Methane (CH4) strongly contributes to observed global warming. As natural CH4 emissions mainly originate from wet ecosystems, it is important to unravel how climate change may affect these emissions. This is especially true for ebullition (bubble flux from sediments), a pathway that has long been underestimated but generally dominates emissions. Here we show a remarkably strong relationship between CH4 ebullition and temperature across a wide range of freshwater ecosystems on different continents using multi-seasonal CH4 ebullition data from the literature. As these temperature–ebullition relationships may have been affected by seasonal variation in organic matter availability, we also conducted a controlled year-round mesocosm experiment. Here 4 °C warming led to 51% higher total annual CH4 ebullition, while diffusion was not affected. Our combined findings suggest that global warming will strongly enhance freshwater CH4 emissions through a disproportional increase in ebullition (6–20% per 1 °C increase), contributing to global warming.

Abstract. Global warming has been shown to affect ecosystems worldwide. Warming may, for instance, disrupt plant herbivore synchrony and bird phenology in terrestrial systems, reduce primary production in oceans, and promote toxic cyanobacterial blooms in freshwater lakes. Responses of communities will not only depend on direct species-specific temperature effects, but also on indirect effects related to bottom-up and top-down processes. Here, we investigated the impact of warming on freshwater phytoplankton community dynamics, and assessed the relative contribution of nutrient availability, fungal parasitism, and grazing therein. For this purpose, we performed an indoor mesocosm experiment following seasonal temperature dynamics of temperate lakes and a warmed (+4°C) scenario from early spring to late summer. We assessed phytoplankton biomass, C:N:P stoichiometry and community composition, dissolved nutrient availabilities, fungal parasite (i.e., chytrid) prevalence, and zooplankton abundance. Warming led to an overall reduction in phytoplankton biomass as well as lower C:P and N:P ratios, while phytoplankton community composition remained largely unaltered. Warming resulted in an earlier termination of the diatom spring bloom, and an epidemic of its fungal parasite ended earlier as well. Furthermore, warming advanced zooplankton phenology, leading to an earlier top-down control on phytoplankton in the period after the spring bloom. Linear model analysis showed that most of the observed variance in phytoplankton biomass was related to seasonal temperature dynamics in combination with zooplankton abundance. Our findings showed that warming advanced grazer phenology and reduced phytoplankton biomass, thereby demonstrating how bottom-up and top-down related processes may shape future phytoplankton dynamics.

Climate change is expected to favour infectious diseases across ecosystems worldwide. In freshwater and marine environments, parasites play a crucial role in controlling plankton population dynamics. Infection of phytoplankton populations will cause a transfer of carbon and nutrients into parasites, which may change the type of food available for higher trophic levels. Some phytoplankton species are inedible to zooplankton, and the termination of their population by parasites may liberate otherwise unavailable carbon and nutrients. Phytoplankton spring blooms often consist of large diatoms inedible for zooplankton, but the zoospores of their fungal parasites may serve as a food source for this higher trophic level. Here, we investigated the impact of warming on the fungal infection of a natural phytoplankton spring bloom and followed the response of a zooplankton community. Experiments were performed in ca. 1000 L indoor mesocosms exposed to a controlled seasonal temperature cycle and a warm (+4 °C) treatment in the period from March to June 2014. The spring bloom was dominated by the diatom Synedra. At the peak of infection over 40% of the Synedra population was infected by a fungal parasite (i.e. a chytrid) in both treatments. Warming did not affect the onset of the Synedra bloom, but accelerated its termination. Peak population density of Synedra tended to be lower in the warm treatments. Furthermore, Synedra carbon: phosphorus stoichiometry increased during the bloom, particularly in the control treatments. This indicates enhanced phosphorus limitation in the control treatments, which may have constrained chytrid development. Timing of the rotifer Keratella advanced in the warm treatments and closely followed chytrid infections. The chytrids' zoospores may thus have served as an alternative food source to Keratella. Our study thus emphasizes the importance of incorporating not only nutrient limitation and grazing, but also parasitism in understanding the response of plankton communities towards global warming.

Signaling through the interleukin-4/interleukin-13 (IL-4/IL-13) receptor complex is a crucial mechanism in the development of bronchial asthma and chronic obstructive pulmonary disease (COPD). In bronchial epithelial cells, this signaling pathway leads to changes in the expression levels of several genes that are possibly involved in protection against and/or pathogenesis of these diseases. The expression of pendrin (SLC26A4), a candidate for the latter category, is upregulated by IL-4/IL-13 and leads to overproduction of mucus and increased viscosity of the airway surface liquid (ASL). Therefore, elucidating the transcriptional regulation of pendrin could aid in the development of new pharmacological leads for asthma and/or COPD therapy. Here we show that IL-4/IL-13 significantly increased human pendrin promoter activity in HEK-Blue cells but not in STAT6-deficient HEK293 Phoenix cells; that mutation of the STAT6 binding site (N(4) GAS motif) rendered the promoter insensitive to IL-4/IL-13; and that addition of the N(4) GAS motif to an IL-4/IL-13-unresponsive sequence of the human pendrin promoter conferred sensitivity to both ILs.