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Down-stream targets of TGFβ/BMP signaling in C. elegans exposed to microbiota CeMbio using RNAseq

ABSTRACT: Only recently, the natural gut microbiome of the model organism Caenorhabditis elegans has been described. C. elegans harbors a distinct gut microbiome that is shaped by environmental conditions, age, and host genotype. However, there is not much known about the genetic factors on the molecular level that the worm employs in order to keep its microbiota at bay. Previously, we have shown that TGFβ/BMP immune signaling is able to control the gut microbiome of C. elegans in particular in regards to Enterobacter species. We now aimed to identify the downstream targets of TGFβ/BMP immune signaling that implement the changes in microbiome composition. Hence, we exposed TGFβ mutants, dbl-1(nk3) and sma-3(e491), overexpression strain ctIs40 [dbl-1(+) + sur-5::GFP], and wild-type N2 to a synthetic microbiota community, CeMbio, and an E. coli OP50 control, and performed RNAseq. CeMbio is a collection of 12 diverse bacterial strains, previously isolated from wild C. elegans, C. elegans grown in microcosms, or substrates with C. elegans. Using the R packages edgeR and limma we are currently analyzing the data to understand the involvement of TGFβ/BMP signaling in host-microbiome interaction.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE186653 | GEO | 2023/10/31

REPOSITORIES: GEO

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Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.

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Down-stream targets of TGFβ/BMP signaling in C. elegans exposed to microbiota CeMbio using RNAseq

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