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Objective: To study the aggravation of clinical symptoms after discontinuation of metal chelating agent therapy in Wilson's disease (WD) patients, analyze the causes of aggravation, and observe the prognosis. Methods: 40 WD patients (cerebral type 30 cases and hepatic type 10 cases) who stopped using metal chelating agent were selected, 40 WD patients with normal therapy, and 10 normal control cases were selected. All patients underwent neurological symptom evaluation using modified Young scale, Child‐Pugh liver function grading, metal metabolism, and disease typing. Magnetic sensitivity imaging (SWI), diffusion tensor imaging (DTI), and magnetic resonance spectroscopy imaging (MRS) were performed. According to the imaging results, WD patients were divided into metal deposition stage, fiber damage stage, and neuron necrosis stage. All patients were treated with metal chelating agent for 6 months. Results: The score of modified Young scale in drug withdrawal group was lower than that in normal treatment group before drug withdrawal (p =.032). The score of modified Young scale was higher after drug withdrawal than before (p =.011). The number of Child‐Pugh B‐grade patients after drug withdrawal was more than that before drug withdrawal and in normal treatment group. The proportion of patients in the stage of neuronal necrosis after drug withdrawal (25%) was higher than that before drug withdrawal (10%) (p =.025). After drug withdrawal, urine copper was significantly higher than that before drug withdrawal and in the normal treatment group (p =.032,.039). After the withdrawal group resumed metal chelating agent treatment, 34.2% of neurological symptoms worsened. Conclusions: WD patients showed neurological symptoms aggravation and increased liver injury after metal chelating agent withdrawal. Increased metal deposition and new nerve injury occurred in the brain. After re‐treatment, the aggravated neurological symptoms of WD patients are difficult to reverse. [ABSTRACT FROM AUTHOR]

Summary: Cluster roots of white lupin are induced by low phosphorus (LP) to efficiently access unavailable P, but how soilborne microbes are associated with cluster root formation (CRF) is unclear.We investigated the roles of soilborne bacteria in CRF response to LP by high‐throughput sequencing and root–bacteria interactions.Cluster root number was significantly decreased in plants grown in sterilized soil compared with nonsterilized soil. Proteobacteria was enriched in CR, as shown by microbiome analysis of soil (bulk, rhizosphere, and rhizosheath) and roots (main, lateral, and CR). Large‐scale gene expression level implicated ethylene mediation in CRF. Klebsiella pneumoniae (P7), a soilborne bacterium belonging to Proteobacteria, was isolated from CR. Among 11 isolated strains, P7 exhibited the highest 1‐aminocyclopropane‐1‐carboxylate deaminase (ACCD) activity; this enzyme inhibits the biosynthesis of ethylene in plants by the cleavage of the ethylene precursor 1‐aminocyclopropane‐1‐carboxylic acid and promotes CRF under LP. We constructed an ACCD‐deficit mutant accd in the P7 genetic background. The loss‐of‐function mutation failed to promote CRF under LP conditions. Also, auxin responses may be involved in K. pneumoniae‐ethylene‐mediated CRF.Overall, we propose that the soilborne bacterium K. pneumoniae promotes CRF of white lupin in response to LP by ethylene mediation. [ABSTRACT FROM AUTHOR]

White lupin (Lupinus albus L.) produces cluster roots to acquire more phosphorus under phosphorus deficiency. Bacillus amyloliquefaciens SQR9 contributes to plant growth, but whether and how it promotes cluster root formation in white lupin remain unclear. Here, we investigated the roles of SQR9 in cluster root formation under low phosphorus conditions using a microbial mutant and virus-induced gene silencing (VIGS) in white lupin. SQR9 substantially enhanced cluster root formation under low phosphorus conditions. The ysnE gene encodes an auxin biosynthesis enzyme in SQR9 and was associated with cluster root formation, as ysnE-defective SQR9 did not trigger cluster root formation. SQR9 inoculation induced the expression of PIN-formed2 (LaPIN2, encoding an auxin transporter) and YUCCA4 (LaYUC4, encoding an auxin biosynthesis enzyme) in white lupin roots. VIGS-mediated knockdown of LaPIN2 and LaYUC4 prevented wild-type SQR9-induced cluster root formation in white lupin. Finally, white lupin LaYUC4-derived auxin and SQR9-derived auxin pools were both transported by LaPIN2, promoting cluster root formation under low phosphorus conditions. Taken together, we propose that B. amyloliquefaciens promotes cluster root formation in white lupin under low phosphorus conditions by stimulating auxin biosynthesis and transport. Our results provide insights into the interplay between bacteria and root auxin in crop phosphorus use efficiency., Competing Interests: Conflict of interest statement. The authors declare they have no conflict of interest., (© The Author(s) 2024. Published by Oxford University Press on behalf of American Society of Plant Biologists.)