Biomedical subjects

Su Li

Publications and source records attributed to Su Li.

3 recordsLinked to original sources

PubMed2026

The transcription factor AtANAC070 enhances zinc tolerance by promoting AtMTP1 expression in Arabidopsis thaliana.

The NAC transcription factor AtANAC070 functions in zinc tolerance by directly activating AtMTP1 transcription to promote vacuolar zinc sequestration and homeostasis in A. thaliana. Zinc (Zn) is an essential micronutrient for plant growth, but it becomes toxic when present in excess. An initial screen of Arabidopsis thaliana T-DNA insertion mutants suggested a positive role of AtANAC070 in tolerance to excess Zn. AtANAC070 expression was induced under excess Zn, and loss of function of AtANAC070 led to increased Zn sensitivity and higher Zn accumulation. Conversely, AtANAC070 overexpression enhanced Zn tolerance and reduced Zn accumulation. Yeast one-hybrid assays identified Metal Tolerance Protein 1 (AtMTP1), which encodes a key transporter mediating vacuolar sequestration of excess Zn, as a downstream target of AtANAC070. Dual-luciferase reporter and real-time quantitative PCR (RT-qPCR) assays confirmed that AtANAC070 directly binds to the AtMTP1 promoter to activate its expression. The atmtp1 mutant accumulated more Zn than the WT and was more sensitive to excess Zn, whereas AtMTP1-overexpressing lines showed the opposite phenotype. The atanac070 atmtp1 double mutant displayed Zn sensitivity comparable to that of atmtp1 mutant, while AtMTP1 overexpression in the atanac070 background reduced Zn accumulation and restored Zn tolerance. These results indicate that AtANAC070 contributes to Zn homeostasis under excess Zn by promoting AtMTP1 expression.

Arabidopsis↗

PubMed2026

Mitophagy-mediated ferroptosis involved in 2,5-hexanedione-induced neurotoxicity in rats.

n-Hexane, a widespread environmental and industrial pollutant, poses serious health risks, particularly neurotoxicity. Chronic exposure primarily induces sensorimotor neuropathy via its metabolite 2,5-hexanedione (HD), yet the mechanisms underlying HD-induced neuronal injury remain unclear. Recent evidence implicates ferroptosis, an iron-dependent form of regulated cell death, in neurodegenerative processes. In this study, Sprague-Dawley (SD) rats were exposed to HD to establish a neuropathy model. Ferroptosis involvement was assessed using the iron chelator deferoxamine (DFO) and the ferroptosis inhibitor Ferrostatin-1. The potential role of mitophagy in HD-induced ferroptosis was evaluated by monitoring mitophagy markers and by autophagy inhibition with chloroquine (CQ). In vitro, SH-SY5Y cells were transfected with PINK-1 siRNA to explore mitophagy-mediated regulation of ferroptosis. HD exposure led to iron accumulation, lipid peroxidation, mitochondrial abnormalities, and decreased GPX4 in rat spinal neurons. DFO or ferrostatin-1 treatment ameliorated these changes and preserved mitochondrial integrity. Mechanistic analyses revealed HD-induced activation of mitophagy, as shown by upregulation of Beclin-1, LC3II, Drp-1, and PINK-1, with concomitant downregulation of P62 in spinal mitochondria. CQ suppressed mitophagy, reduced iron deposition and lipid peroxidation, and improved motor function. Similarly, PINK-1 knockdown in SH-SY5Y cells mitigated HD-induced mitophagy and ferroptosis. These findings demonstrate that HD induces neuronal ferroptosis via mitophagy activation. Inhibition of ferroptosis or mitophagy effectively attenuates HD-induced neurotoxicity, suggesting potential therapeutic strategies to reduce neural damage from environmental n-hexane exposure.

Animals↗

PubMed2025

A suite of enhancer AAVs and transgenic mouse lines for genetic access to cortical cell types.

The mammalian cortex is comprised of cells classified into types according to shared properties. Defining the contribution of each cell type to the processes guided by the cortex is essential for understanding its function in health and disease. We use transcriptomic and epigenomic cortical cell-type taxonomies from mouse and human to define marker genes and putative enhancers and create a large toolkit of transgenic lines and enhancer adeno-associated viruses (AAVs) for selective targeting of cortical cell populations. We report creation and evaluation of fifteen transgenic driver lines, two reporter lines, and >1,000 different enhancer AAV vectors covering most subclasses of cortical cells. The tools reported here have been made publicly available, and along with the scaled process of tool creation, evaluation, and modification, they will enable diverse experimental strategies toward understanding mammalian cortex and brain function.

Animals↗