Project description:Arundo donax L. is one of the most promising bioenergy crop due to its high biomass yield and low irrigation requirement. The resistance to biotic and abiotic stress causes the high invasiveness of this plant, which can grow with very low management input (e.g., pesticides, fertilization, irrigation) even in marginal lands or in fields irrigated with waste or salty water. We report the leaf transcriptome sequencing, de novo assembly and annotation of a giant reed G34 genotype under salt stress. This genotype shows a different transcriptomic response to salinity compared to other A. donax genotypes. This finding was unexpected considering that the genetic variability of this species is supposed to be low due to its vegetative reproductive process. This study aims to direct future efforts towards the A. donax genetic improvement.
Project description:Arundo donax L. is one of the most promising bioenergy crop due to its high biomass yield and low irrigation requirement. The resistance to biotic and abiotic stress causes the high invasiveness of this plant which can grow with very low management input (e.g., pesticides, fertilization, irrigation) even in marginal lands or in fields irrigated with waste or salty water. Despite its economic importance, the A. donax genomic resources are still limited. In particular, no information on its transcriptional response to salt stress is available.We report the leaf transcriptome sequencing, de novo assembly and annotation of a giant reed genotype under two levels of salt stress. The study will be useful for providing insight into the molecular mechanism underlying its extreme adaptability also offering a platform for directing future efforts towards the genetic improvement of this species.
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.
Project description:Aging is associated with declining immunity and inflammation as well as alterations in the gut microbiome with a decrease of beneficial microbes and increase in pathogenic ones. The aim of this study was to investigate aging associated gut microbiome in relation to immunologic and metabolic profile in a non-human primate (NHP) model. 12 old (age>18 years) and 4 young (age 3-6 years) Rhesus macaques were included in this study. Immune cell subsets were characterized in PBMC by flow cytometry and plasma cytokines levels were determined by bead based multiplex cytokine analysis. Stool samples were collected by ileal loop and investigated for microbiome analysis by shotgun metagenomics. Serum, gut microbial lysate and microbe-free fecal extract were subjected to metabolomic analysis by mass-spectrometry. Our results showed that the old animals exhibited higher inflammatory biomarkers in plasma and lower CD4 T cells with altered distribution of naïve and memory T cell maturation subsets. The gut microbiome in old animals had higher abundance of Archaeal and Proteobacterial species and lower Firmicutes than the young. Significant enrichment of metabolites that contribute to inflammatory and cytotoxic pathways was observed in serum and feces of old animals compared to the young. We conclude that aging NHP undergo immunosenescence and age associated alterations in the gut microbiome that has a distinct metabolic profile.