Methylomonadaceae was the active and dominant methanotroph in Tibet lake sediments.

Methane (CH4), an important greenhouse gas, significantly impacts the local and global climate. Our study focused on the composition and activity of methanotrophs residing in the lakes on the Tibetan Plateau, a hotspot for climate change research. Based on the field survey, the family Methylomonadaceae had a much higher relative abundance in freshwater lakes than in brackish and saline lakes, accounting for ~92% of total aerobic methanotrophs. Using the microcosm sediment incubation with 13CH4 followed by high throughput sequencing and metagenomic analysis, we further demonstrated that the family Methylomonadaceae was actively oxidizing CH4. Moreover, various methylotrophs, such as the genera Methylotenera and Methylophilus, were detected in the 13C-labeled DNAs, which suggested their participation in CH4-carbon sequential assimilation. The presence of CH4 metabolism, such as the tetrahydromethanopterin and the ribulose monophosphate pathways, was identified in the metagenome-assembled genomes of the family Methylomonadaceae. Furthermore, they had the potential to adapt to oxygen-deficient conditions and utilize multiple electron acceptors, such as metal oxides (Fe3+), nitrate, and nitrite, for survival in the Tibet lakes. Our findings highlighted the predominance of Methylomonadaceae and the associated microbes as active CH4 consumers, potentially regulating the CH4 emissions in the Tibet freshwater lakes. These insights contributed to understanding the plateau carbon cycle and emphasized the significance of methanotrophs in mitigating climate change.

Inhibition of protein kinase C protects against paraoxon-mediated neuronal cell death.

Paraoxon, the active metabolite of parathion, is an acetylcholinesterases (AChE) inhibitor that kills cultured cerebellar granule cell neurons via an apoptotic mechanism. Protein kinase C is an enzyme with diverse functions but its role in paraoxon-induced cell death is unknown. We show that a neurotoxic concentration of paraoxon increases PKC phosphorylation. We tested whether PKC is involved in paraoxon-induced neuronal cell death by using the PKC activator, phorbol 12-myristate 13-acetate (TPA). TPA increases PKC activity and enhances the neurotoxic effect of paraoxon by 28%. In sharp contrast, addition of the PKC inhibitor Ro-31-8220 protects more than 30% neurons that would otherwise die from paraoxon-induced neuronal cell death in either a pretreatment or post-treatment paradigm and markedly reduces phospho-PKC pan levels. We also show that the pretreatment of Ro-31-8220 blocks paraoxon-induced caspase-3 activity completely. These results suggest that activation of protein kinase C is required for paraoxon neurotoxicity.