As the global threat of plastic pollution has grown in scale and urgency, so have efforts to find sustainable and efficient solutions. Research conducted over the past few years has identified gut environments within insect larvae, including Tenebrio molitor (yellow mealworms), as microenvironments uniquely suited to rapid plastic biodegradation. However, there is currently limited understanding of how the insect host and its gut microbiome collaborate to create an environment conducive to plastic biodegradation. In this work, we provide evidence that T. molitor secretes one or more emulsifying factor(s) (30–100 kDa) that mediate plastic bioavailability. We also demonstrate that the insect gut microbiome secretes factor(s) (<30 kDa) that enhance respiration on polystyrene (PS). We apply these insights to culture PS-fed gut microbiome enrichments, with elevated rates of respiration and degradation compared to the unenriched gut microbiome. Within the enrichment, we identified eight unique gut microorganisms associated with PS biodegradation including Citrobacter freundii, Serratia marcescens, and Klebsiella aerogenes. Our results demonstrate that both the mealworm itself and its gut microbiome contribute to accelerated plastic biodegradation. This work provides new insights into insect-mediated mechanisms of plastic degradation and potential strategies for cultivation of plastic-degrading microorganisms in future investigations and scale-up.

One challenge in engineering organisms is taking responsibility for their behavior over many generations. Spontaneous mutations arising before or during use can impact heterologous genetic functions, disrupt system integration, or change organism phenotype. Here, we propose restructuring the genetic code itself such that point mutations in protein-coding sequences are selected against. Synthetic genetic systems so-encoded should fail more safely in response to most spontaneous mutations. We designed fail-safe codes and simulated their expected effects on the evolution of so-encoded proteins. We predict fail-safe codes supporting expression of 20 or 15 amino acids could slow protein evolution to ∼30% or 0% the rate of standard-encoded proteins, respectively. We also designed quadruplet-codon codes that should ensure all single point mutations in protein-coding sequences are selected against while maintaining expression of 20 or more amino acids. We demonstrate experimentally that a reduced set of 21 tRNAs is capable of expressing a protein encoded by only 20 sense codons, whereas a standard 64-codon encoding is not expressed. Our work suggests that biological systems using rationally depleted but otherwise natural translation systems should evolve more slowly and that such hypoevolvable organisms may be less likely to invade new niches or outcompete native populations.

Objective: Although self-disgust has been implicated in sexual assault-related posttraumatic stress disorder (PTSD), empirical evidence of this association is limited. Method: Participants with sexual assault-related PTSD (n = 19), sexual assault without PTSD (n = 20), and healthy controls (n = 21) completed “trait” measures of disgust proneness, self-disgust, and negative affect (NA; i.e., anxiety and depression). An ecological momentary assessment approach was also employed, where participants reported “state” levels of PTSD symptoms, self-disgust, and NA in the morning, afternoon, and evening for 1 week. Results: Those with PTSD reported more trait disgust proneness, self-disgust, and NA than those who experienced sexual assault without PTSD and controls. However, those experiencing sexual assault without PTSD and controls did not differ from each other. Participants with a history of sexual assault also experienced higher self-disgust and NA during the week than controls. Those with higher PTSD symptoms during the week also experienced more self-disgust and NA. Similarly, changes in PTSD symptoms were associated with changes in self-disgust and NA during the week. Although a temporal association was found where NA predicted subsequent PTSD symptoms (and vice versa) during the week, a temporal link between self-disgust and PTSD symptoms (or vice versa) was not found. Conclusions: These findings suggest that the link between self-disgust and sexual assault-related PTSD is more correlational than causal. The implications of these findings for understanding how trait and state self-disgust fits within the broader emotional network of sexual assault-related PTSD are discussed.

One challenge in engineering organisms is guaranteeing system behavior over many generations. Spontaneous mutations that arise before or during use can impact heterologous genetic functions, disrupt system integration, or change organism phenotype. Here, we propose restructuring the genetic code itself such that all point mutations in protein-coding sequences are selected against. Synthetic genetic systems so-encoded should "fail safely" in response to many individual spontaneous mutations. We designed a family of such fail-safe codes and analyzed their expected effect on the evolution of engineered organisms via simulation. We predict that fail-safe codes supporting expression of 20 or 15 amino acids could slow the evolution of proteins in so-encoded organisms to 30% or 0% the rate of standard-code organisms, respectively. We also designed quadruplet-codon codes that should be capable of encoding at least 20 amino acids while ensuring all single point mutations in protein-coding sequences are selected against. We show by in vitro experiments that a reduced set of 21 tRNA is capable of expressing a protein whose coding sequence is recoded to use a fail-safe code, whereas a standard-code encoding is not expressed. Our work suggests that a rationally depleted but otherwise natural translation system should yield biological systems with intrinsically reduced evolutionary capacity, and that so-encoded hypoevolvable organisms might be less likely to invade new niches or outcompete native populations.