Mulberry (Morus alba) is an essential plant with countless economic benefits; however, its growth and metabolic processes are hampered by boron (B) stresses. Very little research has been performed to elucidate boron tolerance and detoxification mechanisms in this species. The M. alba cultivar, Yu-711, was exposed to five different concentrations of boric acid (HBO), including deficient (T1; 0 mM) moderate B deficiency (T2; 0.02 mM), sufficient (CK; 0.1 mM) and toxic (T3 and T4; 0.5 and 1 mM) levels for 18 days of growth in pots experiment. Transcriptome analysis of B deficiency and toxicity treatments was performed on mulberry leaves. The transcriptome data reveal that a total of 6114 genes were differentially expressed (DEGs), of which 3830 were up-regulated and 2284 were down-regulated. A comparative analysis between treatment groups CK-vs-T1 (deficiency) and CK-vs-T4 (toxicity) indicates that 590 and 1383 genes were down-regulated in both deficiency and B toxicity, respectively. The results show that 206 genes were differentially expressed in all treatments. B deficiency and toxicity significantly altered the expression of the key aquaporins (PIP2-1, PIP2-7, PIP2-4 and NIP3-1) and high-affinity boron transporter genes (BOR1 and BOR7). In addition, boron stress also altered the expression of antioxidants and photosynthesis-related genes. B stresses were found to alter several transcription factors including ERF1B, which is associated with the regulation of boron uptake and the synthesis and signaling of phytohormones. Unravelling the mechanisms of B tolerance and detoxification is important and would give us further insight into how B stresses affect mulberry plants.
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http://dx.doi.org/10.1016/j.plaphy.2023.108316 | DOI Listing |
J Immunother Cancer
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Department of Medical Oncology, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
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View Article and Find Full Text PDFPLoS Negl Trop Dis
January 2025
Department of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, China.
Leishmaniasis, a neglected tropical disease caused by Leishmania parasites, continues to pose global health challenges. Current treatments face issues like resistance, safety, efficacy, and cost. This review covers the discovery, mechanisms of action, clinical applications, and limitations of key antileishmanial agents: pentavalent antimonials, amphotericin B, miltefosine, paromomycin, and pentamidine.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Brain and Mind Research Institute, new york, NY, USA.
Background: DAP12 (DNAX-activation protein 12 or TYROBP) functions as a pivotal adaptor, facilitating signal transmission from surface immune receptors on microglia, including TREM2-a known risk gene for Alzheimer's disease (AD). Previous studies showed that DAP12-deficient mice exhibit resistance to tau toxicity in a tauopathy model, manifesting reduced brain inflammation and improved cognition, despite increased tau pathology. However, the precise mechanism underlying how DAP12 deficiency enhances resilience to tauopathy remains elusive.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background: Adenosine receptor 1 (A1R) is the predominant subtype of adenosine receptors, primarily distributed in memory-associated brain regions such as the cortex, hippocampus, and cerebellum. It actively participates in plasticity-regulated synaptic transmission and is crucial for functions related to sleep, arousal, cognition, learning, and memory. In a recent study, we reported that an elevation in A1R signaling mediates aberrant neuron-glial crosstalk in Alzheimer's disease.
View Article and Find Full Text PDFDrug Des Devel Ther
January 2025
Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy & School of Pharmacy, Xuzhou Medical University, Xuzhou, Jiangsu, 221004, People's Republic of China.
Purpose: Tacrolimus could induce hepatotoxicity during clinical use, and the mechanism was still unclear, which posed new challenge for the prevention and treatment of tacrolimus-induced hepatotoxicity. The aim of this study was to investigate the mechanism of tacrolimus-induced hepatotoxicity and provide reference for drug development target.
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