Project description:Microbes are an integral component of the tumor microenvironment (TME). However, mechanisms that direct microbial recruitment into tumors and the spatial relationship between intratumoral microbes and host cells remain poorly understood. Here, we show that microbes and immune cells have parallel spatial distribution and that the presence of intratumoral microbes is dependent on T cells. Analysis of human pancreatic ductal adenocarcinomas (PDAC) and lung adenocarcinomas (LUAD) revealed a spatially heterogeneous distribution of lipopolysaccharide (LPS) that is associated with T cell infiltration. Using mouse models of PDAC, we found that microbes were more abundant and diverse in tumors that were enriched in T cells compared to tumors that lacked T cells, despite no significant differences in the fecal microbiome. Consistent with these findings, we detected elevated levels of microbial genes in T cell-enriched tumor nests in human PDAC. Compared to microbe-poor tumor nests, microbe-enriched tumor nests displayed a higher number of myeloid cells, B cells, and plasma cells. Microbe-enriched tumor nests also showed upregulation of immune-related processes, including responses to bacteria, and receptors that mediate mucosal immune responses to microbes. Administration of antibiotics to tumor-bearing mice altered the phenotype and presence of intratumoral myeloid cells and B cells but did not alter T cell infiltration. In contrast, depletion of T cells reduced the presence of intratumoral microbes. Our results identify a novel coupling between microbes and the intratumoral immune landscape, with T cells shaping microbial presence and subsequent microbial-host interactions.
Project description:Proximity labeling approach to identify protein inside nuclear envelope blebs arising in Torsin-deficient HeLa cells. WT and TorsinKO cells were engineered to express MLF2-APEX2 fusion. APEX reaction was carried out via 1 mM H2O2 for 1 minute in the presence of biotin phenol. Biotinylated protein were captured via streptavidin beads. Each APEX reaction was accompanied by an untreated (no H2O2) control.
Project description:We identify inducible binding of the transcription factor Oct1 to numerous targets following exposure to hydrogen peroxide. Oct1 bound ChIP fragments were sequenced in the presence and absence of H2O2 exposure using HeLa cells. Both 26 and 36bp reads were generated. Each processed file contains a list of genomic regions (NCBI 36.1, H_sapiens_Mar_2006, hg18) enriched for Oct1 binding. These files were generated by running the EnrichedRegionMaker on ScanSeqs window scored data, see http://useq.sourceforge.net/ . Adjacent and overlapping windows with a q-value FDR of 0.0001 were joined into larger enriched regions. The best scoring window's scores are used to represent the enriched region.
Project description:Enriched cells from coal slurry in the Powder River Basin, Montana, United States - BONCAT cells FG11 rep2 HSBNCT.FG11.300.03.H11 metagenome
Project description:Enriched cells from coal slurry in the Powder River Basin, Montana, United States - Total cells FG11 rep3 HSBNCT.FG11.300.03.J13 metagenome
Project description:Enriched cells from coal slurry in the Powder River Basin, Montana, United States - BONCAT cells N11 rep1 HSBNCT.N11.5000.01.E6 metagenome
Project description:Enriched cells from coal slurry in the Powder River Basin, Montana, United States - Total cells N11 rep1 HSBNCT.N11.5000.01.F3 metagenome
Project description:Enriched cells from coal slurry in the Powder River Basin, Montana, United States - BONCAT cells N11 rep2 HSBNCT.N11.5000.01.H4 metagenome
Project description:Enriched cells from coal slurry in the Powder River Basin, Montana, United States - Total cells N11 rep3 HSBNCT.N11.5000.01.L3 metagenome