Ecotoxicology of microplastics in Daphnia: A review focusing on microplastic properties and multiscale attributes of Daphnia.

The ubiquitous presence of microplastics in aquatic environments is considered a global threat to aquatic organisms. Species of the genus Daphnia provide an important link between aquatic primary producers and consumers of higher trophic levels; furthermore, these organisms exhibit high sensitivity to various environmental pollutants. Hence, the biological effects of microplastics on Daphnia species are well documented. This paper reviews the latest research regarding the ecotoxicological effects of microplastics on Daphnia, including the: 1) responses of individual, population, and community attributes of Daphnia to microplastics; 2) influence of the physical and chemical properties of microplastics; and 3) joint toxicity of microplastics and other pollutants on responses of Daphnia. Our literature review found that the published literature does not provide sufficient evidence to reveal the risks of microplastics at the population and community levels. Furthermore, we emphasized that high-level analysis has more general implications for understanding how individual-level research can reveal the ecological hazards of microplastics on Daphnia. Based on this review, we suggest avenues for future research, including microplastic toxicology studies based on both omics-based and community-level methods, especially the latter.

Microplastics can affect the trophic cascade strength and stability of plankton ecosystems via behavior-mediated indirect interactions.

The negative effects of microplastics on the normal growth of aquatic organisms have been well studied, but relatively little is known about their potential adverse effects on the function and stability of aquatic ecosystems. We investigated here the effects of polyethylene (PE) microplastics on several aspects of plankton ecosystems, including Daphnia magna behavior, the grazing rate of D. magna on Chlorella vulgaris cells, trophic-cascade effects in the C. vulgaris-D. magna-larval damselfly food chain, the life-history of D. magna, and the stability and persistence of the D. magna-larval damselfly system. PE microplastics decreased the D. magna grazing rate as a result of reductions in their heart rate and hopping frequency. In the trophic-cascade experiment, PE microplastics increased the foraging success of larval damselflies on grazers due to hopping inhibition in grazers, which ultimately strengthened the trophic-cascade effect on algal growth. Long-term exposure to PE microplastics reduced the stability and persistence of the grazer population via increased predation risk and reduced reproductive capacity for grazer species. This study provides evidence that microplastics can affect the trophic cascade strength and stability of plankton ecosystems via behavior-mediated indirect interactions, suggesting that microplastics have more extensive impacts on aquatic ecosystems than presently recognized. ENVIROMENTAL IMPLICATION: The massive production and environmental releasing of microplastics have become ubiquitous in the global environment. The negative effects of microplastics on the normal growth of aquatic organisms have been well studied, but little is known about potential adverse effects on the function and stability of aquatic ecosystems. Here, we found that microplastics increased the positive impacts of larval damselflies on algal growth, and reduced the stability and persistence of plankton ecosystems via a behavior-mediated indirect interaction. To our knowledge, this is the first systematic study assessing the effects of microplastics on the community-level characteristics of a freshwater ecosystem. SYNOPSIS: PE microplastics affect trophic cascade strength and reduce the stability and persistence of plankton ecosystems via behavior-mediated indirect interactions.

ATG16L1 phosphorylation is oppositely regulated by CSNK2/casein kinase 2 and PPP1/protein phosphatase 1 which determines the fate of cardiomyocytes during hypoxia/reoxygenation.

Recent studies have shown that the phosphorylation and dephosphorylation of ULK1 and ATG13 are related to autophagy activity. Although ATG16L1 is absolutely required for autophagy induction by affecting the formation of autophagosomes, the post-translational modification of ATG16L1 remains elusive. Here, we explored the regulatory mechanism and role of ATG16L1 phosphorylation for autophagy induction in cardiomyocytes. We showed that ATG16L1 was a phosphoprotein, because phosphorylation of ATG16L1 was detected in rat cardiomyocytes during hypoxia/reoxygenation (H/R). We not only demonstrated that CSNK2 (casein kinase 2) phosphorylated ATG16L1, but also identified the highly conserved Ser139 as the critical phosphorylation residue for CSNK2. We further established that ATG16L1 associated with the ATG12-ATG5 complex in a Ser139 phosphorylation-dependent manner. In agreement with this finding, CSNK2 inhibitor disrupted the ATG12-ATG5-ATG16L1 complex. Importantly, phosphorylation of ATG16L1 on Ser139 was responsible for H/R-induced autophagy in cardiomyocytes, which protects cardiomyocytes from apoptosis. Conversely, we determined that wild-type PPP1 (protein phosphatase 1), but not the inactive mutant, associated with ATG16L1 and antagonized CSNK2-mediated phosphorylation of ATG16L1. Interestingly, one RVxF consensus site for PPP1 binding in the C-terminal tail of ATG16L1 was identified; mutation of this site disrupted its association with ATG16L1. Notably, CSNK2 also associated with PPP1, but ATG16L1 depletion impaired the interaction between CSNK2 and PPP1. Collectively, these data identify ATG16L1 as a bona fide physiological CSNK2 and PPP1 substrate, which reveals a novel molecular link from CSNK2 to activation of the autophagy-specific ATG12-ATG5-ATG16L1 complex and autophagy induction.