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With the globally rising usage of plastics, including polyethylene terephthalate (PET), the environmental risk that disposal of waste plastics to landfills and discharge of microplastics to the marine environment pose have also increased. For example, observation of animal ingestion of fragmented waste plastics (micro-and nano-plastics) has driven awareness for the need of proper environmental risk assessment. In evaluating the biodegradability of PET-derived byproducts and their precursors, most work has focused on hydrolytic enzymes and aerobic or-ganisms that possess such genes, but only few reports on biodegradation in the absence of oxygen (i.e., anaerobic) are available. Here, to elucidate the fate of PET-derived materials under anaerobic environments, a sludge -derived microbial community was cultured with bis(2-hydroxyethyl) terephthalate (BHET) as a model sub-strate for byproducts of PET degradation and dimethyl terephthalate (DMT) as a potential environmental pollutant discharged from the PET manufacturing process. Metagenome-and metabolome-informed microbiome analyses identified anaerobic BHET and DMT degradation pathways, uncultured organisms affiliated with Spi-rochaetota and Negativicutes predominant in the BHET-fed cultures, and Methanomethylovorans and Trepone-ma_G predominant in the DMT-fed cultures. Metagenomic analyses newly identified three BHET-degrading and two DMT-degrading enzymes from the genomes of Spirochaeota. In addition, the Negativicutes in the BHET enrichment cultures possessed genes for acetogenically metabolizing EG and/or ethanol. Overall, this study successfully established anaerobic BHET-and DMT-degrading microbial consortia and newly proposed these degradation mechanisms under anaerobic conditions. This study indicated that the cultivation, microbiome, and metabolome analyses can be powerful tools for elucidating consortia capable of degrading plastics-associated waste compounds and the relevant metabolic mechanisms.

Background: The gut microbiome and fecal metabolites of breastfed infants changes during lactation, and are influenced by breast milk components. This study aimed to investigate dynamic associations of milk components with the infant gut microbiome and fecal metabolites throughout the lactation period in a mother-infant model.Methods: One month after delivery, breast milk and subsequent infant feces were collected in a pair for 5 months from a mother and an exclusively breastfed infant. Composition of the fecal microbiome was determined with 16S rRNA sequencing. Low-molecular-weight metabolites, including human milk oligosaccharides (HMOs), and antibacterial proteins were measured in feces and milk using H-1 NMR metabolomics and enzyme-linked immunosorbent assays. The association of milk bioactive components with the infant gut microbiome and fecal metabolites was determined with Python clustering and correlation analyses.Results: The HMOs in milk did not fluctuate throughout the lactation period. However, they began to disappear in infant feces at the beginning of month 4. Notably, at this time-point, a bifidobacterium species switching (from B. breve to B. longum subsp. infantis) occurred, accompanied by fluctuations in several metabolites including acetate and butyrate in infant feces.Conclusions: Milk bioactive components, such as HMOs, might play different roles in the exclusively breastfed infants depending on the lactation period.

Background: The gut microbiome and fecal metabolites of breastfed infants changes during lactation, and are influenced by breast milk components. This study aimed to investigate dynamic associations of milk components with the infant gut microbiome and fecal metabolites throughout the lactation period in a mother-infant model.Methods: One month after delivery, breast milk and subsequent infant feces were collected in a pair for 5 months from a mother and an exclusively breastfed infant. Composition of the fecal microbiome was determined with 16S rRNA sequencing. Low-molecular-weight metabolites, including human milk oligosaccharides (HMOs), and antibacterial proteins were measured in feces and milk using H-1 NMR metabolomics and enzyme-linked immunosorbent assays. The association of milk bioactive components with the infant gut microbiome and fecal metabolites was determined with Python clustering and correlation analyses.Results: The HMOs in milk did not fluctuate throughout the lactation period. However, they began to disappear in infant feces at the beginning of month 4. Notably, at this time-point, a bifidobacterium species switching (from B. breve to B. longum subsp. infantis) occurred, accompanied by fluctuations in several metabolites including acetate and butyrate in infant feces.Conclusions: Milk bioactive components, such as HMOs, might play different roles in the exclusively breastfed infants depending on the lactation period.

Nishiyama et al. report the biochemical pathway for the conversion of DEHU to alpha-ketoglutarate in the alginate-assimilating marine bacterium Flavobacterium sp. strain UMI-01. They show that a parallel oxidative pathway besides the reductive route is possible, and provide evidence that this pathway might be conserved in other alginate-degrading bacteria. Alginate-assimilating bacteria degrade alginate into an unsaturated monosaccharide, which is converted into 4-deoxy-L-erythro-5-hexoseulose uronic acid (DEHU). DEHU is reduced to 2-keto-3-deoxy-D-gluconate by a DEHU-specific reductase using NAD(P)H. This is followed by pyruvate production via the Entner-Doudoroff pathway. Previously, we identified FlRed as a DEHU reductase in an alginate-assimilating bacterium, Flavobacterium sp. strain UMI-01. Here, we showed that FlRed can also catalyze the oxidation of DEHU with NAD(+), producing 2-keto-3-deoxy-D-glucarate (KDGR). FlRed showed a predilection for NADH and NAD(+) over NADPH and NADP(+), respectively, and the K-m value for NADH was approximately 2.6-fold less than that for NAD(+). Furthermore, we identified two key enzymes, FlDet and FlDeg, for KDGR catabolism. FlDet was identified as an enzyme of the ribonuclease activity regulator A family, which converts KDGR to alpha-ketoglutaric semialdehyde (alpha-KGSA). FlDeg, a type II alpha-KGSA dehydrogenase, generated alpha-ketoglutaric acid by oxidizing the aldehyde group of alpha-KGSA using NAD(P)(+). Consequently, unlike the conventional DEHU reduction pathway, DEHU can be directly converted to alpha-ketoglutaric acid without consuming NAD(P)H. Alginate upregulated the expression of not only FlRed and two enzymes of the DEHU-reduction pathway, but also FlDet and FlDeg. These results revealed dual pathways of DEHU metabolism involving reduction or oxidation by FlRed.

Nishiyama et al. report the biochemical pathway for the conversion of DEHU to alpha-ketoglutarate in the alginate-assimilating marine bacterium Flavobacterium sp. strain UMI-01. They show that a parallel oxidative pathway besides the reductive route is possible, and provide evidence that this pathway might be conserved in other alginate-degrading bacteria. Alginate-assimilating bacteria degrade alginate into an unsaturated monosaccharide, which is converted into 4-deoxy-L-erythro-5-hexoseulose uronic acid (DEHU). DEHU is reduced to 2-keto-3-deoxy-D-gluconate by a DEHU-specific reductase using NAD(P)H. This is followed by pyruvate production via the Entner-Doudoroff pathway. Previously, we identified FlRed as a DEHU reductase in an alginate-assimilating bacterium, Flavobacterium sp. strain UMI-01. Here, we showed that FlRed can also catalyze the oxidation of DEHU with NAD(+), producing 2-keto-3-deoxy-D-glucarate (KDGR). FlRed showed a predilection for NADH and NAD(+) over NADPH and NADP(+), respectively, and the K-m value for NADH was approximately 2.6-fold less than that for NAD(+). Furthermore, we identified two key enzymes, FlDet and FlDeg, for KDGR catabolism. FlDet was identified as an enzyme of the ribonuclease activity regulator A family, which converts KDGR to alpha-ketoglutaric semialdehyde (alpha-KGSA). FlDeg, a type II alpha-KGSA dehydrogenase, generated alpha-ketoglutaric acid by oxidizing the aldehyde group of alpha-KGSA using NAD(P)(+). Consequently, unlike the conventional DEHU reduction pathway, DEHU can be directly converted to alpha-ketoglutaric acid without consuming NAD(P)H. Alginate upregulated the expression of not only FlRed and two enzymes of the DEHU-reduction pathway, but also FlDet and FlDeg. These results revealed dual pathways of DEHU metabolism involving reduction or oxidation by FlRed.

Nishiyama et al. report the biochemical pathway for the conversion of DEHU to alpha-ketoglutarate in the alginate-assimilating marine bacterium Flavobacterium sp. strain UMI-01. They show that a parallel oxidative pathway besides the reductive route is possible, and provide evidence that this pathway might be conserved in other alginate-degrading bacteria. Alginate-assimilating bacteria degrade alginate into an unsaturated monosaccharide, which is converted into 4-deoxy-L-erythro-5-hexoseulose uronic acid (DEHU). DEHU is reduced to 2-keto-3-deoxy-D-gluconate by a DEHU-specific reductase using NAD(P)H. This is followed by pyruvate production via the Entner-Doudoroff pathway. Previously, we identified FlRed as a DEHU reductase in an alginate-assimilating bacterium, Flavobacterium sp. strain UMI-01. Here, we showed that FlRed can also catalyze the oxidation of DEHU with NAD(+), producing 2-keto-3-deoxy-D-glucarate (KDGR). FlRed showed a predilection for NADH and NAD(+) over NADPH and NADP(+), respectively, and the K-m value for NADH was approximately 2.6-fold less than that for NAD(+). Furthermore, we identified two key enzymes, FlDet and FlDeg, for KDGR catabolism. FlDet was identified as an enzyme of the ribonuclease activity regulator A family, which converts KDGR to alpha-ketoglutaric semialdehyde (alpha-KGSA). FlDeg, a type II alpha-KGSA dehydrogenase, generated alpha-ketoglutaric acid by oxidizing the aldehyde group of alpha-KGSA using NAD(P)(+). Consequently, unlike the conventional DEHU reduction pathway, DEHU can be directly converted to alpha-ketoglutaric acid without consuming NAD(P)H. Alginate upregulated the expression of not only FlRed and two enzymes of the DEHU-reduction pathway, but also FlDet and FlDeg. These results revealed dual pathways of DEHU metabolism involving reduction or oxidation by FlRed.

We introduce several novel change of measure inequalities for two families of divergences: $f$-divergences and $\alpha$-divergences. We show how the variational representation for $f$-divergences leads to novel change of measure inequalities. We also present a multiplicative change of measure inequality for $\alpha$-divergences and a generalized version of Hammersley-Chapman-Robbins inequality. Finally, we present several applications of our change of measure inequalities, including PAC-Bayesian bounds for various classes of losses and non-asymptotic intervals for Monte Carlo estimates., Comment: 20 pages