Project description:Marine sponges are essential for coral reefs to thrive and harbour a diverse microbiome that is thought to contribute to host health. Although the overall function of sponge symbionts has been increasingly described, in-depth characterisation of each taxa remains challenging, with many sponge species hosting up to 3,000 distinct microbial species. Recently, the sponge Ianthella basta has emerged as a model organism for symbiosis research, hosting only three dominant symbionts: a Thaumarchaeotum, a Gammaproteobacterium, and an Alphaproteobacterium and a range of other minor taxa. Here, we retrieved metagenome assembled genomes (MAGs) for >90% of I. basta’s microbial community which allowed us to make a complete metabolic reconstruction of the sponge’s microbiome, identifying metabolic complementarity between microbes, as well as the importance of symbionts present in low abundance. We also mined the metagenomes for putative viral sequences, highlighting the contribution of viruses to the overall metabolism of the sponge, and complement this data with metaproteomic sequencing to identify active metabolic pathways in both prokaryotes and viruses. This data now allows us to use I. basta as a model organism for studying host-microbe interactions and provides a basis for future (genomic) manipulative experiments.
Project description:miRNA sponge, a special class of miRNA target, has been emerging as a pivotal player in miRNA mediated regulatory network. Currently, the identified miRNA sponge genes mostly act on sequestering conserved miRNAs (e.g. miR-7, miR-145), however, the existence, potential function and evolutionary process of miRNA sponge genes for species-specific miRNA, especially for human specific miRNA, are largely unknown. In this study, we conducted a systematic analysis including sponge gene identification and subsequent function and evolutionary analyses for an authentic human-specific miRNA, miR-941.
Project description:Exosomal and cellular miRNA expression levels were measured using a microRNA chip array or quantitative reverse transcription PCR (qRT-PCR). miR-24-3p was enriched in T-EXOs from the sera of NPC patients and NPC cells, which was correlated with worse disease-free survival (DFS). Exosomes (miR-24-3p-sponge-EXO) released from miR-24-3p-sponge-TW03 cells failed to inhibit T-cell proliferation and Th1 and Th17 differentiation or to induce Treg differentiation in vitro, compared with controlNC -sponge-EXO. Mechanistic analyses revealed that in miR-24-3p-sponge-EXO-treated T-cells, P-ERK, P-STAT1 and P-STAT3 were up-regulated, whereas P-STAT5 was down-regulated compared with controlNC-sponge-EXO-treated T-cells. FGF11 was identified as a direct target gene of miR-24-3p through in vivo and in vitro assessments. More importantly, the T-EXOs repressed FGF11 expression in T-cells during proliferation and differentiation. Interestingly, when FGF11 expression in T-cells was blocked, miR-24-3p-sponge-EXOs impeded shFGF11-T-cell proliferation and Th1 and Th17 differentiation but induced Treg differentiation, like controlNC-sponge-EXO. When FGF11 was knocked down in miR-24-3p-sponge-EXO-treated T-cells, neither P-ERK, P-STAT1 and P-STAT3 up-regulation or P-STAT5 down-regulation occurred. Interestingly, FGF11 expression in tumor-infiltrating lymphocytes (TILs) was significantly and positively correlated with the number of CD4+ and CD8+ TILs and predicted favorable DFS of the patients (p < 0.05).