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DOE OSTI2021

Assessing dynamic vegetation model parameter uncertainty across Alaskan arctic tundra plant communities

Abstract As the Arctic region moves into uncharted territory under a warming climate, it is important to refine the terrestrial biosphere models (TBMs) that help us understand and predict change. One fundamental uncertainty in TBMs relates to model parameters, configuration variables internal to the model whose value can be estimated from data. We incorporate a version of the Terrestrial Ecosystem Model (TEM) developed for arctic ecosystems into the Predictive Ecosystem Analyzer (PEcAn) framework. PEcAn treats model parameters as probability distributions, estimates parameters based on a synthesis of available field data, and then quantifies both model sensitivity and uncertainty to a given parameter or suite of parameters. We examined how variation in 21 parameters in the equation for gross primary production influenced model sensitivity and uncertainty in terms of two carbon fluxes (net primary productivity and heterotrophic respiration) and two carbon (C) pools (vegetation C and soil C). We set up different parameterizations of TEM across a range of tundra types (tussock tundra, heath tundra, wet sedge tundra, and shrub tundra) in northern Alaska, along a latitudinal transect extending from the coastal plain near Utqiaġvik to the southern foothills of the Brooks Range, to the Seward Peninsula. TEM was most sensitive to parameters related to the temperature regulation of photosynthesis. Model uncertainty was mostly due to parameters related to leaf area, temperature regulation of photosynthesis, and the stomatal responses to ambient light conditions. Our analysis also showed that sensitivity and uncertainty to a given parameter varied spatially. At some sites, model sensitivity and uncertainty tended to be connected to a wider range of parameters, underlining the importance of assessing tundra community processes across environmental gradients or geographic locations. Generally, across sites, the flux of net primary productivity (NPP) and pool of vegetation C had about equal uncertainty, while heterotrophic respiration had higher uncertainty than the pool of soil C. Our study illustrates the complexity inherent in evaluating parameter uncertainty across highly heterogeneous arctic tundra plant communities. It also provides a framework for iteratively testing how newly collected field data related to key parameters may result in more effective forecasting of Arctic change.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2017

Global pattern and controls of soil microbial metabolic quotient

The microbial metabolic quotient (MMQ), microbial respiration per unit of biomass, is a fundamental factor controlling heterotrophic respiration, the largest carbon flux in soils. The magnitude and controls of MMQ at regional scale remain uncertain. We compiled a comprehensive data set of MMQ to investigate the global patterns and controls of MMQ in top 30 cm soils. Published MMQ values, generally measured in laboratory microcosms, were adjusted on ambient soil temperature using long-term (30 yr) average site soil temperature and a Q10 = 2. The area-weighted global average of MMQ_Soil is estimated as 1.8 (1.5–2.2) (95% confidence interval) lmol C•h -1 •mmol -1 microbial biomass carbon (MBC) with substantial variations across biomes and between cropland and natural ecosystems. Variation was most closely associated with biological factors, followed by edaphic and meteorological parameters. MMQ_Soil was greatest in sandy clay and sandy clay loam and showed a pH maximum of 6.7 - 0.1 (mean ± se). At large scale, MMQ_Soil varied with latitude and mean annual temperature (MAT), and was negatively correlated with microbial N:P ratio, supporting growth rate theory. These trends led to large differences in MMQ_Soil between natural ecosystems and cropland. When MMQ was adjusted to 11°C (MMQ_Ref), the global MAT in the top 30 cm of soils, the area-weighted global averages of MMQ_Ref was 1.5 (1.3–1.8) lmol C•mmol MBC -1 •h -1 . The values, trends, and controls of MMQ_Soil add to our understanding of soil microbial influences on soil carbon cycling and could be used to represent microbial activity in global carbon models.

59 BASIC BIOLOGICAL SCIENCES↗

DOE OSTI2016

Disturbance, complexity, and succession of net ecosystem production in North America’s temperate deciduous forests

Century-old forests in the U.S. upper Midwest and Northeast power much of North Amer- ica’s terrestrial carbon (C) sink, but these forests’ production and C sequestration capacity are expected to soon decline as fast-growing early successional species die and are replaced by slower growing late successional species. But will this really happen? Here we marshal empirical data and ecological theory to argue that substantial declines in net ecosystem production (NEP) owing to reduced forest growth, or net primary production (NPP), are not imminent in regrown temperate deciduous forests over the next several decades. Forest age and production data for temperate deciduous forests, synthesized from published literature, suggest slight declines in NEP and increasing or stable NPP during middle successional stages. We revisit long-held hypotheses by EP Odum and others that suggest low-severity, high-frequency disturbances occurring in the region’s aging forests will, against intuition, maintain NEP at higher-than- expected rates by increasing ecosystem complexity, sustaining or enhancing NPP to a level that largely o sets rising C losses as heterotrophic respiration increases. This theoretical model is also supported by biological evidence and observations from the Forest Accelerated Succession Experiment in Michigan, USA. Ecosystems that experience high-severity disturbances that simplify ecosystem complexity can exhibit substantial declines in production during middle stages of succession. However, observations from these ecosystems have exerted a disproportionate in uence on assumptions regarding the trajectory and magnitude of age-related declines in forest production. We conclude that there is a wide ecological space for forests to maintain NPP and, in doing so, lessens the declines in NEP, with signi cant implications for the future of the North American carbon sink. Our intellectual frameworks for understanding forest C cycle dynamics and resilience need to catch up to our more complex and nuanced understanding of ecological succession.

ecological theory↗

DOE OSTI2022

Microbial communities and biogeochemical functioning across peatlands in the Athabasca Oil Sands region of Canada: Implications for reclamation and management

Abstract Peatlands play an important role in global biogeochemical cycles and are essential for multiple ecosystem functions. Understanding the environmental drivers of microbial functioning and community structure can provide insights to enable effective and evidence‐based management. However, it remains largely unknown how microbial diversity contributes to the functioning of belowground processes. Addressing this gap in knowledge will provide a better understanding of microbial‐mediated processes in peatlands that are undergoing restoration or reclamation. This study assessed the changes in microbial community diversity and structure as well as soil function by measuring microbial respiration on a range of substrates from three natural fen types found in the Athabasca Oil Sands region of Alberta, Canada (a poor fen, a hypersaline fen, and a tree‐rich fen) and a nearby constructed fen undergoing reclamation following open pit mining. Overall, substrate induced respiration was significantly higher in the constructed fen. Alpha diversity of fungi and prokaryotes was highest in the tree‐rich fen, and the composition of microbial communities was significantly different between fens. Both fungal and prokaryotic communities were strongly related to pore water pH and temperature, with plant richness also contributing to the shape of fungal communities. In summary, microbial community structure reflects the underlying differences in soil condition across different fens but plays essential roles in the ecological functions of soil. These findings provide a new outlook for the management of peatlands undergoing post‐mining reclamation. Future research on peatland reclamation should consider the dynamic interaction between communities and ecosystem functionality, for which this study forms a useful baseline.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2023

Oxygen consumption of sexually mature adult, first-feeding larval, and yearling Pacific Lampreys

Abstract Objective The Pacific Lamprey Entosphenus tridentatus is considered a first food of Native American tribes, such as the Confederated Tribes of the Umatilla Indian Reservation. Populations of this imperiled species have declined such that harvest for traditional use is limited. As a result, propagation and culture of Pacific Lampreys have been initiated to supply animals for restoration and recovery efforts. These efforts require transport and periodic holding of both adults and larvae under static (no-flow) conditions. Hence, guidelines for ensuring an adequate oxygen supply are needed for all life stages of this species. Methods We measured oxygen consumption rates of mature adults, first-feeding larvae, and yearlings under static conditions at 12–15°C. In addition, we recorded indicators of stress during hypoxia for adults and estimated routine respiration rates during and after larval feeding. Result Adults exhibited surprisingly high metabolic rates when at rest in static chambers. At 12°C, a single adult typically reduced dissolved oxygen levels in 10 L to <2 mg/L in just 90 min (oxygen consumption rates of 100–200 mg/kg/h). Adults often started to climb the walls of open chambers when dissolved oxygen levels approached 2 mg/L, allowing them to raise their branchiopores into air. Larvae remained quiescent, even when oxygen levels dropped below 1 mg/L, and costs of feeding increased routine respiration by 22–56%. Conclusion Based on these observations, we recommend that adult Pacific Lampreys always be transported in aerated containers and with access to air at the top of the tank. Although larvae exhibited hypoxia tolerance, care should be taken to ensure adequate oxygen availability, particularly during and immediately after feeding.

Moser, Mary↗

DOE OSTI2021

Integrating Aquatic Metabolism and Net Ecosystem CO2 Balance in Short- and Long-Hydroperiod Subtropical Freshwater Wetlands

Abstract How aquatic primary productivity influences the carbon (C) sequestering capacity of wetlands is uncertain. We evaluated the magnitude and variability in aquatic C dynamics and compared them to net ecosystem CO 2 exchange (NEE) and ecosystem respiration ( R eco ) rates within calcareous freshwater wetlands in Everglades National Park. We continuously recorded 30-min measurements of dissolved oxygen (DO), water level, water temperature ( T water ), and photosynthetically active radiation (PAR). These measurements were coupled with ecosystem CO 2 fluxes over 5 years (2012–2016) in a long-hydroperiod peat-rich, freshwater marsh and a short-hydroperiod, freshwater marl prairie. Daily net aquatic primary productivity (NAPP) rates indicated both wetlands were generally net heterotrophic. Gross aquatic primary productivity (GAPP) ranged from 0 to − 6.3 g C m −2 day −1 and aquatic respiration ( R Aq ) from 0 to 6.13 g C m −2 day −1 . Nonlinear interactions between water level, T water , and GAPP and R Aq resulted in high variability in NAPP that contributed to NEE. Net aquatic primary productivity accounted for 4–5% of the deviance explained in NEE rates. With respect to the flux magnitude, daily NAPP was a greater proportion of daily NEE at the long-hydroperiod site (mean = 95%) compared to the short-hydroperiod site (mean = 64%). Although we have confirmed the significant contribution of NAPP to NEE in both long- and short-hydroperiod freshwater wetlands, the decoupling of the aquatic and ecosystem fluxes could largely depend on emergent vegetation, the carbonate cycle, and the lateral C flux.

Malone, Sparkle L.↗

DOE OSTI2026

Unlocking plant-microbial interactions in deep Mollisols in the Midwestern US: Linking depth gradients in roots, microbial activity, and soil carbon in agroecosystems

Deep-rooted plants may build soil carbon (C) stocks, but most research has focused on shallow soils, leaving gaps in our understanding of how shifts in the balance between decomposition and C inputs drive soil C accumulation with depth. Thus, our objectives were to: (1) link depth gradients in root biomass with microbial activity and soil C stocks down to 1 m, and (2) examine the potential of simple C inputs to prime soil C across depths. To this end, we dug 5 quantitative soil pits in Argiudolls under mature perennial miscanthus plots in the SoyFACE Farm (Champaign-Urbana, IL). We added 13 C labeled glucose to our soils to determine the fate of simple C inputs with depth. We found that fine root biomass, total soil C, mineral-associated organic C (MAOC), particulate organic C (POC), and microbial activity (as measured by potential enzyme activity) declined with depth. POC declined more rapidly than MAOC, resulting in an increase in the ratio of MAOC-to-POC. Root biomass, enzyme activity (either acid phosphatase or n-acetyl-glucosaminadase) activity, and microbial respiration explained 74% and 38% of the variability in soil total C and MAOC, respectively, while POC was dependent on root biomass and microbial respiration (47%). Although the incorporation of simple 13 C inputs into MAOC was similar across depths, these inputs led to greater net MAOC losses in shallow soils than in deeper soils between 50 and 100 cm. The divergent impact of simple C inputs across depths may suggest that MAOC in shallow soils is more susceptible to priming losses, while C inputs into deep soils may instead be more persistent. Collectively, our results suggest that depth gradients in soil C stocks represents a balance between inputs, decomposition, and microbial necromass production and that increases in root C inputs by deep-rooted plants may have the potential to build stable MAOC.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2020

New soil carbon sequestration with nitrogen enrichment: a meta-analysis

Background and aims: Through agriculture and industry, humans are increasing the deposition and availability of nitrogen (N) in ecosystems worldwide. Carbon (C) isotope tracers provide useful insights into soil C dynamics, as they allow to study soil C pools of different ages. In this study we evaluated to what extent N enrichment affects soil C dynamics in experiments that applied C isotope tracers. Methods: Using meta-analysis, we synthesized data from 35 published papers. We made a distinction between “new C” and “old C” stocks, i.e., soil C derived from plant C input since the start of the isotopic enrichment, or unlabeled, pre-existing soil C. Results: Averaged across studies, N addition increased new soil C stocks (+30.3%), total soil C stocks (+6.1%) and soil C input proxies (+30.7%). Although N addition had no overall, average, effect on old soil C stocks and old soil C respiration, old soil C stocks increased with the amount of N added and respiration of old soil C declined. Nitrogen-induced effects on new soil C and soil C input both decreased with the amount of extraneous N added in control treatments. Conclusion: Although our findings require additional confirmation from long-term field experiments, our analysis provides isotopic evidence that N addition stimulates soil C storage both by increasing soil C input and (at high N rates) by decreasing decomposition of old soil C. Furthermore, we demonstrate that the widely reported saturating response of plant growth to N enrichment also applies to new soil C storage.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2016

Mitochondrial Sirt3 supports cell proliferation by regulating glutamine-dependent oxidation in renal cell carcinoma

Clear cell renal carcinoma (RCC), the most common malignancy arising in the adult kidney, exhibits increased aerobic glycolysis and low mitochondrial respiration due to von Hippel-Lindau gene defects and constitutive hypoxia-inducible factor-α expression. Sirt3 is a major mitochondrial deacetylase that mediates various types of energy metabolism. However, the role of Sirt3 as a tumor suppressor or oncogene in cancer depends on cell types. We show increased Sirt3 expression in the mitochondrial fraction of human RCC tissues. Sirt3 depletion by lentiviral short-hairpin RNA, as well as the stable expression of the inactive mutant of Sirt3, inhibited cell proliferation and tumor growth in xenograft nude mice, respectively. Furthermore, mitochondrial pyruvate, which was used for oxidation in RCC, might be derived from glutamine, but not from glucose and cytosolic pyruvate, due to depletion of mitochondrial pyruvate carrier and the relatively high expression of malic enzyme 2. Depletion of Sirt3 suppressed glutamate dehydrogenase activity, leading to impaired mitochondrial oxygen consumption. Our findings suggest that Sirt3 plays a tumor-progressive role in human RCC by regulating glutamine-derived mitochondrial respiration, particularly in cells where mitochondrial usage of cytosolic pyruvate is severely compromised. -- Highlights: •Sirt3 is required for the maintenance of RCC cell proliferation. •Mitochondrial usage of cytosolic pyruvate is severely compromised in RCC. •Sirt3 supports glutamine-dependent oxidation in RCC.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2016

Anthelmintic drug ivermectin inhibits angiogenesis, growth and survival of glioblastoma through inducing mitochondrial dysfunction and oxidative stress

Glioblastoma is one of the most vascular brain tumour and highly resistant to current therapy. Targeting both glioblastoma cells and angiogenesis may present an effective therapeutic strategy for glioblastoma. In our work, we show that an anthelmintic drug, ivermectin, is active against glioblastoma cells in vitro and in vivo, and also targets angiogenesis. Ivermectin significantly inhibits growth and anchorage-independent colony formation in U87 and T98G glioblastoma cells. It induces apoptosis in these cells through a caspase-dependent manner. Ivermectin significantly suppresses the growth of two independent glioblastoma xenograft mouse models. In addition, ivermectin effectively targets angiogenesis through inhibiting capillary network formation, proliferation and survival in human brain microvascular endothelial cell (HBMEC). Mechanistically, ivermectin decreases mitochondrial respiration, membrane potential, ATP levels and increases mitochondrial superoxide in U87, T98G and HBMEC cells exposed to ivermectin. The inhibitory effects of ivermectin are significantly reversed in mitochondria-deficient cells or cells treated with antioxidants, further confirming that ivermectin acts through mitochondrial respiration inhibition and induction of oxidative stress. Importantly, we show that ivermectin suppresses phosphorylation of Akt, mTOR and ribosomal S6 in glioblastoma and HBMEC cells, suggesting its inhibitory role in deactivating Akt/mTOR pathway. Altogether, our work demonstrates that ivermectin is a useful addition to the treatment armamentarium for glioblastoma. Our work also highlights the therapeutic value of targeting mitochondrial metabolism in glioblastoma. - Highlights: • Ivermectin is effective in glioblastoma cells in vitro and in vivo. • Ivermectin inhibits angiogenesis. • Ivermectin induces mitochondrial dysfunction and oxidative stress. • Ivermectin deactivates Akt/mTOR signaling pathway.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2017

Antibiotic tigecycline enhances cisplatin activity against human hepatocellular carcinoma through inducing mitochondrial dysfunction and oxidative damage

Targeting mitochondrial metabolism has been recently demonstrated to be a promising therapeutic strategy for the treatment of various cancer. In this work, we demonstrate that antibiotic tigecycline is selectively against hepatocellular carcinoma (HCC) through inducing mitochondrial dysfunction and oxidative damage. Tigecycline is more effective in inhibiting proliferation and inducing apoptosis of HCC than normal liver cells. Importantly, tigecycline significantly enhances the inhibitory effects of chemotherapeutic drug cisplatin in HCC in vitro and in vivo. Mechanistically, tigecycline specifically inhibits mitochondrial translation as shown by the decreased protein levels of Cox-1 and -2 but not Cox-4 or Grp78, and increased mRNA levels of Cox-1 and -2 but not Cox-4 in HCC cells exposed to tigecycline. In addition, tigecycline significantly induces mitochondrial dysfunction in HCC cells via decreasing mitochondrial membrane potential, complex I and IV activities, mitochondrial respiration and ATP levels. Tigecycline also increases levels of mitochondrial superoxide, hydrogen peroxide and ROS levels. Consistent with oxidative stress, oxidative damage on DNA, protein and lipid are also observed in tigecycline-treated cells. Importantly, antioxidant N-acetyl-L-cysteine (NAC) reverses the effects of tigecycline, suggesting that oxidative stress is required for the action of tigecycline in HCC cells. We further show that HCC cells have higher level of mitochondrial biogenesis than normal liver cells which might explain the different sensitivity to tigecycline between HCC and normal liver cells. Our work is the first to demonstrate that tigecycline is a promising candidate for HCC treatment and highlight the therapeutic value of targeting mitochondrial metabolism in HCC. - Highlights: • Tigecycline selectively targets HCC in vitro and in vivo. • Tigecycline enhances HCC cell response to chemotherapeutic drug. • Tigecycline inhibits mitochondrial translation and functions in HCC cells. • Tigecycline induces oxidative stress and damage in HCC cells. • Mitochondrial biogenesis and respiration is higher in HCC than normal liver cells.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2017

Resveratrol stimulates mitochondrial fusion by a mechanism requiring mitofusin-2

Resveratrol (RES) is a plant-derived stilbene associated with a wide range of health benefits. Mitochondria are a key downstream target of RES, and in some cell types RES promotes mitochondrial biogenesis, altered cellular redox status, and a shift toward oxidative metabolism. Mitochondria exist as a dynamic network that continually remodels via fusion and fission processes, and the extent of fusion is related to cellular redox status and metabolism. We investigated RES's effects on mitochondrial network morphology in several cell lines using a quantitative approach to measure the extent of network fusion. 48 h continuous treatment with 10–20 μM RES stimulated mitochondrial fusion in C2C12 myoblasts, PC3 cancer cells, and mouse embryonic fibroblasts stimulated significant increases in fusion in all instances, resulting in larger and more highly branched mitochondrial networks. Mitofusin-2 (Mfn2) is a key protein facilitating mitochondrial fusion, and its expression was also stimulated by RES. Using Mfn2-null cells we demonstrated that RES's effects on mitochondrial fusion, cellular respiration rates, and cell growth are all dependent upon the presence of Mfn2. Taken together, these results demonstrate that Mfn2 and mitochondrial fusion are affected by RES in ways that appear to relate to RES's known effects on cellular metabolism and growth. - Highlights: • Resveratrol (RES) stimulated mitochondrial fusion in multiple cell types. • More networks and more branches per network in RES treated cells. • RES effect on mitochondrial fusion was absent in Mitofusin-2 KO cells. • RES effects on cell respiration and growth abolished in Mitofusin-2 KO cells. • Results indicate a key role for Mitofusin-2 in RES effects.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2018

Antibiotic bedaquiline effectively targets growth, survival and tumor angiogenesis of lung cancer through suppressing energy metabolism

Highlights: • Bedaquiline targets lung cancer in vitro and in vivo. • Bedaquiline potently inhibits angiogenesis in vitro and in vivo. • Bedaquiline inhibits mitochondrial respiration and glycolysis. • Bedaquiline causes energy crisis and oxidative damage. Tumor angiogenesis plays essential roles during lung cancer progression and metastasis. Therapeutic agent that targets both tumor cell and vascular endothelial cell may achieve additional anti-tumor efficacy. We demonstrate that bedaquiline, a FDA-approved antibiotic drug, effectively targets lung cancer cells and angiogenesis. Bedaquiline dose-dependently inhibits proliferation and induces apoptosis of a panel of lung cancer cell lines regardless of subtypes and molecular heterogeneity. Bedaquiline also inhibits capillary network formation of human lung tumor associated-endothelial cell (HLT-EC) on Matrigel and its multiple functions, such as spreading, proliferation and apoptosis, even in the presence of vascular endothelial growth factor (VEGF). We further demonstrate that bedaquiline acts on lung cancer cells and HLT-EC via inhibiting mitochondrial respiration and glycolysis, leading to ATP reduction and oxidative stress. Consistently, oxidative damage on DNA, protein and lipid were detected in cells exposed to bedaquiline. Importantly, the results obtained in in vitro cell culture are reproducible in in vivo xenograft lung cancer mouse model, confirming that bedaquiline suppresses lug tumor growth and angiogenesis, and increases oxidative stress. Our findings demonstrating that energy depletion is effectively against lung tumor cells and angiogenesis. Our work also provide pre-clinical evidence to repurpose antibiotic bedaquiline for lung cancer treatment.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2018

A novel role for PTK2B in cultured beige adipocyte differentiation

Highlights: • PTK2B protein levels are higher during cultured beige versus white adipogenesis. • Ptk2b knock-out SVF cells have poor white adipocyte differentiation. • Ptk2b knock-out beige adipocytes have elevated lipid accumulation. • Ptk2b knock-out beige adipocytes have a greatly diminished thermogenic gene program. • Ptk2b knock-out beige adipocytes have altered mitochondrial respiration. Adipocyte differentiation is a tightly regulated process which requires the sequential and organized expression of numerous genes and proteins. Phosphorylation of cytoplasmic proteins and key transcription factors represents a critical regulatory mechanism of the process leading to adipocyte maturation and modulation of associated metabolic pathways. Despite the recognition of the importance of protein phosphorylation in adipocyte biology, relatively little is known about the role of specific kinases in thermogenic (brown or beige) adipocyte differentiation and function. In this study, we demonstrate that the non-receptor protein tyrosine kinase 2 beta (PTK2B) plays a critical role in murine beige adipocyte differentiation. We observed that PTK2B protein expression is associated with beige adipocyte differentiation in cultured, immortalized, inguinal stromal vascular fraction cells. CRISPR/Cas9-mediated knock-out of Ptk2b results in non-differentiating white adipocytes, and differentiated beige adipocytes with significantly reduced thermogenic gene and protein expression, enlarged lipid droplet size, and altered mitochondrial respiration. Together, our data in a cell culture system provides evidence for a role of PTK2B in the differentiation of murine beige adipocytes.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2018

Resistin destroys mitochondrial biogenesis by inhibiting the PGC-1α/ NRF1/TFAM signaling pathway

Highlights: • Resistin caused impairment of mitochondrial biogenesis in neuronal cells. • Resistin induced loss of mitochondrial function by reducing respiration rate and ATP. • Resistin inhibited the PGC-1α/NRF1/TFAM pathway. • PGC-1α abolished the inhibitory effects of resistin in mitochondrial biogenesis. Mitochondrial biogenesis deficits in neuronal cells are associated with the pathological progression of neurodegenerative diseases. Resistin, a secretory adipocytokine, possesses multiple physiological functions in diverse cells and tissues. However, the effects of resistin on mitochondrial biogenesis in neuronal cells are still elusive. In the current study, we found that resistin caused a sustainable decrease in mitochondrial contents, including mitochondrial DNA/nuclear DNA ratio (mtDNA/nDNA), mitochondrial mass, cytochrome b protein expression, and cytochrome c oxidase activity, which were correlated with “loss of mitochondrial function” including reduced mitochondrial respiration rate and ATP production in human SH-SY5Y neuronal cells. Indeed, resistin treatment destroyed the expression of peroxisome proliferator activator receptor gamma-coactivator 1α (PGC-1α), a master regulator of mitochondrial biogenesis, as well as its downstream target genes including nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM). Notably, overexpression of PGC-1α could completely rescue mitochondrial biogenesis and mitochondrial deficits induced by resistin. Mechanistically, inhibition of 5′-adenosine monophosphate-activated protein kinase (AMPK) was shown to mediate the inhibitory effects of resistin on mitochondrial biogenesis.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2023

Correlated particle transport enables biological free energy transduction

Studies of biological transport frequently neglect the explicit statistical correlations among particle site occupancies (i.e., they use a mean-field approximation). Neglecting correlations sometimes captures biological function, even for out-of-equilibrium and interacting systems. Here, we show that neglecting correlations fails to describe free energy transduction, mistakenly predicting an abundance of slippage and energy dissipation, even for networks that are near reversible and lack interactions among particle sites. Interestingly, linear charge transport chains are well described without including correlations, even for networks that are driven and include site-site interactions typical of biological electron transfer chains. We examine three specific bioenergetic networks: a linear electron transfer chain (as found in bacterial nanowires), a near-reversible electron bifurcation network (as in complex III of respiration and other recently discovered structures), and a redox-coupled proton pump (as in complex IV of respiration).

bacterial nanowires↗

DOE OSTI2016

Persistence of the herbicides florasulam and halauxifen-methyl in alluvial and saline alluvial soils, and their effects on microbial indicators of soil quality

In this study, the persistence of florasulam and halauxifen-methyl in combination was investigated in an alluvial (AL) and saline alluvial (SAL) soils under laboratory condition at field recommended (FR) dose (i.e. 12.76 g a.i. ha -1 ), 10 FR and 0FR (control) throughout the experiment. Effect of these herbicides on soil microbial biomass carbon (MBC), basal soil respiration (BSR), substrate induced soil respiration (SIR), hydrolysis of fluorescein diacetate (FDHA) and β-glucosidase activities was also measured under same conditions. The residues of florasulam and haluaxifen-methyl were extracted with acetonitrile using modified QuChERS method, followed by quantification using liquid chromatography-mass spectrometry (LC-MS/MS). Half-lives of florasulam and halauxifen-methyl were in the range of 12.65-16.82 days and 7.13-10.24 days in AL respectively and the same for SAL was 15.28-17.60 days and 7.25-8.88 days. Herbicide treatment inhibited MBC, BSR, SIR, and microbial metabolic quotient (qCO 2 ) up to 30 days of incubation at the applied doses in both the soils. At the end of incubation, FR treated soils became statistically at par with control. However, the FDHA and β-glucosidase activities were affected in both the soils at the applied doses of the herbicide up to 15 days. Thereafter, the FR treated soils were statistically at par with control. Finally, data revealed that, recommended dose of this herbicide formulation did not ultimately impair microbial components of the studied soils.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗

DOE OSTI2024

Non-mercury methylating microbial taxa are integral to understanding links between mercury methylation and elemental cycles in marine and freshwater sediments

The goal of this study was to explore the role of non-mercury (Hg) methylating taxa in mercury methylation and to identify potential links between elemental cycles and Hg methylation. Statistical approaches were utilized to investigate the microbial community and biochemical functions in relation to methylmercury (MeHg) concentrations in marine and freshwater sediments. Sediments were collected from the methylation zone (top 15 cm) in four Hg-contaminated sites. Both abiotic (e.g., sulfate, sulfide, iron, salinity, total organic matter, etc.) and biotic factors (e.g., hgcA, abundances of methylating and non-methylating taxa) were quantified. Random forest and stepwise regression were performed to assess whether non-methylating taxa were significantly associated with MeHg concentration. Co-occurrence and functional network analyses were constructed to explore associations between taxa by examining microbial community structure, composition, and biochemical functions across sites. Regression analysis showed that approximately 80% of the variability in sediment MeHg concentration was predicted by total mercury concentration, the abundances of Hg methylating taxa, and the abundances of the non-Hg methylating taxa. The co-occurrence networks identified Paludibacteraceae and Syntrophorhabdaceae as keystone non Hg methylating taxa in multiple sites, indicating the potential for syntrophic interactions with Hg methylators. Strong associations were also observed between methanogens and sulfate-reducing bacteria, which were likely symbiotic associations. The functional network results suggested that non-Hg methylating taxa play important roles in sulfur respiration, nitrogen respiration, and the carbon metabolism-related functions methylotrophy, methanotrophy, and chemoheterotrophy. Interestingly, keystone functions varied by site and did not involve carbon- and sulfur-related functions only. In conclusion, our findings highlight associations between methylating and non-methylating taxa and sulfur, carbon, and nitrogen cycles in sediment methylation zones, with implications for predicting and understanding the impact of climate and land/sea use changes on Hg methylation.

54 ENVIRONMENTAL SCIENCES↗