Project description:Plants often generate secondary metabolites with antifungal properties as defense mechanisms against parasites. Although some fungi may potentially overcome the barrier of antimicrobial compounds, only a limited number of examples and molecular mechanisms of resistance have been reported. Here, we found an Aglaia plant-parasitizing fungus that overcomes the toxicity of rocalgates, which are translation inhibitors synthesized by the plant, through an amino acid substitution in a translation initiation factor (eIF). De novo transcriptome assembly of the fungus revealed that eIF4A, a molecular target of rocaglates, replaces a critical amino acid in the rocaglate binding site. Moreover, genome-wide ribosome profiling harnessing a cucumber-infecting fungus, Colletotrichum orbiculare, demonstrated that the translational inhibitory effects of rocaglates were largely attenuated by the mutation found in the Aglaia parasite. The engineered Colletotrichum orbiculare showed a survival advantage on cucumber plants with rocaglates. Our study exemplifies a plant-fungus tug-of-war centered on secondary metabolites produced by host plants.
Project description:In order to more accurately discover the cause of drug resistance in tumor treatment, and to provide a new basis for precise treatment.
Therefore, based on the umbrella theory of precision medicine, we carried out this single-center, prospective, and observational study to include patients with liver metastases from colorectal cancer. By combining genome, transcriptome, and proteomic sequencing data, we established a basis for colorectal cancer liver Transfer the multi-omics data of the sample, describe the reason for the resistance of the first-line treatment, and search for new therapeutic targets.
Project description:Gene regulation of bacterial pathogens in the host is not comprehensively understood due to the difficulty in analyzing genome-wide mRNA and protein expression of bacteria during infection. Here, we jointly analyzed transcriptome and proteome of a foliar bacterial pathogen in plants. Bacterial transcriptome changes can explain to a large extent their proteome changes in resistant and susceptible plants. However, a part of bacterial type III secretion system was suppressed by plant immunity preferentially at the protein level. Also, gene co-expression analysis uncovered previously unknown gene regulatory modules underlying bacterial virulence. Collectively, integrated in planta bacterial omics provides molecular insights into multiple layers of bacterial gene regulation that contributes to virulence and roles of plant immunity in controlling it.
Project description:Cryptosporidium parvum is an important opportunistic parasite pathogen for immunocompromised individuals and a common cause of diarrhea in young children in developing countries. Certain parasite molecules can be delivered into host epithelial cells and may act as effector molecules for parasite intracellular development. This study aims to measure the impact of transfection of two parasite low-protein coding potential RNA transcripts, cdg2_FLc_0220 and cdg7_FLc_1000, on the transcriptome profile in intestinal epithelial cells. Human intestinal epithelial INT (FHs 74 Int) cells were grown to 80% confluence and transfected with the cdg2_FLc_0220 or cdg7_FLc_1000full-length or the empty vector for 48h. Total RNA was collected for the genome-wide analysis. The Agilent SurePrint G3 Human Gene Expression Microarray (G4851B) was used for the genome-wide analysis, which provides full coverage of genes and transcripts with the most up-to-date content, including mRNAs and lincRNAs (http://www.chem.agilent.com/store/en_US/Prod-G4851B/G4851B).
2018-02-21 | GSE94128 | GEO
Project description:Repeat composition of Euphrasia (Orobanchaceae) Genomes
Project description:During red-blood-cell-stage infection of Plasmodium falciparum, the parasite undergoes repeated rounds of replication, egress, and invasion. Erythrocyte invasion involves specific interactions between host cell receptors and parasite ligands and coordinated expression of genes specific to this step of the life cycle. We show that a parasite-specific bromodomain protein, PfBDP1, binds to chromatin at transcriptional start sites of invasion-related genes and directly controls their expression. Conditional PfBDP1 knockdown causes a dramatic defect in parasite invasion and growth and results in transcriptional downregulation of multiple invasion-related genes at a time point critical for invasion. Conversely, PfBDP1 overexpression enhances expression of these same invasion-related genes. PfBDP1 binds to acetylated histone H3 and a second bromodomain protein, PfBDP2, suggesting a potential mechanism for gene recognition and control. Collectively, these findings show that PfBDP1 critically coordinates expression of invasion genes and indicate that targeting PfBDP1 could be an invaluable tool in malaria eradication. ChIPseq mapping of the genome wide enrichment profile of the P. falciparum bromodomain protein PfBDP1 in two parasite stages and correlation with RNAseq expression data
Project description:During infections with malaria parasites P. vivax, patients exhibit rhythmic fevers every 48 hours. These fever cycles correspond with the time parasites take to traverse the Intraerythrocytic Cycle (IEC) and may be guided by a parasite-intrinsic clock. Different species of Plasmodia have cycle times that are multiples of 24 hours, suggesting they may be coordinated with the host circadian clock. We utilized an ex vivo culture of whole blood from patients infected with P. vivax to examine the dynamics of the host circadian transcriptome and the parasite IEC transcriptome. Transcriptome dynamics revealed that the phases of the host circadian cycle and the parasite IEC were correlated across multiple patients, suggesting that the cycles are coupled. In mouse model systems, host-parasite cycle coupling appears to provide a selective advantage for the parasite. Thus, understanding how host and parasite cycles are coupled in humans could enable anti-malarial therapies that disrupt this coupling.