Exposure to polycyclic aromatic carbons (PAHs) poses a growing risk to coral reefs due to increasing shipping and petroleum extraction in tropical waters. Damaging effects of specific PAHs can be further enhanced by the presence of ultraviolet radiation, known as phototoxicity. We tested phototoxic effects of the PAHs anthracene and phenanthrene on larvae of the scleractinian coral Acropora tenuis in the presence and absence of UVA (320-400 nm). Activity of superoxide dismutase (SOD) enzyme was reduced by anthracene while phenanthrene and UVA exposure did not have any effect. Gene expression of MnSod remained constant across all treatments. The genes Catalase, Hsp70 and Hsp90 showed increased expression levels in larvae exposed to anthracene, but not phenanthrene. Gene expression of p53 was upregulated in the presence of UVA, but downregulated when exposed to PAHs. The influence on stress-related biochemical pathways and gene expresson in A. tenuis larvae was considerably greater for anthracene than phenanthrene, and UVA-induced phototoxicity was only evident for anthracene. The combined effects of UVA and PAH exposure on larval survival and metamorphosis paralleled the sub-lethal stress responses, clearly highlighting the interaction of UVA on anthracene toxicity and ultimately the coral's development.

Atmospheric transport is a major vector for the long-range transport of microbial communities, maintaining connectivity among them and delivering functionally important microbes, such as pathogens. Though the taxonomic diversity of aeolian microorganisms is well characterized, the genomic functional traits underpinning their survival during atmospheric transport are poorly characterized. Here we use functional metagenomics of dust samples collected on the Global Dust Belt to initiate a Gene Catalogue of Aeolian Microbiome (GCAM) and explore microbial genetic traits enabling a successful aeolian lifestyle in Aeolian microbial communities. The GCAM reported here, derived from ten aeolian microbial metagenomes, includes a total of 2,370,956 non-redundant coding DNA sequences, corresponding to a yield of ~31 × 10⁶ predicted genes per Tera base-pair of DNA sequenced for the aeolian samples sequenced. Two-thirds of the cataloged genes were assigned to bacteria, followed by eukaryotes (5.4%), archaea (1.1%), and viruses (0.69%). Genes encoding proteins involved in repairing UV-induced DNA damage and aerosolization of cells were ubiquitous across samples, and appear as fundamental requirements for the aeolian lifestyle, while genes coding for other important functions supporting the aeolian lifestyle (chemotaxis, aerotaxis, germination, thermal resistance, sporulation, and biofilm formation) varied among the communities sampled.

Intake of high-protein (HP) diets has increased over the last years, mainly due to their popularity for body weight control. Liver is the main organ handling ingested macronutrients and it is associated with the beginning of different pathologies. We aimed to deepen our knowledge on molecular pathways affected by long-term intake of an HP diet. We performed a transcriptome analysis on liver of rats chronically fed with a casein-rich HP diet and analyzed molecular parameters related to liver injury. Chronic increase in the dietary protein/carbohydrate ratio up-regulated processes related with amino acid uptake/metabolism and lipid synthesis, promoting a molecular environment indicative of hepatic triacylglycerol (TG) deposition. Moreover, changes in expression of genes involved in acid-base maintenance and oxidative stress indicate alterations in the pH balance due to the high acid load of the diet, which has been linked to liver/health damage. Up-regulation of immune-related genes was also observed. In concordance with changes at gene expression level, we observed increased liver TG content and increased serum markers of hepatic injury/inflammation (aspartate transaminase, C-reactive protein and TNF-alpha). Moreover, the HP diet strongly increased hepatic mRNA and protein levels of HSP90, a marker of liver injury. Thus, we show for the first time that long-term consumption of an HP diet, resulting in a high acid load, results in a hepatic transcriptome signature reflecting increased TG deposition and increased signs of health risk (increased inflammation, alterations in the acid-base equilibrium and oxidative stress). Persistence of this altered metabolic status could have unhealthy consequences.