So far, how the animals evade the environmental nanomaterials is still largely unclear. In this study, we employed in vivo assay system of Caenorhabditis elegans to investigate the aversive behavior of nematodes to graphene oxide (GO) and the underlying neuronal basis. In this assay model, we detected the significant aversive behavior of nematodes to GO at concentrations more than 50 mg/L. Loss-of-function mutation of nlg-1 encoding a neuroligin with the function in connecting pre- and post-synaptic neurons suppressed the aversive behavior of nematodes to GO. Moreover, based on the neuron-specific activity assay, we found that the NLG-1 activity in AIY or AIB interneurons was required for the regulation of aversive behavior to GO. The neuron-specific activities of NLG-1 in AIY or AIB interneurons were also required for the regulation of GO toxicity. Using nlg-1 mutant as a genetic tool, we identified the AIY and AIB interneurons required for the regulation of aversive behavior to GO. Our results provide an important neuronal basis for the aversive response of animals to environmental nanomaterials.

The interaction between nanoplastics and bacteria remains still largely unclear. In this study, we determined the effect of nanopolystyrene particle (NP) on a bacterial pathogen of Acinetobacter johnsonii AC15. Scanning electron microscopy (SEM) analysis indicated the aggregation of NPs from 10 μg/L to 100 μg/L on surface of A. johnsonii AC15, suggesting that A. johnsonii AC15 acted as the vector for NPs. Exposure to 100–1000 μg/L NPs increased the growth and colony-forming unit (CFU) of A. johnsonii AC15. In addition, exposure to 100–1000 μg/L NPs enhanced the amount of formed biofilm of A. johnsonii AC15. Alterations in expressions of 3 survival-related (zigA, basD, and zur), 5 biofilm formation-related (ompA, bap, adeG, csuC, and csuD), and 3 serum resistance-related virulence genes (lpxC, lpxL, and pbpG) were observed after exposure to 1000 μg/L NPs. Moreover, both CFU and survival rate of A. johnsonii AC15 in normal human serum (NHS) were significantly increased by 1–1000 μg/L NPs, suggesting the enhancement in serum resistance of Acinetobacter pathogen by NPs. In the NHS, expressions of 3 survival-related (zigA, basD, and zur), 9 biofilm formation-related (ompA, bap, adeF, adeG, csuA/B, csuC, csuD, csuE, and hlyD), and 3 serum resistance-related virulence genes (lpxC, lpxL, and pbpG) were affected by 1000 μg/L NPs. Expressions of 1 survival-related (zigA), 5 biofilm formation-related (bap, adeG, csuC, csuD, and csuE), and 3 serum resistance-related virulence genes (lpxC, lpxL, and pbpG) were also altered by 10 μg/L NPs after the addition of NHS. Therefore, exposure to NPs in the range of μg/L has the potential to enhance bacterial virulence by increasing their growth, biofilm formation, and serum resistance.

As the primary energy source for a plant host and microbe to sustain life, sugar is generally exported by Sugars Will Eventually be Exported Transporters (SWEETs) to the host extracellular spaces or the apoplast. There, the host and microbes compete for hexose, sucrose, and other important nutrients. The host and microbial monosaccharide transporters (MSTs) and sucrose transporters (SUTs) play a key role in the “evolutionary arms race”. The result of this competition hinges on the proportion of sugar distribution between the host and microbes. In some plants (such as Arabidopsis, corn, and rice) and their interacting pathogens, the key transporters responsible for sugar competition have been identified. However, the regulatory mechanisms of sugar transporters, especially in the microbes require further investigation. Here, the key transporters that are responsible for the sugar competition in the host and pathogen have been identified and the regulatory mechanisms of the sugar transport have been briefly analyzed. These data are of great significance to the increase of the sugar distribution in plants for improvement in the yield.

Nanoplastics and microbial pathogens are both widely distributed in the environment; however, their combined toxicity remains largely unclear. Using Caenorhabditis elegans as an animal model, we examined the possible effect of exposure to polystyrene nanoparticle (PS-NP) in Acinetobacter johnsonii AC15 (a bacterial pathogen) infected animals. Exposure to PS-NP at the concentrations of 0.1-10 μg/L significantly enhanced the toxicity of Acinetobacter johnsonii AC15 infection on lifespan and locomotion behaviors. In addition, after exposure to 0.1-10 μg/L PS-NP, the accumulation of Acinetobacter johnsonii AC15 in body of nematodes was also increased. Meanwhile, the innate immune response indicated by the increase of antimicrobial gene expressions in Acinetobacter johnsonii AC15 infected nematodes was suppressed by exposure to 0.1-10 μg/L PS-NP. Moreover, expressions of egl-1, dbl-1, bar-1, daf-16, pmk-1, and elt-2 governing the bacterial infection and immunity in Acinetobacter johnsonii AC15 infected nematodes were further inhibited by exposure to 0.1-10 μg/L PS-NP. Therefore, our data suggested the possible exposure risk of nanoplastic at predicted environmental concentrations in enhancing the toxic effects of bacterial pathogens on environmental organisms.