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Ressl, S.

Publications and source records attributed to Ressl, S..

3 recordsLinked to original sources

Single-molecule nanophotonic resolution of binding dynamics from apo to fully liganded for a cyclic nucleotide-gated ion channel in cell-derived vesicles

Many biological macromolecules are activated upon ligand binding at multiple specific binding domains. However, how these domains interact and the transient intermediate conformations that connect binding events to protein activity are typically unknown. Ensemble-averaged measures over stochastic binding events are challenged to resolve the underlying asynchronous dynamics. Single-molecule resolution of these dynamics offers an attractive approach to investigate the ligand-activation process. Optical methods using fluorescently labeled ligands enable observation of individual binding events that report on the energetics of early ligand-bound conformational changes. However, diffraction-limited microscopy limits these methods to low ligand concentrations, often below what is required for physiologically relevant activation. Here, we overcome this limitation using nanophotonic zero-mode waveguides to observe the sequential binding of a fluorescent cyclic nucleotide to each of four subunits in TAX-4 cyclic nucleotide-gated ion channels in cell-derived vesicles. Our observations suggest that binding at one domain positively promotes binding at other domains, and that binding induces an isomerization of the binding domain in individual subunits which we attribute to a sequence of pre-activated intermediate states. This approach provides a broadly applicable tool to dissect the energetic landscape of ligand-binding at macromolecules in native cell membranes.

biophysics↗

Brain-wide mapping and synaptic localization of C1QL3 using a novel epitope-tagged knock-in mouse

Synapse formation and function are coordinated spatially and temporally by a host of synaptic proteins that regulate neuronal signaling, synapse specificity, and plasticity; many of which are implicated in neuropsychiatric disorders. Members of the C1q/TNF superfamily function as synaptic organizers, shaping synapse assembly and maintenance. Among them, C1QL3 plays a putative role in trans-synaptic adhesion and modulation of synaptic strength, but the lack of a reliable antibody to detect it has severely limited the ability to map its endogenous localization and study its biochemical properties. Here, we present a novel epitope-tagged knock-in mouse line (C1ql32HA), in which two hemagglutinin (HA) epitopes were inserted near the N-terminus of the endogenous C1QL3 protein. This model enables purification, detection, and subcellular localization of native C1QL3 protein (C1QL3-2HA) with high specificity, eliminating the need for overexpression or custom antibodies. We validated that C1ql32HA mice maintain normal mRNA expression, biochemical properties, and behavior. Using native PAGE, we determined the endogenous oligomeric state of C1QL3-2HA. Brain-wide light-sheet microscopy uncovered an expanded neuroanatomical map of C1QL3-2HA expression, including newly identified populations in cortical and subcortical regions as well as the retina. Dual immunohistochemistry confirmed cell type-specific expression patterns, and super-resolution STED microscopy localized C1QL3-2HA to hippocampal mossy fiber synapses, positioned between pre- and post-synaptic markers, supporting its hypothesized role in trans-synaptic complexes. This knock-in mouse line is a powerful tool for studying the anatomical, molecular, and synaptic biology of C1QL3 in all cellular/tissue contexts, enabling future studies into its potential roles in the nervous system and beyond.

neuroscience↗

New functional identity of the essential inner membrane protein YejM: the cardiolipin translocator is also a metalloenzyme

Recent recurrent outbreaks of Gram-negative bacteria show the critical need to target essential bacterial mechanisms to fight the increase of antibiotic resistance. Pathogenic Gram-negative bacteria have developed several strategies to protect themselves against the host immune response and antibiotics. One strategy is to remodel the outer membrane where several genes are involved. yejM was discovered as an essential gene in E. coli and S. typhimurium that plays a critical role in their virulence by changing the outer membrane permeability by translocating and increasing the cardiolipin lipid concentration. How the inner membrane protein YejM with its periplasmic domain acts as a cardiolipin translocator remains unknown. Despite overwhelming structural similarity of the periplasmic domains of two YejM homologues with hydrolases like arylsulfatases, no enzymatic activity has been reported for YejM. Our studies reveal an intact active site with bound metal ions in the structure of YejM periplasmic domain. Furthermore, we show that YejM has a phosphatase activity that is dependent on the presence of magnesium ions and is linked to its cardiolipin translocation properties. Understanding the molecular mechanism by which YejM is involved in OM remodeling will help to identify a new drug target in the fight against the increased antibiotic resistance.

biophysics↗