Antibiotics as a silent driver of climate change? A case study investigating methane production in freshwater sediments

Methane (CH4) is the second most important greenhouse gas after carbon dioxide (CO2) and is inter alia produced in natural freshwater ecosystems. Given the rise in CH4 emissions from natural sources, researchers are investigating environmental factors and climate change feedbacks to explain this increment. Despite being omnipresent in freshwaters, knowledge on the influence of chemical stressors of anthropogenic origin (e.g., antibiotics) on methanogenesis is lacking. To address this knowledge gap, we incubated freshwater sediment under anaerobic conditions with a mixture of five antibiotics at four levels (from 0 to 5000 mu g/L) for 42 days. Weekly measurements of CH4 and CO2 in the headspace, as well as their compound-specific delta C-13, showed that the CH4 production rate was increased by up to 94% at 5000 mu g/L and up to 29% at field-relevant concentrations (i.e., 50 mu g/L). Metabarcoding of the archaeal and eubacterial 16S rRNA gene showed that effects of antibiotics on bacterial community level (i.e., species composition) may partially explain the observed differences in CH4 production rates. Despite the complications of transferring experimental CH4 production rates to realistic field conditions, the study indicated that chemical stressors contribute to the emissions of greenhouse gases by affecting the methanogenesis in freshwaters

The ER protein Ema19 facilitates the degradation of non-imported mitochondrial precursor proteins

For the biogenesis of mitochondria, hundreds of proteins need to be targeted from the cytosol into the various compartments of this organelle. The intramitochondrial targeting routes these proteins take to reach their respective location in the organelle are well understood. However, the early targeting processes, from cytosolic ribosomes to the membrane of the organelle, are still largely unknown. In this study, we present evidence that an integral membrane protein of the endoplasmic reticulum (ER), Ema19, plays a role in this process. Mutants lacking Ema19 show an increased stability of mitochondrial precursor proteins, indicating that Ema19 promotes the proteolytic degradation of non-productive precursors. The deletion of Ema19 improves the growth of respiration-deficient cells, suggesting that Ema19-mediated degradation can compete with productive protein import into mitochondria. Ema19 is the yeast representative of a conserved protein family. The human Ema19 homolog is known as sigma 2 receptor or TMEM97. Though its molecular function is not known, previous studies suggested a role of the sigma 2 receptor as a quality control factor in the ER, compatible with our observations about Ema19. More globally, our data provide an additional demonstration of the important role of the ER in mitochondrial protein targeting