Project description:Transcriptomic analyses (RNA-seq) on RNA isolated from rice embryo at 3 h, 6 h, and 12 h pot-imbibition was performed to identify changes in gene expression in response to CSA.
2024-01-01 | GSE178972 | GEO
Project description:Fertilization evaluation of OEPF through pot experiments
| PRJNA1261813 | ENA
Project description:Microbial community of cotton in pot experiments
Project description:A cultivation facility that can assist users in controlling the soil water condition is needed for accurately phenotyping plants under drought stress in an artificial environment. Here we report the Internet of Things (IoT)-based pot system controlling optional treatment of soil water condition (iPOTs), an automatic irrigation system that mimics the drought condition in a growth chamber. The Wi-Fi-enabled iPOTs system allows water supply from the bottom of the pot, based on the soil water level set by the user, and automatically controls the soil water level at a desired depth. The iPOTs also allows users to monitor environmental parameters, such as soil temperature, air temperature, humidity, and light intensity, in each pot. To verify whether the iPOTs mimics the drought condition, we conducted a drought stress test on rice varieties and near-isogenic lines, with diverse root system architecture, using the iPOTs system installed in a growth chamber. Similar to the results of a previous drought stress field trial, the growth of shallow-rooted rice accessions was severely affected by drought stress compared with that of deep-rooted accessions. The microclimate data obtained using the iPOTs system increased the accuracy of plant growth evaluation. Transcriptome analysis revealed that pot positions in the growth chamber had little impact on plant growth. Together, these results suggest that the iPOTs system represents a reliable platform for phenotyping plants under drought stress.
2021-08-24 | GSE171578 | GEO
Project description:bahiagrass and stylo pot experiments phoD and pqqC sequecing
Project description:The facultative intracellular bacterium Fusobacterium nucleatum (Fn), mediates tumorigenesis and progression in CRC. However, the origin of intracellular Fn and the role of Fn-infected phagocytes in tumor microenvironment remains unclear. Here, we observed Fn-infected neutrophils/macrophages (PMNs/MΦ) is accumulated in CRC tumor tissues. Fn can survive inside of PMNs by reducing intracellular ROS levels. The lysozyme inhibitor Fn-MliC induced the expression of the CX3CR1 which suppressed apoptosis of phagocytes. Fn-infected phagocytes can transfer Fn to tumor cells, and Fn-infected CRC cells recruited PMNs and MΦ/monocytes through the CXCL2/8-CXCR2 and CCL5/CCR5 axis. Intracellular Fn upregulated PD-L1 expression through activating NF-κB/STAT3 pathway in PMNs. PD-L1+ PMNs infiltration promotes CRC metastasis and weaken the efficacy of immunotherapy, and eradication intracellular Fn infection retarded the Fn promoted tumor progressing in mice. These results suggest that Fn volved efficient strategies to exploit phagocytes to home to tumor tissues, inhibited immune responses and facilitate tumor metastasis.
Project description:The facultative intracellular bacterium Fusobacterium nucleatum (Fn) mediates tumorigenesis and progression in esophageal squamous cell carcinoma (ESCC). The intracellular survival strategy of Fn and whether Fn can spread through cell‒cell contact in intratumoral tissues and, if so, the underlying mechanisms and implications are currently unknown. Here, we observed that Fn accumulates in macrophages from ESCC tumors and paracancerous normal tissues. We further found that Fn-induced macrophage mitophagy through the PINK1-Parkin-independent pathway decreases excessive mitochondrial ROS production to promote survival. Furthermore, Fn drives a biphasic metabolic switch between glycolysis and oxidative phosphorylation in macrophages to support the bioenergetic demands of survival. Notably, Fn is carried and delivered to tumors by macrophages, where it promotes tumor metastasis via the CCL2-CCR2 axis in ESCC. Treatment with a mitochondrial division inhibitor (mdivi-1) reduced the intracellular Fn concentration and inhibited Fn-positive tumor metastasis in mice. These findings indicate that mitophagy inhibitors or mitophagy machinery targeting may serve as efficient therapeutic strategies to treat Fn-positive tumors.