SUMMARY
Phosphorus (P) is a major element required for plant growth and development. To cope with P shortage, plants activate local and long‐distance signaling pathways, such as an increase in the production and exudation of strigolactones (SLs). The role of the latter in mitigating P deficiency is, however, still largely unknown. To shed light on this, we studied the transcriptional response to P starvation and replenishment in wild‐type rice and a SL mutant, dwarf10 (d10), and upon exogenous application of the synthetic SL GR24. P starvation resulted in major transcriptional alterations, such as the upregulation of P TRANSPORTER, SYG1/PHO81/XPR1 (SPX) and VACUOLAR PHOSPHATE EFFLUX TRANSPORTER. Gene Ontology (GO) analysis of the genes induced by P starvation showed enrichment in phospholipid catabolic process and phosphatase activity. In d10, P deficiency induced upregulation of genes enriched for sesquiterpenoid production, secondary shoot formation and metabolic processes, including lactone biosynthesis. Furthermore, several genes induced by GR24 treatment shared the same GO terms with P starvation‐induced genes, such as oxidation reduction, heme binding and oxidoreductase activity, hinting at the role that SLs play in the transcriptional reprogramming upon P starvation. Gene co‐expression network analysis uncovered a METHYL TRANSFERASE that displayed co‐regulation with known rice SL biosynthetic genes. Functional characterization showed that this gene encodes an enzyme catalyzing the conversion of carlactonoic acid to methyl carlactonoate. Our work provides a valuable resource to further studies on the response of crops to P deficiency and reveals a tool for the discovery of SL biosynthetic genes.
Most land plants entertain a mutualistic symbiosis known as arbuscular mycorrhiza with fungi (Glomeromycota) that provide them with essential mineral nutrients, in particular phosphate (Pi), and protect them from biotic and abiotic stress. Arbuscular mycorrhizal (AM) symbiosis increases plant productivity and biodiversity, and is therefore relevant for both, natural plant communities and crop production. However, AM fungal populations suffer from intense farming practices in agricultural soils, in particular Pi fertilization. The dilemma between natural fertilization from AM symbiosis and chemical fertilization has raised major concern and emphasizes the need to better understand the mechanisms by which Pi suppresses AM symbiosis. Here, we test the hypothesis that Pi may interfere with AM symbiosis via the phytohormone gibberellic acid (GA) in the Solanaceous model systems Petunia hybrida and Nicotiana tabacum. Indeed, we find that GA is inhibitory to AM symbiosis, and that Pi may cause GA levels to increase in mycorrhizal roots. Consistent with a role of endogenous GA as an inhibitor of AM development, GA-defective N. tabacum lines expressing a GA-metabolizing enzyme (GA methyltransferase; GAMT), are colonized more quickly by the AM fungus Rhizoglomus irregulare, and exogenous Pi is less effective in inhibiting AM colonization in these lines. Systematic gene expression analysis of GA-related genes reveals a complex picture, in which GA degradation by GA2 oxidase plays a prominent role. These findings reveal potential targets for crop breeding that could reduce Pi suppression of AM symbiosis, thereby reconciling the advantages of Pi fertilization with the diverse benefits of AM symbiosis.
Postoperative cognitive dysfunction (POCD) is a common postsurgical complication in elderly individuals, significantly impacting the quality of life of patients; however, there is currently no effective clinical treatment for POCD. Recent studies have shown that Icariin (ICA) has antiaging effects and improves cognitive function, but its effect in POCD has not been studied. In this study, we investigated the influence of ICA on cognitive function and the TLR4/NF-κB signaling pathway in a POCD rat model. We found that ICA reduced surgery-induced memory impairment, decreased hippocampal inflammatory responses, ameliorated neuronal injury in the hippocampus and inhibited microglial activation. In addition, we also observed that ICA inhibited activation of the TLR4/NF-κB signaling pathway. In summary, our research suggest that ICA can ameliorate surgery-induced memory impairment and that the improvements resulting from administration of ICA may be associated with inhibition of hippocampal neuroinflammation. Our research findings also provide insight into potential therapeutic targets and methods for POCD.
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