, and airway tissues are protected from external contaminants by cilia-driven mucosal flow over the top of the airway epithelium. OBJECTIVE: A previous study reported that reduction of Ribc2 protein leads to disruption of ciliary beating in multi-ciliated cells. However, knowledge regarding the molecular function of Ribc2 is limited, thus currently available information is also limited. Therefore, we evaluated the importance of proteins involved in the interaction with Ribc2 in the process of ciliary beating. METHODS: Immunoprecipitation and mass spectrometry analysis was performed for the discovery of proteins involved in the interaction with Ribc2. Expression of the target gene was inhibited by injection of antisense morpholinos and measurement of the fluid flow on the embryonic epidermis of Xenopus was performed using fluorescent beads for examination of the ciliary beating of multi cilia. In addition, the flag-tagged protein was expressed by injection of mRNA and the changes in protein localization in the cilia were measured by immunostaining and western blot analysis for analysis of the molecular interaction between Ribc2 and Ribc2 binding proteins in multi-cilia. RESULTS: The IP/MS analysis identified Ckb and Ybx2 as Ribc2 binding proteins and our results showed that localization of both Ckb and Ybx2 occurs at the axoneme of multi-cilia on the embryonic epithelium of Xenopus laevis. In addition, our findings confirmed that knock-down of Ckb or Ybx2 resulted in abnormal ciliary beating and reduction of cilia-driven fluid flow on multi-cilia of Xenopus laevis. In addition, significantly decreased localization of Ckb or Ybx2 in the ciliary axoneme was observed in Ribc2-depleted multi-cilia. CONCLUSION: Ckb and Ybx2 are involved in the interaction with Ribc2 and are necessary for the ciliary beating of multi-cilia.

GJA1 depletion causes ciliary defects by affecting Rab11 trafficking to the ciliary base.

The gap junction complex functions as a transport channel across the membrane. Among gap junction subunits, gap junction protein α1 (GJA1) is the most commonly expressed subunit. A recent study showed that GJA1 is necessary for the maintenance of motile cilia; however, the molecular mechanism and function of GJA1 in ciliogenesis remain unknown. Here, we examined the functions of GJA1 during ciliogenesis in human retinal pigment epithelium-1 and Xenopus laevis embryonic multiciliated-cells. GJA1 localizes to the motile ciliary axonemes or pericentriolar regions beneath the primary cilium. GJA1 depletion caused malformation of both the primary cilium and motile cilia. Further study revealed that GJA1 depletion affected several ciliary proteins such as BBS4, CP110, and Rab11 in the pericentriolar region and basal body. Interestingly, CP110 removal from the mother centriole was significantly reduced by GJA1 depletion. Importantly, Rab11, a key regulator during ciliogenesis, was immunoprecipitated with GJA1 and GJA1 knockdown caused the mislocalization of Rab11. These findings suggest that GJA1 regulates ciliogenesis by interacting with the Rab11-Rab8 ciliary trafficking pathway.

Advanced Atomic Layer Deposition: Ultrathin and Continuous Metal Thin Film Growth and Work Function Control Using the Discrete Feeding Method.

The ultrathin and continuous ruthenium (Ru) film was deposited through an improved atomic layer deposition (ALD) process with a discrete feeding method (DFM), called DF-ALD, employing a cut-in purge step during the precursor feeding. The excess precursor molecules can be physically adsorbed onto the chemisorbed precursors on the substrate during precursor feeding, which screens the reactive sites on the surface. Using DF-ALD, surface coverage of precursors was enhanced because the cut-in purge removes the physisorbed precursors securing the reactive sites beneath them; thus, nucleation density was greatly increased. Therefore, the grain size decreased, which changed the microstructure and increased oxygen impurity concentration. However, a more metallic Ru thin film was formed due to thermodynamic stability and improved physical density. Consequently, DF-ALD enables the deposition of the ultrathin (3 nm) and continuous Ru film with a low resistivity of ∼60 µΩ cm and a high effective work function of ∼4.8 eV.

Black Si Photocathode with a Conformal and Amorphous MoSx Catalytic Layer Grown Using Atomic Layer Deposition for Photoelectrochemical Hydrogen Evolution.

We demonstrated how the photoelectrochemical (PEC) performance was enhanced by conformal deposition of an amorphous molybdenum sulfide (a-MoSx) thin film on a nanostructured surface of black Si using atomic layer deposition (ALD). The a-MoSx is found to predominantly consist of an octahedral structure (S-deficient metallic phase) that exhibits high electrocatalytic activity for the hydrogen evolution reaction with a Tafel slope of 41 mV/dec in an acid electrolyte. The a-MoSx has a smaller work function (4.0 eV) than that of crystalline 2H-MoS2 (4.5 eV), which induces larger energy band bending at the p-Si surface, thereby facilitating interface charge transfer. These features enabled us to achieve an outstanding kinetic overpotential of ∼0.2 V at 10 mA/cm2 and an onset potential of 0.27 V at 1 mA/cm2. Furthermore, the a-MoSx layer provides superior protection against corrosion of the Si surface, enabling long-term PEC operation of more than 50 h while maintaining 87% or more performance. This work highlights the remarkable advantages of the ALD a-MoSx layer and leads to a breakthrough in the architectural design of PEC cells to ensure both high performance and stability.

Precision targeting tumor cells using cancer-specific InDel mutations with CRISPR-Cas9.

An ideal cancer therapeutic strategy involves the selective killing of cancer cells without affecting the surrounding normal cells. However, researchers have failed to develop such methods for achieving selective cancer cell death because of shared features between cancerous and normal cells. In this study, we have developed a therapeutic strategy called the cancer-specific insertions-deletions (InDels) attacker (CINDELA) to selectively induce cancer cell death using the CRISPR-Cas system. CINDELA utilizes a previously unexplored idea of introducing CRISPR-mediated DNA double-strand breaks (DSBs) in a cancer-specific fashion to facilitate specific cell death. In particular, CINDELA targets multiple InDels with CRISPR-Cas9 to produce many DNA DSBs that result in cancer-specific cell death. As a proof of concept, we demonstrate here that CINDELA selectively kills human cancer cell lines, xenograft human tumors in mice, patient-derived glioblastoma, and lung patient-driven xenograft tumors without affecting healthy human cells or altering mouse growth.

Augmented ERAD (ER-associated degradation) activity in chondrocytes is necessary for cartilage development and maintenance.

Chondrocytes secrete massive extracellular matrix (ECM) molecules that are produced, folded, and modified in the endoplasmic reticulum (ER). Thus, the ER-associated degradation (ERAD) complex-which removes misfolded and unfolded proteins to maintain proteostasis in the ER- plays an indispensable role in building and maintaining cartilage. Here, we examined the necessity of the ERAD complex in chondrocytes for cartilage formation and maintenance. We show that ERAD gene expression is exponentially increased during chondrogenesis, and disruption of ERAD function causes severe chondrodysplasia in developing embryos and loss of adult articular cartilage. ERAD complex malfunction also causes abnormal accumulation of cartilage ECM molecules and subsequent chondrodysplasia. ERAD gene expression is decreased in damaged cartilage from patients with osteoarthritis (OA), and disruption of ERAD function in articular cartilage leads to cartilage destruction in a mouse OA model.

Integrin ß-like 1 protein (ITGBL1) promotes cell migration by preferentially inhibiting integrin-ECM binding at the trailing edge.

BACKGROUND: Cell migration is a basic cellular behavior involved in multiple phenomena in the human body such as embryonic development, wound healing, immune reactions, and cancer metastasis. For proper cell migration, integrin and the ECM binding complex must be disassembled for the retraction of trailing edges. OBJECTIVE: Integrin must be differentially regulated at leading edges or trailing edges during cell migration. Previously, we showed that ITGBL1 was a secreted protein and inhibits integrin activity. Therefore, we examined the function of ITGBL1 on the retraction of trailing edges during cell migration. METHODS: To examined the function of ITGBL1 on cell migration, we knocked-down or overexpressed ITGBL1 by using ITGBL1 siRNA or ITGBL1 plasmid DNA in human chondrocytes or ATDC5 cells. We then characterized cellular migration and directionality by performing wound healing assays. Also, to analyze leading-edge formation and trailing-edge retraction, we labeled cell membranes with membrane-GFP and performed live imaging of migrating cells and. Finally, we specifically detected active forms of integrin, FAK and Vinculin using specific antibodies upon ITGBL1 depletion or overexpression. RESULT: In this study, ITGBL1 preferentially inhibited integrin activity at the trailing edges to promote cell migration. ITGBL1-depleted cells showed increased focal adhesions at the membranous traces of trailing edges to prevent the retraction of trailing edges. In contrast, overexpression of ITGBL1 upregulated directional cell migration by promoting focal adhesion disassembly at the trailing edges. CONCLUSION: ITGBL1 facilitates directional cell migration by promoting disassembly of the trailing edge focal adhesion complex.

Antiviral role of nanomaterials: a material scientist's perspective.

The present world continues to face unprecedented challenges caused by the COVID-19 pandemic. Collaboration between researchers of multiple disciplines is the need of the hour. There is a need to develop antiviral agents capable of inhibiting viruses and tailoring existing antiviral drugs for efficient delivery to prevent a surge in deaths caused by viruses globally. Biocompatible systems have been designed using nanotechnological principles which showed appreciable results against a wide range of viruses. Many nanoparticles can act as antiviral therapeutic agents if synthesized by the correct approach. Moreover, nanoparticles can act as carriers of antiviral drugs while overcoming their inherent drawbacks such as low solubility, poor bioavailability, uncontrolled release, and side effects. This review highlights the potential of nanomaterials in antiviral applications by discussing various studies and their results regarding antiviral potential of nanoparticles while also suggesting future directions to researchers.

Physiological Functions of Thiol Peroxidases (Gpx1 and Prdx2) during Xenopus laevis Embryonic Development.

Glutathione peroxidase 1 (Gpx1) and peroxiredoxin 2 (Prdx2) belong to the thiol peroxidase family of antioxidants, and have been studied for their antioxidant functions and roles in cancers. However, the physiological significance of Gpx1 and Prdx2 during vertebrate embryogenesis are lacking. Currently, we investigated the functional roles of Gpx1 and Prdx2 during vertebrate embryogenesis using Xenopus laevis as a vertebrate model. Our investigations revealed the zygotic nature of gpx1 having its localization in the eye region of developing embryos, whereas prdx2 exhibited a maternal nature and were localized in embryonic ventral blood islands. Furthermore, the gpx1-morphants exhibited malformed eyes with incompletely detached lenses. However, the depletion of prdx2 has not established its involvement with embryogenesis. A molecular analysis of gpx1-depleted embryos revealed the perturbed expression of a cryba1-lens-specific marker and also exhibited reactive oxygen species (ROS) accumulation in the eye regions of gpx1-morphants. Additionally, transcriptomics analysis of gpx1-knockout embryos demonstrated the involvement of Wnt, cadherin, and integrin signaling pathways in the development of malformed eyes. Conclusively, our findings indicate the association of gpx1 with a complex network of embryonic developmental pathways and ROS responses, but detailed investigation is a prerequisite in order to pinpoint the mechanistic details of these interactions.

Xenopus gpx3 Mediates Posterior Development by Regulating Cell Death during Embryogenesis.

Glutathione peroxidase 3 (GPx3) belongs to the glutathione peroxidase family of selenoproteins and is a key antioxidant enzyme in multicellular organisms against oxidative damage. Downregulation of GPx3 affects tumor progression and metastasis and is associated with liver and heart disease. However, the physiological significance of GPx3 in vertebrate embryonic development remains poorly understood. The current study aimed to investigate the functional roles of gpx3 during embryogenesis. To this end, we determined gpx3's spatiotemporal expression using Xenopus laevis as a model organism. Using reverse transcription polymerase chain reaction (RT-PCR), we demonstrated the zygotic nature of this gene. Interestingly, the expression of gpx3 enhanced during the tailbud stage of development, and whole mount in situ hybridization (WISH) analysis revealed gpx3 localization in prospective tail region of developing embryo. gpx3 knockdown using antisense morpholino oligonucleotides (MOs) resulted in short post-anal tails, and these malformed tails were significantly rescued by glutathione peroxidase mimic ebselen. The gene expression analysis indicated that gpx3 knockdown significantly altered the expression of genes associated with Wnt, Notch, and bone morphogenetic protein (BMP) signaling pathways involved in tailbud development. Moreover, RNA sequencing identified that gpx3 plays a role in regulation of cell death in the developing embryo. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and phospho-histone 3 (PH3) staining confirmed the association of gpx3 knockdown with increased cell death and decreased cell proliferation in tail region of developing embryos, establishing the involvement of gpx3 in tailbud development by regulating the cell death. Furthermore, these findings are inter-related with increased reactive oxygen species (ROS) levels in gpx3 knockdown embryos, as measured by using a redox-sensitive fluorescent probe HyPer. Taken together, our results suggest that gpx3 plays a critical role in posterior embryonic development by regulating cell death and proliferation during vertebrate embryogenesis.

Direct Evidence of Electronic Interaction at the Atomic-Layer-Deposited MoS2 Monolayer/SiO2 Interface.

The electronic structure of an atomic-layer-deposited MoS2 monolayer on SiO2 was investigated using X-ray absorption spectroscopy (XAS) and synchrotron X-ray photoelectron spectroscopy (XPS). The angle-dependent evolution of the XAS spectra and the photon-energy-dependent evolution of the XPS spectra were analyzed in detail using an ab initio electronic structure simulation. Although similar to the theoretical spectra of an ideal free-standing MoS2 ML, the experimental spectra exhibit features that are distinct from those of an ideal ML, which can be interpreted as a consequence of S-O van der Waals (vdW) interactions. The strong consensus among the experimental and theoretical spectra suggests that the vdW interactions between MoS2 and adjacent SiO2 layers can influence the electronic structure of the system, manifesting a substantial electronic interaction at the MoS2-SiO2 interface.