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ABSTRACT Wildlife can be exposed to antimicrobial-resistant bacteria (ARB) via multiple pathways. Spatial overlap with domestic animals is a prominent exposure pathway. However, most studies of wildlife-domestic animal interfaces have focused on livestock and little is known about the wildlife-companion animal interface. Here, we investigated the prevalence and phylogenetic relatedness of extended-spectrum cephalosporin-resistant (ESC-R) Escherichia coli from raccoons ( Procyon lotor ) and domestic dogs ( Canis lupus familiaris ) in the metropolitan area of Chicago, IL, USA. To assess the potential importance of spatial overlap with dogs, we explored whether raccoons sampled at public parks (i.e., parks where people and dogs could enter) differed in prevalence and phylogenetic relatedness of ESC-R E. coli to raccoons sampled at private parks (i.e., parks where people and dogs could not enter). Raccoons had a significantly higher prevalence of ESC-R E. coli (56.9%) than dogs (16.5%). However, the richness of ESC-R E. coli did not vary by host species. Further, core single-nucleotide polymorphism (SNP)-based phylogenetic analyses revealed that isolates did not cluster by host species, and in some cases displayed a high degree of similarity (i.e., differed by less than 20 core SNPs). Spatial overlap analyses revealed that ESC-R E. coli were more likely to be isolated from raccoons at public parks than raccoons at private parks, but only for parks located in suburban areas of Chicago, not urban areas. That said, ESC-R E. coli isolated from raccoons did not genetically cluster by park of origin. Our findings suggest that domestic dogs and urban/suburban raccoons can have a diverse range of ARB, some of which display a high degree of genetic relatedness (i.e., differ by less than 20 core SNPs). Given the differences in prevalence, domestic dogs are unlikely to be an important source of exposure for mesocarnivores in urbanized areas. IMPORTANCE Antimicrobial-resistant bacteria (ARB) have been detected in numerous wildlife species across the globe, which may have important implications for human and animal health. Wildlife can be exposed to ARB via numerous pathways, including via spatial overlap with domestic animals. However, the interface with domestic animals has mostly been explored for livestock and little is known about the interface between wild animals and companion animals. Our work suggests that urban and suburban wildlife can have similar ARB to local domestic dogs, but local dogs are unlikely to be a direct source of exposure for urban-adapted wildlife. This finding is important because it underscores the need to incorporate wildlife into antimicrobial resistance surveillance efforts, and to investigate whether certain urban wildlife species could act as additional epidemiological pathways of exposure for companion animals, and indirectly for humans. 

Abstract Sugar supply is a key component of hypoxia tolerance and acclimation in plants. However, a striking gap remains in our understanding of mechanisms governing sugar impacts on low-oxygen responses. Here, we used a maize (Zea mays) root-tip system for precise control of sugar and oxygen levels. We compared responses to oxygen (21 and 0.2%) in the presence of abundant versus limited glucose supplies (2.0 and 0.2%). Low-oxygen reconfigured the transcriptome with glucose deprivation enhancing the speed and magnitude of gene induction for core anaerobic proteins (ANPs). Sugar supply also altered profiles of hypoxia-responsive genes carrying G4 motifs (sources of regulatory quadruplex structures), revealing a fast, sugar-independent class followed more slowly by feast-or-famine-regulated G4 genes. Metabolite analysis showed that endogenous sugar levels were maintained by exogenous glucose under aerobic conditions and demonstrated a prominent capacity for sucrose re-synthesis that was undetectable under hypoxia. Glucose abundance had distinctive impacts on co-expression networks associated with ANPs, altering network partners and aiding persistence of interacting networks under prolonged hypoxia. Among the ANP networks, two highly interconnected clusters of genes formed around Pyruvate decarboxylase 3 and Glyceraldehyde-3-phosphate dehydrogenase 4. Genes in these clusters shared a small set of cis-regulatory elements, two of which typified glucose induction. Collective results demonstrate specific, previously unrecognized roles of sugars in low-oxygen responses, extending from accelerated onset of initial adaptive phases by starvation stress to maintenance and modulation of co-expression relationships by carbohydrate availability. 

Plants have evolved the ability to derive the benzenoid moiety of the respiratory cofactor and antioxidant, ubiquinone (coenzyme Q), either from the β-oxidative metabolism of p-coumarate or from the peroxidative cleavage of kaempferol. Here, isotopic feeding assays, gene co-expression analysis and reverse genetics identified Arabidopsis 4-COUMARATE-COA LIGASE 8 (4-CL8; At5g38120) as a contributor to the β-oxidation of p-coumarate for ubiquinone biosynthesis. The enzyme is part of the same clade (V) of acyl-activating enzymes than At4g19010, a p-coumarate CoA ligase known to play a central role in the conversion of p-coumarate into 4-hydroxybenzoate. A 4-cl8 T-DNA knockout displayed a 20% decrease in ubiquinone content compared with wild-type plants, while 4-CL8 overexpression boosted ubiquinone content up to 150% of the control level. Similarly, the isotopic enrichment of ubiquinone's ring was decreased by 28% in the 4-cl8 knockout as compared with wild-type controls when Phe-[Ring-13C6] was fed to the plants. This metabolic blockage could be bypassed via the exogenous supply of 4-hydroxybenzoate, the product of p-coumarate β-oxidation. Arabidopsis 4-CL8 displays a canonical peroxisomal targeting sequence type 1, and confocal microscopy experiments using fused fluorescent reporters demonstrated that this enzyme is imported into peroxisomes. Time course feeding assays using Phe-[Ring-13C6] in a series of Arabidopsis single and double knockouts blocked in the β-oxidative metabolism of p-coumarate (4-cl8; at4g19010; at4g19010 × 4-cl8), flavonol biosynthesis (flavanone-3-hydroxylase), or both (at4g19010 × flavanone-3-hydroxylase) indicated that continuous high light treatments (500 µE m−2 s−1; 24 h) markedly stimulated the de novo biosynthesis of ubiquinone independently of kaempferol catabolism.