Project description:Root rot is one of the most severe diseases affecting agricultural productivity worldwide, particularly wolfberry. However, the mechanisms underlying wolfberry resistance to root rot pathogens remain unclear. In this study, we selected Chinese wolfberry (Lycium chinense Mill., LC) and Ningxia wolfberry ‘Ningqi No.5’ (Lycium barbarum L., N5) as research materials, which have been reported to show different tolerances to root rot.
Project description:In terrestrial ecosystems plants take up phosphate predominantly via association with arbuscular mycorrhizal fungi (AMF). We discovered that the loss of responsiveness to AMF in the rice deletion mutant hebiba is encoded by the alpha/beta fold hydrolase, DWARF 14 LIKE (D14L), which is one of the 26 deleted genes. It is a component of an intracellular receptor complex involved in the detection of the smoke-compound karrikin. On the basis of the early and pronounced hebiba mutant phenotype, we hypothesized that functional D14L is required for the perception of AM fungi prior to contact. Germinated spore exudates of AMF activate pre-contact plant responses. Therefore, we used RNAseq to monitor the transcriptional changes of hebiba and wild type roots in response to germinated spore exudates, and also karrikin, over the first 24 hours post treatment. WT seedlings were treated with GSE, Karrikin or a mock and iho seedlings with GSE or a mock. Root material was collected for sequencing at 0, 3, 6, 9, 12 and 24 hours. This gave a total of 27 samples (WT+Mock: 6, WT+GSE: 5, WT+Karrikin:5, iho+Mock:6, iho+GSE: 5).
Project description:Purpose: To date, the biological activity of AMF has not been fully investigated. We set out to analyze how AMF regulates gene expression in HepG2 cells. Conclusions: we performed clustering analysis on the various expressed genes associated with autophagy, and the pathways confirmed in the KEGG and BP analysis
Project description:Traditional surgery plus radiotherapy or chemotherapy, existing targeted therapies failed to significantly improve the survival rate of recurrent endometrial cancer, so suggesting that mechanism of recurrence and progression that modulates in endometrial cancer is clinically important. Here, we show that GPER(G protein-coupled estrogen receptor 1) was binded to AMF, and the complex were translocation form plasma to cytoplasmic. Mechanistic investigations elucidated that interaction of AMF with GPER triggers phosphoinositide-3-kinase (PI3K) signaling activating and accelerating the ability of endometrial cancer cells growth. Furthermore, we found that AMF may contribute to GPER-mediated endometrial cancer progression using animal experiments and human histological experiments which be consistent with the above conclusions. On the basis of these evidences including invivo and invitro, our findings suggest that AMF–GPER interaction might be novel key molecular targets for therapeutic management of patients with endometrial cancer, whose disease were progression and recurrence.