Project description:Self-inhibition of pollen tubes plays a key role in SI, but the underlying mechanism in Camellia oleifera is poorly understood. Collection of secreted proteins from Camellia oleifera pollen tubes and ovaries for high-throughput sequencing.
Project description:We report the expression analysis of seed kernel in Camellia oleifera cultivars. In total 221 cultivars are sequenced by the Illumina sequencing experiments to obtain the gene expression profiles.
Project description:To identify the important genetic resources of tea oil accumulation and quality formation in Camellia oleifera, an important woody edible oil tree native to Southern China, we have designed and customized an expression profile chip of C. oleifera with 8×60 K on the basis of transcriptome sequencing of multiple tissue samples including kernels, roots, and leaves from multiple varieties. we used the mcroarrays to determine the gene expressions in kernel development of C. oleifera elite varieties'Huashuo' , 'Huaxin' , 'Huajin' and 'Jujian' respectively. Microarray results indicated a total of 10710 gene probes showed stable differential expression in the comparation of August vs June and 9987 in the comparation of October vs August. PATHWAY enrichment results of DEGs indicated that the oil synthesis and accumulation occured in the whole kernel development of C. oleifera, but were mainly concentrated from the nutrition high-speed synthesis period to the seed mature period, which was consistent with the variation trend of oil content and fatty acide composition in C. oleifera kernel development.
Project description:Microbes play key roles in diverse biogeochemical processes including nutrient cycling. However, responses of soil microbial community at the functional gene level to long-term fertilization, especially integrated fertilization (chemical combined with organic fertilization) remain unclear. Here we used microarray-based GeoChip techniques to explore the shifts of soil microbial functional community in a nutrient-poor paddy soil with long-term (21 years).The long-term fertilization experiment site (set up in 1990) was located in Taoyuan agro-ecosystem research station (28°55’N, 111°27’E), Chinese Academy of Sciences, Hunan Province, China, with a double-cropped rice system. fertilization at various regimes.
Project description:Background: Tumor necrosis factor α-induced protein 1 (TNFAIP1) is frequently downregulated in cancer cell lines and promotes cancer cell apoptosis. However, its role, clinical significance and molecular mechanisms in hepatocellular carcinoma (HCC) are unknown. Methods: The expression of TNFAIP1 in HCC tumor tissues and cell lines was measured by Western blot and immunohistochemistry. The effects of TNFAIP1 on HCC proliferation, apoptosis, metastasis, angiogenesis and tumor formation were evaluated by Cell Counting Kit-8 (CCK8), Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL), transwell, tube formation assay in vitro and nude mice experiments in vivo. The interaction between TNFAIP1 and CSNK2B was validated by liquid chromatography-tandem mass spectrometry (LC-MS/MS), Co-immunoprecipitation and Western blot. The mechanism of how TNFAIP1 regulated nuclear factor-kappaB (NF-κB) pathway was analyzed by dual-luciferase reporter, immunofluorescence, quantitative Real-time polymerase chain reaction (RT-qPCR) and Western blot. Findings: The TNFAIP1 expression is significantly decreased in HCC tissues and cell lines, and negatively correlated with the increased HCC histological grade. Overexpression of TNFAIP1 inhibits HCC cell proliferation, metastasis, angiogenesis and promotes cancer cell apoptosis both in vitro and in vivo, whereas the knockdown of TNFAIP1 in HCC cell displays opposite effects. Mechanistically, TNFAIP1 interacts with CSNK2B and promotes its ubiquitin-mediated degradation with Cul3, causing attenuation of CSNK2B-dependent NF-κB trans-activation in HCC cell. Moreover, the enforced expression of CSNK2B counteracts the inhibitory effects of TNFAIP1 on HCC cell proliferation, migration, and angiogenesis in vitro and in vivo. Interpretation: Our results support that TNFAIP1 can act as a tumor suppressor of HCC by modulating TNFAIP1/CSNK2B/NF-κB pathway, implying that TNFAIP1 may represent a potential marker and a promising therapeutic target for HCC. Fund: This work was supported in part by the financial support from the China Natural Science Foundation (No. 81972642, No. 81601122 and No. 81770389), Hunan Natural Science Foundation (No. 2017JJ3205), Cooperative Innovation Center of Engineering and New Products for Developmental Biology of Hunan Province (No. 20134486), and the Scientific Research Fund of Hunan Provincial Education Department (17B162).