Search bioRxiv⌕ Search

Biology subjects

Arenas, F.

Publications and source records attributed to Arenas, F..

3 recordsLinked to original sources

Reduced glutathione levels in Enterococcus faecalis trigger metabolic and transcriptional compensatory adjustments during iron exposure.

Enterococcus faecalis, a facultative anaerobic pathogen and common constituent of the gastrointestinal microbiota, must navigate varying iron levels within the host. This study explores its response to iron supplementation in a glutathione-deficient mutant strain ({Delta}gsh). We examined the transcriptomic and metabolic responses of a glutathione synthetase mutant strain ({Delta}gsh) exposed to iron supplementation, integrating these data into a genome-scale metabolic model (GSMM). Our results show that under glutathione deficiency, E. faecalis reduces intracellular iron levels and shifts its transcriptional response to prioritize energy production genes. Notably, basal metabolites, including arginine, increase. The GSMM highlights the importance of arginine metabolism, particularly the arc operon (anaerobic arginine catabolism), as a compensatory mechanism for reduced glutathione during iron exposure. These findings provide insights into how E. faecalis adjusts metal homeostasis and transcriptional/metabolic processes to mitigate the effects of oxidative stress caused by iron. IMPORTANCEIron is essential for bacterial survival, yet its excess can be harmful through increase of oxidative stress. Enterococcus faecalis, a bacterium common member of the human gut, must carefully balance its iron levels in order to survive in changing environments. This study studies how E. faecalis compensates the reduced levels of glutathione --a key antioxidant-- when exposed to high iron concentrations. We discovered that E. faecalis lowers its intracellular iron levels under glutathione decrease and reprograms its metabolism to prioritize energy production. These findings provide valuable insights into bacterial adaptation mechanisms under oxidative stress conditions, which could influence the development of new strategies to combat bacterial infections.

systems biology↗

Heat Stress on the brown Seaweed Ascophyllum nodosum: differential population sensitivity to future climate.

Accurate forecasts of the biological impacts of climate change require a better understanding of how small-scale temperature variability affects individual physiology and population dynamics. But doing so for intertidal species with large distribution ranges, while also accounting for the effect of local adaptation, presents numerous technical challenges. Here, we assessed the macroecological consequences of thermal stress on the cold-adapted brown seaweed Ascophyllum nodosum across its European distribution. We collected specimens from ten populations spanning latitudes 41{degrees}N to 60{degrees}N and subjected them to simulated intertidal heat stress using a novel, custom-built experimental setup that replicated realistic conditions, including tidal cycles, light conditions, and temperature trajectories based on in situ data. Our factorial design comprised eight experimental treatments, combining two high-tide water temperatures (15 {degrees}C and 20.5 {degrees}C) with four low-tide peak temperatures (28.5 {degrees}C to 40.5 {degrees}C). Physiological performance was evaluated through measurements of growth, mortality, and oxygen production. Results indicate that thermal stress is more closely associated with the magnitude of temperature change between high and low tides rather than the absolute maximum temperatures reached. Algae exposed to warmer water temperatures (20.5 {degrees}C) consistently outperformed those in colder water (15 {degrees}C), suggesting that cold upwelled waters at the species southern limit may not be essential for survival. Southern populations demonstrated higher resilience to thermal stress than central and northern counterparts. Integrating these physiological responses with climate projections, we employed demographic models to forecast long-term population dynamics. The models predict that future climatic conditions could exceed the thermal resilience of specific populations, leading to uneven impacts across the European distribution of the species. Notwithstanding, range contractions may occur at the warm edge of the distribution, where populations, though more resilient to thermal stress, could still be overwhelmed by the pace of warming. This study underscores the importance of realistic experimental simulations in evaluating species thermal tolerance and highlights the potential for climate change to differentially impact populations along large latitudinal gradients.

ecology↗

Soft-metal(loid)s induce protein aggregation in Escherichia coli

Metal(loid) salts have been used to treat infectious diseases due to their exceptional biocidal properties at low concentrations. However, the mechanism of their toxicity has yet to be fully elucidated. The production of reactive oxygen species (ROS) has been linked to the toxicity of soft metal(loid)s such as Ag(I), Au(III), As(III), Cd(II), Hg(II), and Te(IV). Nevertheless, few reports have described the direct, or ROS-independent, effects of some of these soft-metal(loid)s on bacteria, including the dismantling of iron-sulphur clusters [4Fe-4S] and the accumulation of porphyrin IX. Here, we used genome-wide genetic, proteomic, and biochemical approaches under anaerobic conditions to evaluate the direct mechanisms of toxicity of these metal(loid)s in Escherichia coli. We found that certain soft-metal(loid)s promote protein aggregation in a ROS-independent manner. This aggregation occurs during translation in the presence of Ag(I), Au(III), Hg(II), or Te(IV) and post-translationally in cells exposed to Cd(II) or As(III). We determined that aggregated proteins were involved in several essential biological processes that could lead to cell death. For instance, several enzymes involved in amino acid biosynthesis were aggregated after soft-metal(loid) exposure, disrupting intracellular amino acid concentration. We also propose a possible mechanism to explain how soft-metal(loid)s act as proteotoxic agents.

microbiology↗