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:Puccinia graminis f. sp. tritici is the cause of wheat stem rust. A microarray was designed from genes predicted from the P. graminis f. sp. tritici genome assembly, and gene expression measured for four conditions which include wheat or barley infecting growth stages initiated by urediniospores. mRNA was prepared from fresh urediniospores, uredinospores germinated for 24 hr, wheat seedlings infected with urediniospores for 8 days, and barley seedlings infected with urediniospores for 8 days. The asexual uredinial infection cycle on wheat produces additional urediniospores, which can start new cycles of wheat infection and are readily spread by aerial transport. This expression data is further described in Duplessis et al, Obligate Biotrophy Features Unraveled by the Genomic Analysis of the Rust Fungi, Melampsora larici-populina and Puccinia graminis f. sp. tritici
Project description:Puccinia graminis f. sp. tritici is the cause of wheat stem rust. A microarray was designed from genes predicted from the P. graminis f. sp. tritici genome assembly, and gene expression measured for four conditions which include wheat or barley infecting growth stages initiated by urediniospores. mRNA was prepared from fresh urediniospores, uredinospores germinated for 24 hr, wheat seedlings infected with urediniospores for 8 days, and barley seedlings infected with urediniospores for 8 days. The asexual uredinial infection cycle on wheat produces additional urediniospores, which can start new cycles of wheat infection and are readily spread by aerial transport. This expression data is further described in Duplessis et al, Obligate Biotrophy Features Unraveled by the Genomic Analysis of the Rust Fungi, Melampsora larici-populina and Puccinia graminis f. sp. tritici A total of 12 samples were analyzed, including three biological replicates of the four conditions.
Project description:Macrophages play fundamental roles in regulation of inflammatory responses to pathogens, resolution of inflammation and tissue repair, and maintenance of tissue homeostasis. The long (L) and short (S) isoforms of SP-R210/MYO18A, a macrophage receptor for surfactant protein A (SP-A) and C1q, regulate basal and inflammatory macrophage phenotype at multiple gene expression, translational, and subcellular levels in addition to their SP-A and C1q-mediated functions; disruption of L renders macrophages hyper-inflammatory, although the underlying mechanism had previously been unexplored. We questioned whether disruption of the L isoform would alter the global genomic responses. RNA sequencing analysis of SP-R210L(DN) macrophages revealed basal and influenza induced upregulation of genes associated with inflammatory pathways, including TLR, RIG-I, NOD, and cytoplasmic DNA signaling, whereas knockdown of both SP-R210 isoforms (L and S) only resulted in increased RIG-I and NOD signaling. Chromatin immunoprecipitation sequencing (ChIP-seq) analysis showed increased genome-wide deposition of the pioneer transcription factor PU.1 in SP-R210L(DN) compared to WT cells. ChIP-seq analysis of histone H3 methylation showed alterations in both repressive (H3K9me3 and H3K27me3) and transcriptionally active (H3K9me3) histone marks. Influenza A virus (IAV) infection, which stimulates an array of cytosolic and TLR-mediated antiviral mechanisms, resulted in differential redistribution between proximal promoter and distal sites and decoupling of PU.1 binding from Toll-like receptor regulated gene promoters in SP-R210L(DN) cells. Our findings suggest that SP-R210L-deficient macrophages are poised with an open PU.1-primed chromatin conformation to rapidly respond to inflammatory and metabolic stimuli.