Project description:Engineered nanoparticles (ENPs) are increasingly used to generate innovative industrial and medical goods. Because of their broad applications, they form a new class of pollutants with potential eco-toxicological impacts on marine ecosystems. Attempting to evaluate the risk, we investigated the toxicity of Iron and Zinc oxide ENPs on three picophytoplanktonic strains of algae: Micromonas commoda, Ostreococcus tauri and Nannochloris sp. Microalgae responses are highly species-dependent, Micromonas commoda growth being severely impaired by both ENP types whereas Ostreococcus tauri or Nannochloris sp. are resistant. ZnO ENPs have higher toxicity than iron ENPs though growth of M. commoda was severely inhibited by Fe2O3 ENPs. Transcriptome-wide analysis after exposure of M. commoda to ENPs shows that the altered biological processes mainly take place in the cytoplasm and that the response to ENPs is largely metabolic in nature: stimulation of carbohydrate metabolism, light harvesting processes and alteration of the nitrogen pathway. In addition, a severe disruption of ribosome structure and translation processes is observed.
Project description:Micromonas implements a sustained non-photochemical quenching response to phosphate limitation, driven by light harvesting family protein LHCSR. This protein, allows stable growth under P-limitation and increased growth without major LCH adjustment as phosphate becomes more available. Proteomics results show this alga integrates unique strategies to optimize growth under dynamic ocean nutrient conditions.
Project description:BACKGROUND: Human SP-A1 and SP-A2, encoded by SFTPA1 and SFTPA2 and their genetic variants differentially impact alveolar macrophage (AM) functions and regulation, including the miRNome. We investigated whether miRNome differences previously observed between AM from SP-A2 and SP-A1/SP-A2 mice are due to continued qualitative differences or a delayed response of mice carrying a single gene. METHODS: Human transgenic (hTG) mice, carrying SP-A2 or both SP-A genes and SP-A-KO mice were exposed to filtered air (FA) or O3. AM miRNA levels, target gene expression and pathways determined 18 h after O3 exposure. RESULTS: We found: (a) Differences in miRNome due to sex, SP-A genotype, and exposure; (b) miRNome of both sexes was largely downregulated by O3 ; co-ex had fewer changed (≥2X) miRNAs than either group. (c) the number and direction of expression of genes with significant changes in males and females in co-ex is almost the opposite of those in SP-A2; (iv) The same pathways were found in the studied groups; (e) O3 exposure attenuated sex differences; a higher number of genotype-dependent and genotype-independent miRNAs was common in both sexes after O3 exposure. CONCLUSION: Qualitative differences between SP-A2 and co-ex persist 18 h post-O3, and O3 attenuates sex differences.
Project description:Human SP-A1 and SP-A2, encoded by SFTPA1 and SFTPA2 and their genetic variants differentially impact alveolar macrophage (AM) functions and regulation, including the miRNome. single dose of SP-A exogenous treatment of SP-A-KO mice prior to infection, after infection, or at the time of infection significantly improved survival. we investigated the role of exogenous SP-A protein treatment on the regulation of AM miRNome in SP-A-KO mice at the time of infection. Towards this, SP-A-KO male and female mice were infected with K. pneumoniae alone or in combination with exogenous SP-A2 (1A0) protein for 6 h, and the expression levels of AM miRNAs, target mRNAs of the significant miRNAs, and pathways involved were studied. We found (i) significant differences in AM miRNome of KO in terms of sex and exposure; (ii) the expression of the overwhelming majority of miRNA targets in KO males were increased in response to infection and exogenous SP-A2 (1A0) protein treatment at the time of infection; (iii) miRNA-mRNA targets were involved in the pro-inflammatory response, anti-apoptosis, cell cycle, cellular growth and proliferation pathways. These data may assist in studying molecular mechanisms of exogenous SP-A mediated the AM miRNome regulation and potentially identify novel therapeutic targets for K. pneumoniae infection.