Brown-fat-mediated tumour suppression by cold-altered global metabolism.

Glucose uptake is essential for cancer glycolysis and is involved in non-shivering thermogenesis of adipose tissues1-6. Most cancers use glycolysis to harness energy for their infinite growth, invasion and metastasis2,7,8. Activation of thermogenic metabolism in brown adipose tissue (BAT) by cold and drugs instigates blood glucose uptake in adipocytes4,5,9. However, the functional effects of the global metabolic changes associated with BAT activation on tumour growth are unclear. Here we show that exposure of tumour-bearing mice to cold conditions markedly inhibits the growth of various types of solid tumours, including clinically untreatable cancers such as pancreatic cancers. Mechanistically, cold-induced BAT activation substantially decreases blood glucose and impedes the glycolysis-based metabolism in cancer cells. The removal of BAT and feeding on a high-glucose diet under cold exposure restore tumour growth, and genetic deletion of Ucp1-the key mediator for BAT-thermogenesis-ablates the cold-triggered anticancer effect. In a pilot human study, mild cold exposure activates a substantial amount of BAT in both healthy humans and a patient with cancer with mitigated glucose uptake in the tumour tissue. These findings provide a previously undescribed concept and paradigm for cancer therapy that uses a simple and effective approach. We anticipate that cold exposure and activation of BAT through any other approach, such as drugs and devices either alone or in combination with other anticancer therapeutics, will provide a general approach for the effective treatment of various cancers.

The PDK1-FoxO1 signaling in adipocytes controls systemic insulin sensitivity through the 5-lipoxygenase-leukotriene B4 axis.

Although adipocytes are major targets of insulin, the influence of impaired insulin action in adipocytes on metabolic homeostasis remains unclear. We here show that adipocyte-specific PDK1 (3'-phosphoinositide-dependent kinase 1)-deficient (A-PDK1KO) mice manifest impaired metabolic actions of insulin in adipose tissue and reduction of adipose tissue mass. A-PDK1KO mice developed insulin resistance, glucose intolerance, and hepatic steatosis, and this phenotype was suppressed by additional ablation of FoxO1 specifically in adipocytes (A-PDK1/FoxO1KO mice) without an effect on adipose tissue mass. Neither circulating levels of adiponectin and leptin nor inflammatory markers in adipose tissue differed between A-PDK1KO and A-PDK1/FoxO1KO mice. Lipidomics and microarray analyses revealed that leukotriene B4 (LTB4) levels in plasma and in adipose tissue as well as the expression of 5-lipoxygenase (5-LO) in adipose tissue were increased and restored in A-PDK1KO mice and A-PDK1/FoxO1KO mice, respectively. Genetic deletion of the LTB4 receptor BLT1 as well as pharmacological intervention to 5-LO or BLT1 ameliorated insulin resistance in A-PDK1KO mice. Furthermore, insulin was found to inhibit LTB4 production through down-regulation of 5-LO expression via the PDK1-FoxO1 pathway in isolated adipocytes. Our results indicate that insulin signaling in adipocytes negatively regulates the production of LTB4 via the PDK1-FoxO1 pathway and thereby maintains systemic insulin sensitivity.

Development of a screening system for agents that modulate taste receptor expression with the CRISPR-Cas9 system in medaka.

Taste recognition mediated by taste receptors is critical for the survival of animals in nature and is an important determinant of nutritional status and quality of life in humans. However, many factors including aging, diabetes, zinc deficiency, infection with influenza or cold viruses, and chemotherapy can trigger dysgeusia, for which a standard treatment has not been established. We here established an engineered strain of medaka (Oryzias latipes) that expresses green fluorescent protein (GFP) from the endogenous taste 1 receptor 3 (T1R3) gene locus with the use of the CRISPR-Cas9 system. This T1R3-GFP knock-in (KI) strain allows direct visualization of expression from this locus by monitoring of GFP fluorescence. The pattern of GFP expression in the T1R3-GFP KI fish thus mimicked that of endogenous T1R3 gene expression. Furthermore, exposure of T1R3-GFP KI medaka to water containing monosodium glutamate or the anticancer agent 5-fluorouracil resulted in an increase or decrease, respectively, in GFP fluorescence intensity, effects that also recapitulated those on T1R3 mRNA abundance. Finally, screening for agents that affect GFP fluorescence intensity in T1R3-GFP KI medaka identified tryptophan as an amino acid that increases T1R3 gene expression. The establishment of this screening system for taste receptor expression in medaka provides a new tool for the development of potential therapeutic agents for dysgeusia.

Leucine induces cardioprotection in vitro by promoting mitochondrial function via mTOR and Opa-1 signaling.

BACKGROUND AND AIMS: Coronary heart disease is a major global health concern. Further, severity of this condition is greatly influenced by myocardial ischemia/reperfusion (I/R) injury. Branched-chain amino acids (BCAAs) have cardioprotective effects against I/R via mammalian target of rapamycin (mTOR) activity, wherein Leu is considered to particularly regulate mTOR activation. However, the mechanism underlying cardioprotective effects of Leu via mTOR activity is not fully elucidated. Here, we aimed to study the signaling pathway of cardioprotection and mitochondrial function induced by Leu treatment. METHODS AND RESULTS: Cardiac myocytes isolated from adult male Wistar rats were incubated and exposed to simulated I/R (SI/R) injury by replacing the air content. Cardiac myocytes were treated with Leu and subsequently, their survival rate was calculated. To elucidate the signaling pathway and mitochondrial function, immunoblots and mitochondrial permeability transition pore were examined. Cell survival rate was decreased with SI/R but improved by 160 µM Leu (38.5 ± 3.6% vs. 64.5 ± 4.2%, respectively, p < 0.001). Although rapamycin (mTOR inhibitor) prevented this cardioprotective effect induced by Leu, wortmannin (PI3K inhibitor) did not interfere with this effect. In addition, we indicated that overexpression of Opa-1 and mitochondrial function are ameliorated via Leu-induced mitochondrial biogenesis. In contrast, knockdown of Opa-1 suppressed Leu-induced cardioprotection. CONCLUSION: Leu treatment is critical in rendering a cardioprotective effect exhibited by BCAAs via mTOR signaling. Furthermore, Leu improved mitochondrial function.

Assessment of insulin resistance in the skeletal muscle of mice using positron emission tomography/computed tomography imaging.

Measuring glucose uptake in the skeletal muscle in vivo is an effective method to determine glucose metabolism abnormalities as the skeletal muscle is the principal tissue responsible for glucose disposal and is a major site of peripheral insulin resistance. In this study, we investigated the pathological glucose metabolism dynamics of the skeletal muscle of C57BL/6J mice in a noninvasive and time-sequential manner using positron emission tomography/computed tomography (PET/CT), an imaging technique that uses radioactive substances to visualize and measure metabolic processes in the body, with [18F]-fluoro-2-deoxy-D-glucose (FDG). FDG-PET/CT imaging revealed that insulin administration and exercise load significantly increased FDG accumulation in the skeletal muscle of C57BL/6J mice. FDG accumulation was lower in the skeletal muscle of 14-week-old db/db diabetic model mice exhibiting remarkable insulin resistance compared to that of 7-week-old db/db mice. Based on the continuous observation of FDG accumulation over time in diet-induced obese (DIO) mice, FDG accumulation significantly decreased in 17-week-old mice after the acquisition of insulin resistance. Although insulin-induced glucose uptake in the skeletal muscle was markedly attenuated in 20-week-old DIO mice that had already developed insulin resistance, exercise load effectively increased FDG uptake in the skeletal muscle. Thus, we successfully confirmed that glucose uptake accompanied by insulin administration and exercise load increased in the skeletal muscle using PET-CT. FDG-PET/CT might be an effective tool that could noninvasively capture the chronological changes of metabolic abnormalities in the skeletal muscle of mice.

DNA methylation status influences insulin-induced glucose transport in 3T3-L1 adipocytes by mediating p53 expression.

Researchers frequently use 3T3-L1 adipocytes as a fat cell line, but the capacity of this line for insulin-mediated glucose transport is lower than that of primary isolated fat cells. In this study, we found that 5-azacytidine (5-aza-C), DNA methyltransferase 1 inhibitor, enhanced insulin-stimulated 2-deoxyglucose (2-DG) transport in 3T3-L1 cells after adipogenic differentiation. We next examined the expression of the genes related to glucose transport and insulin signal transduction. The insulin independent glucose transporter, glucose transporter 1 (GLUT1), showed lower expression in 5-aza-C pre-treated 3T3-L1 adipocytes, than in un-treated control adipocytes, while the expression of insulin dependent transporter GLUT4 remained unchanged. In addition, insulin receptor substrate-1 (IRS-1) was highly expressed in 5-aza-C pre-treated adipocytes. Based on DNA microarray and functional annotation analysis, we noticed that 5-aza-C pretreatment activated the tumor suppressor p53 pathway. We confirmed that in 5-aza-C adipocytes, p53 expression was markedly higher, and the methylation level of CpGs in its promoter region was lower than in un-treated control adipocytes. Moreover, pharmacological inhibition of p53 restored GLUT1 and IRS-1 expression to the same level as in un-treated 3T3-L1 adipocytes, and significantly decreased insulin-mediated 2-DG uptake. These results suggest that glucose transport capacity in adipocytes is influenced by DNA methylation status, and demethylation induced by 5-aza-C increased it possibly through the p53 signaling pathway.

Differential regulation of Actn2 and Actn3 expression during unfolded protein response in C2C12 myotubes.

ACTN2 and ACTN3 encode sarcomeric α-actinin-2 and α-actinin-3 proteins, respectively, that constitute the Z-line in mammalian skeletal muscle fibers. In human ACTN3, a nonsense mutation at codon 577 that encodes arginine (R) produces the R577X polymorphism. Individuals having a homozygous 577XX genotype do not produce α-actinin-3 protein. The 577XX genotype reportedly occurs in sprint and power athletes in frequency lower than in the normal population, suggesting that α-actinin-3 deficiency diminishes fast-type muscle function. Among humans who carry 577R alleles, varying ACTN3 expression levels under certain conditions can have diverse effects on atheletic and muscle performance. However, the factors that regulate ACTN3 expression are unclear. Here we investigated whether the unfolded protein response (UPR) under endoplasmic reticulum (ER) stress regulates expression of Actn3 and its isoform Actn2 in mouse C2C12 myotubes. Among UPR-related transcription factors, XBP1 upregulated Actn2, whereas XBP1, ATF4 and ATF6 downregulated Actn3 promoter activity. Chemical induction of ER stress increased Actn2 mRNA levels, but decreased those for Actn3. ER stress also decreased α-actinin-3 protein levels, whereas levels of α-actinin-2 were unchanged. The intracellular composition of muscle contraction-related proteins was altered under ER stress, in that expression of parvalbumin (a fast-twitch muscle-specific protein) and troponin I type 1 (skeletal, slow) was suppressed. siRNA-induced suppression of Actn3 mimicked the inhibitory effect of ER stress on parvalbumin levels. Thus, endogenous expression levels of α-actinin-3 can be altered by ER stress, which may modulate muscle performance and athletic aptitudes, particularly in humans who carry ACTN3 577R alleles.

Carbon sources that enable enrichment of 1,4-dioxane-degrading bacteria in landfill leachate.

1,4-Dioxane (DX) is a recalcitrant cyclic ether that has gained attention as an emerging pollutant in the aquatic environment. Enrichment of indigenous DX-degrading bacteria, which are considered to be minor populations even in DX-impacted environments, is the key for efficient biological DX removal. Therefore, this study aimed to explore carbon sources applicable for the enrichment of DX-degrading bacteria present in landfill leachate, which is a potential source of DX pollution. Microorganisms collected from landfill leachate were cultivated on six different carbon sources (DX, tetrahydrofuran (THF), 1,3,5-trioxane (TX), ethylene glycol (EG), diethylene glycol (DEG), and 1,4-butanediol (BD)) in a sequential batch mode. Consequently, enrichment cultures cultivated on THF in addition to DX improved the DX degradation ability compared to that of the original leachate sample, while those on the other test carbon sources did not. The results indicated that THF can be an alternative carbon source to enrich DX-degrading bacteria, and that TX, EG, DEG and BD are not applicable to concentrate DX-degrading bacteria in complex microbial consortia. In addition, sequencing analyses of 16S rRNA and soluble di-iron monooxygenase (SDIMO) genes revealed notable dominance of thm/dxm genes involved in group 5 SDIMO both in DX- and THF-enrichment cultures. The analysis also showed a predominance of Pseudonocardia in THF-enrichment culture, suggesting that Pseudonocardia harboring thm/dxm genes contributes to enhanced DX degradation in THF-enrichment culture.

Colonization and Competition Dynamics of Plant Growth-Promoting/Inhibiting Bacteria in the Phytosphere of the Duckweed Lemna minor.

Despite the considerable role of aquatic plant-associated bacteria in host plant growth and nutrient cycling in aquatic environments, the mode of their plant colonization has hardly been understood. This study examined the colonization and competition dynamics of a plant growth-promoting bacterium (PGPB) and two plant growth-inhibiting bacteria (PGIB) in the aquatic plant Lemna minor (common duckweed). When inoculated separately to L. minor, each bacterial strain quickly colonized at approximately 106 cells per milligram (plant fresh weight) and kept similar populations throughout the 7-day cultivation time. The results of two-membered co-inoculation assays revealed that the PGPB strain Aquitalea magnusonii H3 consistently competitively excluded the PGIB strain Acinetobacter ursingii M3, and strain H3 co-existed at almost 1:1 proportion with another PGIB strain, Asticcacaulis excentricus M6, regardless of the inoculation ratios (99:1-1:99) and inoculation order. We also found that A. magnusonii H3 exerted its growth-promoting effect over the negative effects of the two PGIB strains even when only a small amount was inoculated, probably due to its excellent competitive colonization ability. These experimental results demonstrate that there is a constant ecological equilibrium state involved in the bacterial colonization of aquatic plants.

Biosynthesis of bismuth selenide nanoparticles using chalcogen-metabolizing bacteria.

Cost and energy reductions in the production process of bismuth chalcogenide (BC) semiconductor materials are essential to make thermoelectric generators comprised of BCs profitable and CO2 neutral over their life cycle. In this study, as an eco-friendly production method, bismuth selenide (Bi2Se3) nanoparticles were synthesized using the following five strains of chalcogen-metabolizing bacteria: Pseudomonas stutzeri NT-I, Pseudomonas sp. RB, Stenotrophomonas maltophilia TI-1, Ochrobactrum anthropi TI-2, and O. anthropi TI-3 under aerobic conditions. All strains actively volatilized selenium (Se) by reducing selenite, possibly to organoselenides. In the growth media containing bismuth (Bi) and Se, all strains removed Bi and Se concomitantly and synthesized nanoparticles containing Bi and Se as their main components. Particles synthesized by strain NT-I had a theoretical elemental composition of Bi2Se3, whereas those synthesized by other strains contained a small amount of sulfur in addition to Bi and Se, making strain NT-I the best Bi2Se3 synthesizer among the strains used in this study. The particle sizes were 50-100 nm in diameter, which is sufficiently small for nanostructured semiconductor materials that exhibit quantum size effect. Successful synthesis of Bi2Se3 nanoparticles could be attributed to the high Se-volatilizing activities of the bacterial strains. Selenol-containing compounds as intermediates of Se-volatilizing metabolic pathways, such as methane selenol and selenocysteine, may play an important role in biosynthesis of Bi2Se3.

Potential of waste activated sludge to accumulate polyhydroxyalkanoates and glycogen using industrial wastewater/liquid wastes as substrates.

Recovery of the organics in industrial wastewaters/liquid wastes as polyhydroxyalkanoate (PHA) and/or glycogen (GLG) in waste activated sludge is a useful strategy to not only improve the resource value of waste activated sludge but also reduce the energy and cost of waste disposal and wastewater treatment. This study aimed to evaluate the potential of activated sludge to accumulate PHA and GLG using complex substrates (actual and simulated industrial wastewaters/liquid wastes) in addition to various simple organic substrates (organic acids, saccharides, and glycerol). The 24 h PHA and GLG accumulation experiments resulted in the accumulation of up to 25.5%, 6.0% and 14.1% of polyhydroxybutyrate (PHB), polyhydroxyvalerate (PHV) and GLG, respectively, from simple substrates, and up to 9.8%, 0.1% and 14.6%, respectively, from complex substrates. The results indicated that activated sludge can accumulate PHA and GLG even from complex wastewater substrates, although the accumulated PHA and GLG levels were not sufficiently high. The results also indicated that the PHA and GLG accumulation abilities of activated sludge from complex substrates can be drastically enhanced by a short-term acclimation to the corresponding substrate. This study will present the practical implications for value-added resource production through the combined use of waste activated sludge and industrial wastewaters.

Readthrough of ACTN3 577X nonsense mutation produces full-length α-actinin-3 protein.

The ACTN3 gene encodes α-actinin-3 protein, which stabilizes the contractile apparatus at the Z-line in skeletal muscle cell fast fibers. A nonsense mutation of the arginine (R) at the codon for amino acid 577 of the ACTN3 gene generates a premature termination codon (PTC) and produces the R577X polymorphism in humans (X specifies translational termination). The ACTN3 577X genotype abolishes α-actinin-3 protein production due to targeted degradation of the mutant transcript by the cellular nonsense-mediated mRNA decay (NMD) system, which requires mRNA splicing. In humans, α-actinin-3 deficiency can decrease sprinting and power performance as well as skeletal muscle mass and strength. Here we investigated whether suppression of the in-frame PTC induced by treatment with the aminoglycosides gentamicin and G418 that promote termination codon readthrough could allow production of full-length α-actinin-3 protein from ACTN3 577X. We constructed expression plasmids encoding mature mRNA that lacks introns or pre-mRNA, which carries introns for the ACTN3 577X gene (X and Xpre, respectively) and transfected the constructs into HEK293 cells. Similar constructs for the ACTN3 577R gene were used as controls. HEK293 cells carrying the X gene, but not the Xpre gene, expressed exogenous truncated α-actinin-3 protein, indicating NMD-mediated suppression of exogenous Xpre expression. Cells treated with aminoglycosides produced exogenous full-length α-actinin-3 protein in X-transfected cells, but not in Xpre-transfected cells. The NMD inhibitor caffeine prevented suppression of Xpre expression and thereby induced production of full-length α-actinin-3 protein in the presence of aminoglycoside. Together these results indicate that the ACTN3 R577X polymorphism could be a novel target for readthrough therapy, which may affect athletic and muscle performance in humans.

Characterization of moderately halotolerant selenate- and tellurite-reducing bacteria isolated from brackish areas in Osaka.

Moderately halotolerant selenate- and tellurite-reducing bacteria were characterized for wastewater treatment applications. A selenate-reducing strain 9a was isolated from the biofilm of a leachate treatment plant at a sea-based waste disposal site. A tellurite-reducing strain Taa was isolated from an enrichment culture derived from brackish sediment. Both bacterial strains were Shewanella species. Strain 9a could anaerobically remove 45-70% of 1.0 mM selenate and selenite from water containing up to 3% NaCl within 4 days, while strain Taa could anaerobically and aerobically remove 70-90% of 0.4 mM tellurite from water containing up to 6% NaCl within 3 days. Globular particles of insoluble selenium were observed both outside and inside the cells of strain 9a. The insoluble tellurium formed by strain Taa was globular under microaerobic conditions but nanorod under aerobic conditions. These bacteria will yield a range of useful selenium and tellurium nanomaterials as well as wastewater treatment applications.

Endoplasmic Reticulum Stress in Mice Increases Hepatic Expression of Genes Carrying a Premature Termination Codon via a Nutritional Status-Independent GRP78-Dependent Mechanism.

Nonsense-mediated mRNA decay (NMD) degrades mRNAs carrying a premature termination codon (PTC) in eukaryotes. Cellular stresses, including endoplasmic reticulum (ER) stress, inhibit NMD, and up-regulate PTC-containing mRNA (PTC-mRNA) levels in several cell lines. However, whether similar effects exist under in vivo conditions that involve systemic nutritional status is unclear. Here, we compared the effects of pharmacological induction of ER stress with those of nutritional interventions on hepatic PTC-mRNA levels in mice. In mouse livers, the ER stress inducer tunicamycin increased PTC-mRNA levels of endogenous marker genes. Tunicamycin decreased body weight and perturbed nutrient metabolism in mice. Food restriction or deprivation mimicked the effect of tunicamycin on weight loss and metabolism, but did not increase PTC-mRNA levels. Hyperphagia-induced obesity also had little effect on hepatic PTC-mRNA levels. Meanwhile, in mouse liver phosphorylation of eIF2α, a factor that regulates NMD, was increased by both tunicamycin and nutritional interventions. Hepatic expression of GRP78, a central chaperone in ER stress responses, was increased by tunicamycin but not by the nutritional interventions. In cultured liver cells (Hepa), exogenous overexpression of a phosphomimetic eIF2α failed to increase PTC-mRNA levels. However, GRP78 overexpression in Hepa cells increased PTC-mRNA and PTC-mRNA-derived protein levels. ER stress promoted localization of GRP78 to mitochondria, and exogenous expression of a GRP78 fusion protein targeted to mitochondria mimicked the effect of wild type GRP78. These results indicate that GRP78, but not nutritional status, is a potent up-regulator of hepatic PTC-mRNA levels during induction of ER stress in vivo. J. Cell. Biochem. 118: 3810-3824, 2017. © 2017 Wiley Periodicals, Inc.

[Role of vitamin D and calcium in obesity and type 2 diabetes].

Obesity, induced by unhealthy lifestyle choices, could be involved in the development of chronic diseases like type 2 diabete. Obesity is largely due to the imbalance of energy intake and expenditure, therefore we have put more emphasis on the amount of macronutrients including carbohydrates, fats and proteins as dietary therapy for obesity and related-conditions. On the other hand, several studies revealed obese or diabetic patients were more likely to have micronutrient deficiencies such as vitamins and minerals. Besides the effects on bone metabolism, vitamin D and calcium might contribute to metabolic disorder accompanied by obesity. However, it has not been concluded supplementation of these two nutrients has a benefit in obese or diabetic individuals. Further studies are needed.

Complete genome sequences of six duckweed-associated bacterial strains for studying community assembly in synthetic plant microbiome.

We report the complete genome sequences of six bacterial strains isolated from a floating macrophyte, duckweed. These six strains, representing the six dominant families of the natural duckweed microbiome, establish a simple model ecosystem when inoculated onto sterilized duckweed. Their genomes would provide insights into community assembly in plant microbiome.

Draft genome sequence of Pelosinus sp. IPA-1, a bacterium isolated from arsenic-contaminated soil in Japan.

Pelosinus sp. strain IPA-1 is a bacterium isolated from arsenic-contaminated soil in Japan. We here report the draft genome sequence of strain IPA-1.

Umami taste sensitivity is associated with food intake and oral environment in subjects with diabetes.

OBJECTIVE: Dysgeusia is a serious problem in patients with diabetes because it often leads to overeating, which is associated with disease progression. This study aimed to investigate the association between taste sensitivity, eating habits, and the oral environment. SUBJECTS AND METHODS: In this cross-sectional study of 75 subjects with diabetes, gustatory function was assessed using the whole-mouth method, and lingual taste receptor gene expression was measured by real-time PCR. Food intake was evaluated using a food frequency questionnaire based on food groups. The oral environment was assessed using xerostomia and periodontal comprehensive examination. RESULTS: In total, 45.3%, 28.0%, and 18.7% of subjects showed lower umami taste sensitivity, low sweet taste sensitivity, and low salt taste sensitivity, respectively. Lower umami sensitivity correlated with lower estimated glomerular filtration rate and higher energy-source food intake. Subjects with diabetes with higher plaque control record showed significantly higher T1R3 gene expression than those with lower plaque control record. CONCLUSION: Reduced umami taste sensitivity is associated with decreased renal function and high energy food intake in diabetes. Subjects with diabetes with higher plaque control record showed significantly higher T1R3 gene expression, suggesting that the oral environment affects taste gene expression. J. Med. Invest. 70 : 241-250, February, 2023.

Genome-wide identification of bacterial colonization and fitness determinants on the floating macrophyte, duckweed.

Bacterial communities associated with aquatic macrophytes largely influence host primary production and nutrient cycling in freshwater environments; however, little is known about how specific bacteria migrate to and proliferate at this unique habitat. Here, we separately identified bacterial genes involved in the initial colonization and overall fitness on plant surface, using the genome-wide transposon sequencing (Tn-seq) of Aquitalea magnusonii H3, a plant growth-promoting bacterium of the floating macrophyte, duckweed. Functional annotation of identified genes indicated that initial colonization efficiency might be simply explained by motility and cell surface structure, while overall fitness was associated with diverse metabolic and regulatory functions. Genes involved in lipopolysaccharides and type-IV pili biosynthesis showed different contributions to colonization and fitness, reflecting their metabolic cost and profound roles in host association. These results provide a comprehensive genetic perspective on aquatic-plant-bacterial interactions, and highlight the potential trade-off between bacterial colonization and proliferation abilities on plant surface.

Draft Genome Sequence of Stutzerimonas stutzeri NT-I, Which Reduces Selenium Oxyanions into Elemental Selenium and Volatile Selenium Species.

Stutzerimonas stutzeri strain NT-I effectively reduces selenate and selenite into elemental selenium and volatile selenium species. It is thus a promising biological agent for treatment of selenium-contaminated wastewater. We here report the draft genome sequence of this strain.