Project description:We employed a proteogenomics workflow to identify microproteins encoded by small Open Reading Frames (ORFs) in the genome of Mycobacterium smegmatis strain mc²155.
Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mycobacterium smegmatis C2 155. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of Mycobacterium smegmatis C2 155. We find that amino acids synthesis and degradation genes, genes that are expressed.The ratio of gene expression based on transcriptome substantiate an enhanced TCA cycle. The upregulation of Lys1 was found to prompt this degradation of lysine. The transformation from glutamine to glutamate as well as arginine was mediated by glsA (MSMEG_3818) , of which glutamate engaged into the TCA cycle via α-ketoglutarate. The phenylalanine was degraded into fumarate via mhpB. The succinate formation from asparate degradation was mediated by methylcitrate dehydratase (MSMEG_6645), carboxyvinyl-carboxyphosphonate phosphorylmutase (MSMEG_2506) and MSMEG_6855. and therefore reflect metabolism state of strains. Data from sample treated with rifampicin/glutamine reveals the upregulation of respiration.
Project description:How the complex interaction between Mycobacterium tuberculosis (Mtb) and the host is regulated during infection is still not well understood. Using a systems biology approach, we demonstrate here that miR-155 is one of several microRNAs that regulate host gene expression over the first 48 hours of Mtb infection in macrophages. miR-155 regulates the cell survival of Mtb-infected macrophages through SHIP1/AKT signaling. Using timecourse gene expression data, we constructed a miRNA regulatory network for the innate immune response to Mtb infection by WT macrophages. The network suggested a role for seven miRNAs in regulating the host response to Mtb, with miR-155 being one of them. We then validated a role for miR-155 by comparing the response between WT and miR-155-/- macrophages.
Project description:How the complex interaction between Mycobacterium tuberculosis (Mtb) and the host is regulated during infection is still not well understood. Using a systems biology approach, we demonstrate here that miR-155 is one of several microRNAs that regulate host gene expression over the first 48 hours of Mtb infection in macrophages. miR-155 regulates the cell survival of Mtb-infected macrophages through SHIP1/AKT signaling. Using timecourse gene expression data, we constructed a miRNA regulatory network for the innate immune response to Mtb infection by WT macrophages. The network suggested a role for seven miRNAs in regulating the host response to Mtb, with miR-155 being one of them. We then validated a role for miR-155 by comparing the response between WT and miR-155-/- macrophages.
Project description:We measured global RNA levels using RNA-seq in Mycobacterium smegmatis MC2 155 wild-type cells versus cells with deletions of genes encoding small ORFs MSMEG_0945 and MSMEG_1916.
