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Abstract
The gut microbiome produces vitamins, nutrients, and neurotransmitters, and helps to modulate the host immune system—and also plays a major role in the metabolism of many exogenous compounds, including drugs and chemical toxicants. However, the extent to which specific microbial species or communities modulate hazard upon exposure to chemicals remains largely opaque. Focusing on the effects of collateral dietary exposure to the widely used herbicide atrazine, we applied integrated omics and phenotypic screening to assess the role of the gut microbiome in modulating host resilience in Drosophila melanogaster. Transcriptional and metabolic responses to these compounds are sex-specific and depend strongly on the presence of the commensal microbiome. Sequencing the genomes of all abundant microbes in the fly gut revealed an enzymatic pathway responsible for atrazine detoxification unique to Acetobacter tropicalis. We find that Acetobacter tropicalis alone, in gnotobiotic animals, is sufficient to rescue increased atrazine toxicity to wild-type, conventionally reared levels. This work points toward the derivation of biotic strategies to improve host resilience to environmental chemical exposures, and illustrates the power of integrative omics to identify pathways responsible for adverse health outcomes.
Brown et al. apply integrated omics and phenotypic screening to assess the role of the gut microbiome in modulating host resilience in Drosophila melanogaster. They find that Acetobacter tropicalis in gnotobiotic animals, is sufficient to rescue increased atrazine toxicity, which could pave the way for biotic strategies to improve host resilience to environmental chemical exposure.
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1 Environmental Genomics and Systems Biology Division, Lawrence Berkeley National Laboratory, Berkeley, USA (GRID:grid.184769.5) (ISNI:0000 0001 2231 4551); Centre for Computational Biology, University of Birmingham, Edgbaston, Birmingham, UK (GRID:grid.6572.6) (ISNI:0000 0004 1936 7486); University of California Berkeley, Department of Statistics, Berkeley, USA (GRID:grid.47840.3f) (ISNI:0000 0001 2181 7878); Arva Intelligence, Inc, Salt Lake City, USA (GRID:grid.47840.3f)
2 Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, USA (GRID:grid.184769.5) (ISNI:0000 0001 2231 4551)
3 Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, USA (GRID:grid.184769.5) (ISNI:0000 0001 2231 4551); Genentech Inc., 1 DNA Way, South San Francisco, USA (GRID:grid.418158.1) (ISNI:0000 0004 0534 4718)
4 School of Biosciences, University of Birmingham, Edgbaston, Birmingham, UK (GRID:grid.6572.6) (ISNI:0000 0004 1936 7486); Berlin Institute of Health@Charité, Berlin, Germany (GRID:grid.6572.6)
5 School of Biosciences, University of Birmingham, Edgbaston, Birmingham, UK (GRID:grid.6572.6) (ISNI:0000 0004 1936 7486)