Controlled condensation by liquid contact-induced adaptations of molecular conformations in self-assembled monolayers.

Surface condensation control strategies are crucial but commonly require relatively tedious, time-consuming, and expensive techniques for surface-chemical and topographical engineering. Here we report a strategy to alter surface condensation behavior without resorting to any molecule-type or topographical transmutations. After ultrafast contact of liquids with and removal from surfaces, the condensation rate and density of water droplets on the surfaces decrease, the extent of which is positively correlated with the polarity of the liquid and the duration of contact. The liquid contact-induced condensation rate/density decrease (LCICD) can be attributed to the decrease of nucleation site density resulted from the liquid contact-induced adaption of surface molecular conformation. Based on this, we find that LCICD is applicable to various surfaces, on condition that there are flexible segments capable of shielding at least part of nucleation sites through changing the conformation under liquid contact induction. Leveraging the LCICD effect, we achieve erasable information storage on diverse substrates. Furthermore, our strategy holds promise for controlling condensation of other substances since LCICD is not specific to the water condensation process.

Kaistella yananensis sp. nov., a Novel Indoleacetic Acid-Producing Bacterium Isolated from the Root Nodules of Sophora davidii (Franch.) Skeels.

A novel endophytic bacterium, designated strain BT6-1-3T, was isolated from the root nodules of a leguminous shrub named Sophora davidii (Franch.) Skeels, found growing wild in Yan'an, Shaanxi Province, China. Cells were Gram-staining-negative, non-motile, catalase-positive, oxidase-positive, and did not produce H2S. Strain BT6-1-3T grew at 15-40 °C (optimum 30 °C), at pH 6.0-10.0 (optimum pH 9.0), and with 0-1% (w/v) NaCl (optimum 0.5%). The quinone system was menaquinone 6. The major fatty acids present in BT6-1-3T were iso-C11:0, iso-C15:0, and C16:0. The G+C content of genomic DNA was 39.4 mol% by whole genome sequencing. According to the analysis of 16S rRNA gene sequence, the closest relative was Kaistella montana WG4 (nucleotide identity was 97.6%). The genome of strain BT6-1-3T was sequenced, and the genome similarity was calculated using average nucleotide identity and genome-to-genome distance analysis with the genomes of other strains of Kaistella. Both strongly supported that the strain BT6-1-3T belonged to the genus Kaistella as a representative of a new species. Based on phylogenetic analysis, chemotaxonomic data, and physiological and biochemical characteristics, strain BT6-1-3T represents a new species of the genus Kaistella and is named as Kaistella yananensis sp. nov. Type strain is BT6-1-3T (= NBRC 115452T = CGMCC 1.60032T).

Developmental basis for intestinal barrier against the toxicity of graphene oxide.

BACKGROUND: Intestinal barrier is crucial for animals against translocation of engineered nanomaterials (ENMs) into secondary targeted organs. However, the molecular mechanisms for the role of intestinal barrier against ENMs toxicity are still largely unclear. The intestine of Caenorhabditis elegans is a powerful in vivo experimental system for the study on intestinal function. In this study, we investigated the molecular basis for intestinal barrier against toxicity and translocation of graphene oxide (GO) using C. elegans as a model animal. RESULTS: Based on the genetic screen of genes required for the control of intestinal development at different aspects using intestine-specific RNA interference (RNAi) technique, we identified four genes (erm-1, pkc-3, hmp-2 and act-5) required for the function of intestinal barrier against GO toxicity. Under normal conditions, mutation of any of these genes altered the intestinal permeability. With the focus on PKC-3, an atypical protein kinase C, we identified an intestinal signaling cascade of PKC-3-SEC-8-WTS-1, which implies that PKC-3 might regulate intestinal permeability and GO toxicity by affecting the function of SEC-8-mediated exocyst complex and the role of WTS-1 in maintaining integrity of apical intestinal membrane. ISP-1 and SOD-3, two proteins required for the control of oxidative stress, were also identified as downstream targets for PKC-3, and functioned in parallel with WTS-1 in the regulation of GO toxicity. CONCLUSIONS: Using C. elegans as an in vivo assay system, we found that several developmental genes required for the control of intestinal development regulated both the intestinal permeability and the GO toxicity. With the focus on PKC-3, we raised two intestinal signaling cascades, PKC-3-SEC-8-WTS-1 and PKC-3-ISP-1/SOD-3. Our results will strengthen our understanding the molecular basis for developmental machinery of intestinal barrier against GO toxicity and translocation in animals.

Antimicrobial proteins in the response to graphene oxide in Caenorhabditis elegans.

Upon exposure to environmental engineered nanomaterials (ENMs), animals will activate certain response signals to protect themselves from the toxic effects. However, the underlying molecular mechanisms for this response are still largely unclear. Using in vivo assay system of Caenorhabditis elegans, we here found that antimicrobial proteins of LYS-1, LYS-8, SPP-1, DOD-6, and F55G11.4 were activated by graphene oxide (GO) exposure. These antimicrobial proteins functioned as molecular targets of transcriptional factor DAF-16 in insulin signaling pathway, and acted in intestine to regulate the response to GO. Among these antimicrobial proteins, DOD-6, F55G11.4, and SPP-1 participated in the formation of signaling cascade of DAF-16-DOD-6-SOD-3-F55G11.4/SPP-1 in response to GO exposure by activating the antioxidation system. Different from this, LYS-1 and LYS-8, two lysozymes, mediated TUB-2 signaling and DAF-8-DAF-5 signaling cascade, respectively, to regulate the response to GO exposure. During the regulation of response to GO exposure, LYS-1 and LYS-8 acted synergistically, which could be largely explained by the observed synergistic interaction between TUB-2 and DAF-8. Therefore, our results demonstrate the crucial protection role of antimicrobial proteins for animals in response to environmental ENMs' exposure. The elucidated different signaling cascades mediated by antimicrobial proteins provide important molecular targets for future toxicity assessment and chemical modification of GO.

Wnt Ligands Differentially Regulate Toxicity and Translocation of Graphene Oxide through Different Mechanisms in Caenorhabditis elegans.

In this study, we investigated the possible involvement of Wnt signals in the control of graphene oxide (GO) toxicity using the in vivo assay system of Caenorhabditis elegans. In nematodes, the Wnt ligands, CWN-1, CWN-2, and LIN-44, were found to be involved in the control of GO toxicity. Mutation of cwn-1 or lin-44 gene induced a resistant property to GO toxicity and resulted in the decreased accumulation of GO in the body of nematodes, whereas mutation of cwn-2 gene induces a susceptible property to GO toxicity and an enhanced accumulation of GO in the body of nematodes. Genetic interaction assays demonstrated that mutation of cwn-1 or lin-44 was able to suppress the susceptibility to GO toxicity shown in the cwn-2 mutants. Loss-of-function mutations in all three of these Wnt ligand genes resulted in the resistance of nematodes to GO toxicity. Moreover, the Wnt ligands might differentially regulate the toxicity and translocation of GO through different mechanisms. These findings could be important in understanding the function of Wnt signals in the regulation of toxicity from environmental nanomaterials.

A mir-231-Regulated Protection Mechanism against the Toxicity of Graphene Oxide in Nematode Caenorhabditis elegans.

Recently, several dysregulated microRNAs (miRNAs) have been identified in organisms exposed to graphene oxide (GO). However, their biological functions and mechanisms of the action are still largely unknown. Here, we investigated the molecular mechanism of mir-231 in the regulation of GO toxicity using in vivo assay system of Caenorhabditis elegans. We found that GO exposure inhibited the expression of mir-231::GFP in multiple tissues, in particular in the intestine. mir-231 acted in intestine to regulate the GO toxicity, and overexpression of mir-231 in intestine caused a susceptible property of nematodes to GO toxicity. smk-1 encoding a homologue to mammalian SMEK functioned as a targeted gene for mir-231, and was also involved in the intestinal regulation of GO toxicity. Mutation of smk-1 gene induced a susceptible property to GO toxicity, whereas the intestinal overexpression of smk-1 resulted in a resistant property to GO toxicity. Moreover, mutation of smk-1 gene suppressed the resistant property of mir-231 mutant to GO toxicity. In nematodes, SMK-1 further acted upstream of the transcriptional factor DAF-16/FOXO in insulin signaling pathway to regulate GO toxicity. Therefore, mir-231 may encode a GO-responsive protection mechanism against the GO toxicity by suppressing the function of the SMK-1 - DAF-16 signaling cascade in nematodes.