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High-precision mapping of endogenous proteins is essential for understanding the molecular mechanism underlying neuronal functions in the brain. The SLENDR (single-cell labeling of endogenous proteins by clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9-mediated homology-directed repair) technique provides single-cell endogenous protein labeling with genetically encoded tags within the mammalian brain through precise genome editing via homology-directed repair (HDR). This technique is based on the introduction of HDR-mediated genome editing into neuronal progenitors in embryonic brains by in utero electroporation. Subsequent histological analyses enable high-resolution interrogation of the subcellular distribution of endogenous proteins within a single neuron using conventional fluorescent microscopy. Here, we describe a step-by-step protocol for the SLENDR technique to label endogenous proteins with genetically encoded tags in single pyramidal cells of the mouse primary somatosensory cortex. This protocol would be helpful to visualize the molecular organization underlying biological processes at single-neuron levels in the brain, such as signal processing from synaptic inputs to neuronal outputs across different scales.
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http://dx.doi.org/10.1007/s12565-025-00866-x | DOI Listing |
Free Radic Biol Med
September 2025
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center. Electronic address:
Background: Excessive oxidative stress is well known to participate in the pathogenesis of hypertension. A major regulator of oxidative stress is the transcription factor Nuclear factor erythroid 2-related factor 2 (Nrf2). However, the role of Nrf2 in the pathogenesis of hypertension is not completely understood, especially at the endothelial cell level.
View Article and Find Full Text PDFJ Biol Chem
September 2025
Department of Integrative Structural and Computational Biology, The Scripps Research Institute, La Jolla, California, USA.
Aminoacyl-tRNA synthetases (aaRSs) catalyze the aminoacylation of tRNA with their cognate amino acids, an essential step in protein biosynthesis. While biallelic mutations in aaRSs often result in severe multi-organ dysfunction accompanied by developmental delays, monoallelic mutations typically cause milder, tissue-specific symptoms. However, a de novo monoallelic nonsense mutation (R534*) in the asparaginyl-tRNA synthetase (AsnRS)-resulting in a premature stop codon and 15-residue C-terminal truncation-has been identified in multiple families and is associated with severe neurodevelopmental symptoms.
View Article and Find Full Text PDFMol Cell
August 2025
Lingang Laboratory, Shanghai 200031, China. Electronic address:
YAP/TAZ are transcriptional co-activators that pair with transcription factor TEA/ATTS domains (TEADs) for modulating the Hippo pathway. Previous works propose the potential role of YAP/TAZ phase separation for transcriptional activation, yet the biomolecular basis of endogenous YAP/TAZ-TEAD condensates remains unclear. Here, we dissect their endogenous morphology, revealing that YAP/TAZ are client proteins recruited to TEAD condensates in various human cell lines.
View Article and Find Full Text PDFMol Pharmacol
August 2025
Department of Pharmacology, University of Michigan, Ann Arbor, Michigan.
μ-Opioid receptor (MOR) agonists are a mainstay in acute pain management. However, they also produce adverse effects and are frequently misused, increasing susceptibility for opioid use disorder. Thus, a strategy for improving the safety of opioid analgesics is needed.
View Article and Find Full Text PDFJ Neurochem
September 2025
Department of Biology and Biotechnologies "Charles Darwin", Sapienza University of Rome, Rome, Italy.
Patients with Duchenne muscular dystrophy (DMD) may experience neurobehavioral and cognitive concerns, including psychiatric symptoms, due to the absence of full-length dystrophin (Dp427), frequently accompanied by deficiencies in shorter isoforms. The lack of dystrophin affects neurophysiological processes from the uterine phase, impacting neural circuitry in brain regions such as the prefrontal cortex, hippocampus, and cerebellum. This leads to reduced inhibitory GABAergic transmission and altered hippocampal glutamatergic signaling.
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