Putman, J. | Search bioRxiv

bioRxiv2025

Enantiomer-Specific Malathion Degradation by Gut Microbes of the Colorado Potato Beetle

Symbiotic microbes play pivotal roles in insect ecology, including the detoxification of insecticides, which reduces target host mortality and diminishes the efficacy of chemical pest control agents. Quantifying the prevalence of symbiont-mediated insecticide detoxification across the microbiome is necessary to understand its contributions to pesticide resistance, and to understand how pesticides alter gut microbial communities. Here, we investigated the prevalence and mechanisms of pesticide degradation within the gut microbiota of the Colorado potato beetle (Leptinotarsa decemlineata), a significant agricultural pest that has driven ongoing insecticide innovation for decades. Beetles were collected from an organic farm in Tyler, TX, and 18 bacterial isolates representing the diversity of their gut microbiota were screened for their ability to degrade three common insecticides in vitro: imidacloprid, fenitrothion, and malathion. Among these, Acinetobacter calcoaceticus, Pseudomonas protegens, and an unnamed Microbacterium species degraded malathion as a sole carbon source, with distinct enantiomer-specific preferences. Untargeted GC-MS analysis revealed breakdown products, providing initial insights into the metabolic pathways utilized by these microbes. These findings suggest that microbial association with resistant insect hosts may select for microbial insecticide utilization, potentially enhancing resistance development in agricultural pests and influencing the surrounding soil microbiome.

microbiology↗

bioRxiv2025

Loss of Sarm1 Mitigates Axonal and Neuronal Degeneration and Promotes Neuronal Repair After Ischemic Stroke

Axonal degeneration is a core feature of ischemic brain injury that limits functional recovery. The pro-degenerative molecule Sarm1 is required for Wallerian axon degeneration after traumatic and chemotoxic nerve injuries, however it is unclear if a similar mechanism mediates axonal degradation after ischemic injury. Here we show that loss of Sarm1 results in profound attenuation of axonal degeneration after focal ischemia to the subcortical white matter as well as to the cortex. Moreover, absence of Sarm1 significantly promotes the survival of neurons remote from but connected to the infarct after ischemic injuries to the subcortical white matter as well as to the cortex. Notably, loss of Sarm1 also significantly ameliorates early and late motor as well as cognitive deficits following white matter stroke. To further understand the mechanism of Sarm1-/- mediated neuronal protection, we performed differential gene expression analyses of wildtype and Sarm1-/- stroke-injured neurons and found that the loss of Sarm1 activates a pro-growth molecular program that promotes gene expression programs involved in axonogenesis and synaptogenesis after white matter ischemia. Using a functional genomics approach to recapitulate such a molecular program in Sarm1-/- neurons, we identify molecular compounds sufficient to enhance cortical neurite outgrowth in vitro, and all of which elicit a conserved epigenetic signature promoting axonogenesis. These results indicate that Sarm1 promotes axonal degeneration and concurrently inhibits an axonal reparative program encoded at the level of the epigenome that can be modulated pharmacologically. Our findings thus reveal a novel role for Sarm1 as a crucial regulator of both axonal degeneration and axonal repair after ischemic stroke.

neuroscience↗