Project description:Transcription profile of WT compare to sigma factor sigI deletion mutant at OD1 and OD2. This microarray is simple comparison of wild type strain of M. tuberculosis CDC1551 and its sigma factor gene deletion mutant (sigI) at OD1 and OD2, respectively.
Project description:We employed a quantitative differential proteomics approach to compare the protein expression levels between WT and rss03 deletion mutant (Δrss03), revealing significant differences in some proteins.
Project description:Transcriptional profiling of H37Rv (WT), Mut1 and Comp1 bacteria under aerobic (Aer/0 day, i.e 0 D) and hypoxic conditions (Hyp/5 days standing culture, i.e 5 D). Mut1: H37Rv carrying devR gene disruption by in frame insertion of kanamycin resistance cassette and expressing DevRN-Kan fusion protein. Comp1: Mut1 complemented with low copy number plasmid carrying devR gene expressed from its native constitutive upstream promoter. (Reference: Majumdar et al., 2010, PLoS One 5:e9448). Goal is to compare transcriptional patterns of WT, Mut1 and Comp1 strains under aerobic (0 D) and hypoxic (5 D) conditions in vitro.
Project description:Comparison of gene expression profile of the whiB4 mutant strain of Mycobacterium tuberculosis with the wild type Mycobacterium tuberculosis H37RV Mtb WhiB4 mutant mRNA was compared with the mRNA of wtMtb H37RV under aerobic conditons Aerbic conditions OD600 nm of 0.4, MtbWhiB4KO vs wtMtb, biological replicates: 3 wt Mtb H37RV and 3 MtbWhiB4 KO
Project description:Tuberculosis remains one of the most difficult to control infectious diseases in the world. Many different factors contribute to the complexity of this disease. These include the ability of the host to control the infection which may directly relate to nutritional status, presence of co-morbidities and genetic predisposition. Pathogen factors, in particular the ability of different Mycobacterium tuberculosis strains to respond to the harsh environment of the host granuloma, which includes low oxygen and nutrient availability and the presence of damaging radical oxygen and nitrogen species, also play an important role in the success of different strains to cause disease. In this study we evaluate the impact of a naturally occurring 12 gene 15 Kb genomic deletion on the physiology and virulence of M. tuberculosis. The strains denominated ON-A WT (wild type) and ON-A NM (natural mutant) were isolated from a previously reported TB outbreak in an inner city under-housed population in Toronto, Canada. Here we subjected these isogenic strains to transcriptomic (via RNA-seq) and proteomic analyses and identified several gene clusters with differential expression in the natural mutant, including the DosR regulon and the molybdenum cofactor biosynthesis genes, both of which were found in lower abundance in the natural mutant. We also demonstrated lesser virulence of the natural mutant in the guinea pig animal model. Overall, our findings suggest that the ON-A natural mutant is less fit to cause disease, supporting the general idea that even low virulent strains have the potential to cause extended transmission in at risk populations.
Project description:Analyses of the Wild type and the sigma 54 mutant strain NZ7306 with and without peroxide treatment: A Lactobacillus plantarum strain with a deletion in the alternative sigma factor 54 (?54) encoding gene rpoN, displayed a 100 fold higher sensitivity to peroxide as compared to its parental strain. This feature could be due to ?54-dependent regulation of genes involved in peroxide stress response. However, transcriptome analyses of the wild type and the mutant strain during peroxide exposure did not support such a role for ?54. Subsequent experiments revealed that the impaired expression of the mannose PTS operon in the rpoN mutant caused the observed increased peroxide sensitivity. Keywords: genetic modification
Project description:We identified mce3R and ctpD as genes that could alter M tuberculosis (Mtb) response to isoniazid when perturbed using a regulatory network-based TRIP screen [see associated data at PRJNA483505]. To investigate the mechanisms underlying this response, we performed RNAseq on genetically perturbed mutant strains either in the presence or absence of isoniazid.