Cross species multi-omics reveals cell wall sequestration and elevated global transcript abundance as mechanisms of boron tolerance in plants.

Boron toxicity is a world-wide problem for crops, yet we have a limited understanding of the genetic responses and adaptive mechanisms to this stress in plants. We employed a cross-species comparison between boron stress-sensitive Arabidopsis thaliana and its boron stress-tolerant extremophyte relative Schrenkiella parvula, and a multi-omics approach integrating genomics, transcriptomics, metabolomics and ionomics to assess plant responses and adaptations to boron stress. Schrenkiella parvula maintains lower concentrations of total boron and free boric acid than Arabidopsis when grown with excess boron. Schrenkiella parvula excludes excess boron more efficiently than Arabidopsis, which we propose is partly driven by SpBOR5, a boron transporter that we functionally characterize in this study. Both species use cell walls as a partial sink for excess boron. When accumulated in the cytoplasm, excess boron appears to interrupt RNA metabolism. The extremophyte S. parvula facilitates critical cellular processes while maintaining the pool of ribose-containing compounds that can bind with boric acid. The S. parvula transcriptome is pre-adapted to boron toxicity. It exhibits substantial overlaps with the Arabidopsis boron-stress responsive transcriptome. Cell wall sequestration and increases in global transcript levels under excess boron conditions emerge as key mechanisms for sustaining plant growth under boron toxicity.

Trophodynamics and mercury bioaccumulation in reef and open-ocean fishes from The Bahamas with a focus on two teleost predators.

Identifying prey resource pools supporting fish biomass can elucidate trophic pathways of pollutant bioaccumulation. We used multiple chemical tracers (carbon [δ13C] and nitrogen [δ15N] stable isotopes and total mercury [THg]) to identify trophic pathways and measure contaminant loading in upper trophic level fishes residing at a reef and open-ocean interface near Eleuthera in the Exuma Sound, The Bahamas. We focused predominantly on the trophic pathways of mercury bioaccumulation in dolphinfish Coryphaena hippurus and wahoo Acanthocybium solandri, 2 commonly consumed pelagic sportfish in the region. Despite residing within close proximity to productive and extensive coral reefs, both dolphinfish and wahoo relied almost exclusively on open-ocean prey over both short and long temporal durations. A larger isotopic niche of dolphinfish suggested a broader diet and some potential prey differentiation between the 2 species. THg concentrations in dolphinfish (0.2 ± 0.1 ppm) and wahoo (0.3 ± 0.3 ppm) were mostly below recommended guidelines for humans (US Environmental Protection Agency (EPA) = 0.3 ppm, US Food and Drug Administration (FDA)= 1.0 ppm) and were within ranges previously reported for these species. However, high THg concentrations were observed in muscle and liver tissue of commonly consumed reef-associated fishes, identifying a previously unrecognized route of potentially toxic Hg exposure for human consumers on Eleuthera and neighboring islands.

Mercury and selenium levels, and Se:Hg molar ratios in freshwater fish from South Louisiana.

Ample historical evidence has demonstrated the neurotoxicity of organic Hg. However, several studies have suggested that Se effectively sequesters MeHg. The affinity of Hg is up to ≈106 times higher for Se molecules than for comparable sulfur molecules, most of which are components of brain enzymes. The neurotoxicity of MeHg is associated with its binding to Se and the resultant interference with selenoenzymes (Ralston & Raymond, Global Advances in Selenium Research from Theory to Application, 2016). Therefore, having ample Se reserves is an effective way to mitigate MeHg's toxicity. When the molar ratios of Se to Hg in fish exceed 1.0, ingestion of the fish is unlikely to deplete Se reserves. The goal of this study was to determine the Hg and Se levels, and the Se:Hg molar ratios in freshwater fish from south Louisiana and the implications of those ratios with respect to fish consumption and Hg advisories. Five waterbodies were surveyed (University lake, Calcasieu lake, Toledo Bend, the Atchafalaya River and Henderson Lake). The sampled species included black drum (Pogonias cromis), catfish sp., largemouth bass (Micropterus salmoides) and bluegill (Eupomotis macrochirus). All fish were assayed for total Hg and Se. The average Hg concentration was 0.001 µmol g-1 (0.21 ppm), and all concentrations were below the 1 ppm US FDA action level (from 3.1 × 10-5 to 0.003 µmol g-1). Se concentrations exceeded Hg concentrations in most cases. The average Se concentration was 0.003 µmol g-1 (0.27 ppm), all concentrations were around or less than 1.0 ppm (from 3.7 × 10-4 to 0.017 µmol g-1). Hence, the Se:Hg molar ratios were >1 in all fish except largemouth bass from Henderson Lake. In general, Se was detected in sufficient amounts to sequester Hg, but consumption of largemouth bass from Henderson Lake would pose no risk only if anglers followed the posted Hg advisory. For advisory purposes, perhaps, both Hg and Se levels and Se:Hg molar ratios should be considered. In general, the results indicated that risk assessment will require consideration of both the fish species and body of water, because both can influence Se and Hg concentrations and Se:Hg molar ratios.

Multiple episodes of extensive marine anoxia linked to global warming and continental weathering following the latest Permian mass extinction.

Explaining the ~5-million-year delay in marine biotic recovery following the latest Permian mass extinction, the largest biotic crisis of the Phanerozoic, is a fundamental challenge for both geological and biological sciences. Ocean redox perturbations may have played a critical role in this delayed recovery. However, the lack of quantitative constraints on the details of Early Triassic oceanic anoxia (for example, time, duration, and extent) leaves the links between oceanic conditions and the delayed biotic recovery ambiguous. We report high-resolution U-isotope (δ238U) data from carbonates of the uppermost Permian to lowermost Middle Triassic Zal section (Iran) to characterize the timing and global extent of ocean redox variation during the Early Triassic. Our δ238U record reveals multiple negative shifts during the Early Triassic. Isotope mass-balance modeling suggests that the global area of anoxic seafloor expanded substantially in the Early Triassic, peaking during the latest Permian to mid-Griesbachian, the late Griesbachian to mid-Dienerian, the Smithian-Spathian transition, and the Early/Middle Triassic transition. Comparisons of the U-, C-, and Sr-isotope records with a modeled seawater PO43- concentration curve for the Early Triassic suggest that elevated marine productivity and enhanced oceanic stratification were likely the immediate causes of expanded oceanic anoxia. The patterns of redox variation documented by the U-isotope record show a good first-order correspondence to peaks in ammonoid extinctions during the Early Triassic. Our results indicate that multiple oscillations in oceanic anoxia modulated the recovery of marine ecosystems following the latest Permian mass extinction.

Rapid expansion of oceanic anoxia immediately before the end-Permian mass extinction.

Periods of oceanic anoxia have had a major influence on the evolutionary history of Earth and are often contemporaneous with mass extinction events. Changes in global (as opposed to local) redox conditions can be potentially evaluated using U system proxies. The intensity and timing of oceanic redox changes associated with the end-Permian extinction horizon (EH) were assessed from variations in (238)U/(235)U (δ(238)U) and Th/U ratios in a carbonate section at Dawen in southern China. The EH is characterized by shifts toward lower δ(238)U values (from -0.37‰ to -0.65‰), indicative of an expansion of oceanic anoxia, and higher Th/U ratios (from 0.06 to 0.42), indicative of drawdown of U concentrations in seawater. Using a mass balance model, we estimate that this isotopic shift represents a sixfold increase in the flux of U to anoxic facies, implying a corresponding increase in the extent of oceanic anoxia. The intensification of oceanic anoxia coincided with, or slightly preceded, the EH and persisted for an interval of at least 40,000 to 50,000 y following the EH. These findings challenge previous hypotheses of an extended period of whole-ocean anoxia prior to the end-Permian extinction.