Project description:We used RNA-seq to examine transcriptional proflies of midguts with suppression of Imd in progenitors (e_* samples) or enterocytes (M_* samples) . We found significant differences between the contributions of enterocyte IMD and progenitor IMD to intestinal homeostasis.
Project description:The inner membrane domain (IMD) is a metabolically active and laterally discrete membrane domain initially discovered in Mycobacterium smegmatis that correlates both temporally and spatially with polar cell envelope elongation. While it has remained unclear whether a similar membrane domain exists in pathogenic species, this study specifically demonstrates that the IMD is a conserved membrane structure found in Mycobacterium tuberculosis. Following isolation of the membrane domains by density gradient fractionation, proteomic analysis revealed that the IMD is enriched in metabolic enzymes that are involved in the synthesis of conserved cell envelope components such as peptidoglycan, arabinogalactan, and phosphatidylinositol mannosides. Further, by demonstrating that the IMD is concentrated in the polar region of the rod-shaped cells, where active cell envelope biosynthesis takes place, proteomic analysis further revealed the enrichment of enzymes involved in synthesis of phthiocerol dimycocerosates and phenolic glycolipids. Overall, these proteomic data support that the functional compartmentalization of the membrane is an evolutionarily conserved feature found in both M. tuberculosis and M. smegmatis.
Project description:The purpose of this RNAseq is to analyse the effect of compound IMD-0354 on gene expression in melanoma A375 cells. RNAseq analysis identified unfolded protein response, cell cycle and DNA damage pathways to be effected by IMD-0354.
Project description:We used RNA-seq to examine transcriptional profiles of midgut progenitor cells with suppression of Imd in progenitors. We found significant differences between the contributions of progenitor IMD to intestinal homeostasis.
Project description:Long noncoding RNAs (lncRNAs), as a class of emerging regulators, play crucial role in regulating the strength and duration of innate immunity. However, little is known about how these Drosophila Imd immunity-related lncRNAs are regulated. Herein, we firstly revealed that overexpression of lncRNA-CR33942 could strengthen the expression of Imd pathway antimicrobial peptides Diptericin (Dpt) and Attacin-A (AttA) after infection, and vice versa. Secondly, RNA-seq analysis of post-infected lncRNA-CR33942-overexpressing flies further confirmed that lncRNA-CR33942 positively regulates the Drosophila Imd pathway. Mechanistically, we indicated that lncRNA-CR33942 interacts with NF-κB transcription factor Relish to promote its binding to Dpt and AttA promoters, thereby facilitating Dpt and AttA expression. Interestingly, we found that Relish can also directly promote lncRNA-CR33942 transcription by binding to its promoter. Finally, rescue experiments and dynamic expression profiling post-infection demonstrated the vital role of the Relish/lncRNA-CR33942/AMPs regulatory axis in enhancing inadequate Imd immune responses and maintaining immune homeostasis. Taken together, our study not only elucidates a novel mechanism about lncRNA in Drosophila Imd immune regulation, but also has important guiding significance for elucidating the complex regulatory mechanism of animal innate immune response.
