Multi-omics analysis reveals the roles of purple acid phosphatases in organic phosphorus utilization by the tropical legume Stylosanthes guianensis.

Stylo (Stylosanthes guianensis) is a tropical legume known for its exceptional tolerance to low phosphate (Pi), a trait believed to be linked to its high acid phosphatase (APase) activity. Previous studies have observed genotypic variations in APase activity in stylo; however, the gene encoding the crucial APase responsible for this variation remains unidentified. In this study, transcriptomic and proteomic analyses were employed to identify eight Pi starvation-inducible (PSI) APases belonging to the purple APase (PAP) family in the roots of stylo and seven in the leaves. Among these PSI-PAPs, SgPAP7 exhibited a significantly positive correlation in its expression levels with the activities of both internal APase and root-associated APase across 20 stylo genotypes under low-Pi conditions. Furthermore, the recombinant SgPAP7 displayed high catalytic activity toward adenosine 5'-diphosphate (ADP) and phosphoenolpyruvate (PEP) in vitro. Overexpression (OE) of SgPAP7 in Arabidopsis facilitated exogenous organic phosphorus utilization. Moreover, SgPAP7 OE lines showed lower shoot ADP and PEP levels than the wild type, implying that SgPAP7 is involved in the catabolism and recycling of endogenous ADP and PEP, which could be beneficial for plant growth in low-Pi soils. In conclusion, SgPAP7 is a key gene with a major role in stylo adaptation to low-Pi conditions by facilitating the utilization of both exogenous and endogenous organic phosphorus sources. It may also function as a PEP phosphatase involved in a glycolytic bypass pathway that minimizes the need for adenylates and Pi. Thus, SgPAP7 could be a promising target for improving tolerance of crops to low-Pi availability.

Metabolic alterations provide insights into Stylosanthes roots responding to phosphorus deficiency.

BACKGROUND: Phosphorus (P) deficiency is one of the major constraints limiting plant growth, especially in acid soils. Stylosanthes (stylo) is a pioneer tropical legume with excellent adaptability to low P stress, but its underlying mechanisms remain largely unknown. RESULTS: In this study, the physiological, molecular and metabolic changes in stylo responding to phosphate (Pi) starvation were investigated. Under low P condition, the growth of stylo root was enhanced, which was attributed to the up-regulation of expansin genes participating in root growth. Metabolic profiling analysis showed that a total of 256 metabolites with differential accumulations were identified in stylo roots response to P deficiency, which mainly included flavonoids, sugars, nucleotides, amino acids, phenylpropanoids and phenylamides. P deficiency led to significant reduction in the accumulation of phosphorylated metabolites (e.g., P-containing sugars, nucleotides and cholines), suggesting that internal P utilization was enhanced in stylo roots subjected to low P stress. However, flavonoid metabolites, such as kaempferol, daidzein and their glycoside derivatives, were increased in P-deficient stylo roots. Furthermore, the qRT-PCR analysis showed that a set of genes involved in flavonoids synthesis were found to be up-regulated by Pi starvation in stylo roots. In addition, the abundances of phenolic acids and phenylamides were significantly increased in stylo roots during P deficiency. The increased accumulation of the metabolites in stylo roots, such as flavonoids, phenolic acids and phenylamides, might facilitate P solubilization and cooperate with beneficial microorganisms in rhizosphere, and thus contributing to P acquisition and utilization in stylo. CONCLUSIONS: These results suggest that stylo plants cope with P deficiency by modulating root morphology, scavenging internal Pi from phosphorylated metabolites and increasing accumulation of flavonoids, phenolic acids and phenylamides. This study provides valuable insights into the complex responses and adaptive mechanisms of stylo roots to P deficiency.

Lipopolysaccharide/Toll-like receptor 4 signaling pathway involved Qingdu decoction treating severe liver injury merging with endotoxemia.

OBJECTIVE: To investigate the protective effects and underlying mechanism of Qingdu decoction (QDD) on experimental rats with severe liver injury induced by thioacetamide (TAA). METHODS: A total of 40 Wistar rats were randomly divided into normal group (n = 10) and experimental group (n = 30). Rats were administrated the same content of saline in normal group. The rats in the experimental group were pretreated with TAA at dose of 12 mg/kg lasting 8 weeks, and from 9th week to 12th week, with TAA at concentration of 36 mg/kg. During the 9th week to 12th week period, the rats were randomly divided into three subgroups (n = 10 each) simultaneously based on the treatment categories: model group, lactulose (LA, 3.5 mL/kg) group and QDD (5.95 g/kg) group, orally once per day respectively. At the 12th week, the content of serum alanine transaminase (ALT), aspartate transaminase (AST), total bilirubin (TBIL), endotoxin (ET) and tumor necrosis factor a (TNF-a) was detected by automatic biochemical analyzer. The plasma prothrombin time (PT), prothrombin time-international normalized ratio (PTR) and prothrombin time activity (PTA) were measured by automatic coagulation analyzer. The level of lipopolysaccharide (LPS)-binding protein (LBP), cluster differentiation 14 (CD14) and Toll-like receptor 4 (TLR4) expressions was measured by both western blot (WB) and real-time polymerase chain reaction (real-time PCR). RESULTS: Compared with the model group, hepatic morphology in the QDD group was improved under light microscope and transmission electron microscope; at the same time, the contents of serum ALT, AST, TBIL, ET and TNF-α, and level of LBP, CD14 and TLR4 expressions in liver tissues were significantly decreased compared with the model group (P < 0.05), while PTA in the QDD group was enhanced (P < 0.05). CONCLUSION: QDD has the functional effect on improving the injured liver through inhibiting the LPS/TLR4 signaling pathway thus decreasing the level of the inflammatory medicators.