Biology subjects

Kwon, S.-K.

Publications and source records attributed to Kwon, S.-K..

7 recordsLinked to original sources

bioRxiv2026

Who Formed All That Iron?: A Novel Antarctic Chemolithotroph Drives Iron Biomineralization

Iron mineralization has profoundly influenced Earths biogeochemical history1,2, yet the specific mechanisms underlying banded iron formation (BIF) remain unresolved3-5. Here we profile the microbiomes of Holocene sediments beneath the Larsen C Ice Shelf (LCIS), Antarctica6-8, through stratigraphic analysis of sedimentary ancient DNA combined with metagenomics. Distinct microbial phases aligned with glacial facies boundaries, with sub-ice shelf communities dominated by chemolithoautotrophs including an uncultured Thermodesulfovibrionia. This bacterium, visualized by fluorescence in situ hybridization and designated Candidatus Mariimomonas ferrooxydans (phylum Nitrospirota), emerged as a keystone taxon with high network centrality. Its genome encodes Cyc2, a fused porin-cytochrome outer membrane protein implicated in Fe(II) oxidation. Heterologous expression of Cyc2 in Escherichia coli confirmed its ability to catalyze iron oxidation, supporting iron precipitation under dark, anoxic conditions. These pristine LCIS sediments, unaltered since the last glacial maximum, provide a modern analogue for synglacial BIFs deposited during Neoproterozoic Snowball Earth events. Our findings deliver direct genomic and functional evidence for chemolithotrophic iron oxidation, challenge phototroph-centric models of BIF genesis, and highlight microbial iron cycling as a recurring force in Earths geochemical evolution. Beyond Earth, these insights inform interpretations of iron deposits on other planetary bodies.

microbiology↗

bioRxiv2025

Asymmetric distribution of mitochondrial Ca2+ regulators specifies compartment-specific mitochondrial function and neuronal development

Neuronal polarization is essential for functional compartmentalization, enabling dendritic synaptic integration and axonal action potential generation. While structural differences in mitochondria across compartments have been identified, their functional distinctions remain unclear. Here, we uncovered compartment-specific mitochondrial Ca2+ dynamics and their molecular determinants. In axonal mitochondria, Ca2+ uptake through MCU occurs independently of ER-stored Ca2+ release, with faster matrix Ca2+ clearance than dendritic mitochondria, where Ca2+ uptake predominantly originates from ER Ca2+. The ER-independent mitochondrial Ca2+ uptake in axonal mitochondria is mediated by enriched MCU-regulating proteins, MICU1 and MICU2, while higher NCLX expression facilitates rapid Ca2+ clearance. Moreover, NCLX knockdown, which functionally mimics a mental retardation-associated mutation, caused more significant axonal branching defects compared to dendrites in vivo, aligning with its enrichment in axons. These findings highlight fundamental Ca2+-modulating features and developmental importance of neuronal mitochondria in a compartment-specific manner and reveal the key underlying molecular mechanisms.

neuroscience↗

bioRxiv2024

Investigation of neural functional connectivity in thick acute mouse brain slices with novel multi-region 3D neural probe arrays

There are significant limitations in investigating complex neural circuits in vivo, including drawbacks to midline-adjacent surgeries, limited accessibility to deep brain regions and number of feasible regional targets for simultaneous recordings, and analytical or experimental biases from recording one columnar plane. On the other hand, recording extracellular neural signals ex vivo or in vitro using planar microelectrode arrays (MEAs) only permits slice surface recordings, and since conventional slices under 400 m-thick or dissociated cultures are used, no experiments contain a physiological multi-region circuit, drastically limiting conclusions about connectivity and pharmacology. Using thick, tract-preserving acute brain slices to record otherwise unassailable neural circuits ex vivo combines the strengths of both types of experiments, but is assumed to precipitate ischemic injury due to oxygen scarcity within the slice. Here, we report the first application of custom, multi-region silicon neural probe arrays to record spontaneous activity & optogenetically-induced functional connectivity acrosshe mesocorticolimbic pathway within tract-preserving 800 m sagittal mouse brain slices, compared with 400 m slices, among three brain regions: the ventral tegmental area (VTA), ventral striatum (VS), & medial prefrontal cortex (mPFC). We show that most single-unit signals are an order of magnitude below the noise floor seen using silicon probes in vivo, providing unit yields far higher than previously assumed, allowing for a deep functional understanding of acute slice condition compared to the assumed deterioration due to ischemia. Overall, our method allows for acute circuit manipulations beyond what is available in vivo, with far more information than conventional slice preparations.

neuroscience↗

bioRxiv2023

A marine bacterium elicits the type III secretion-dependent nonhost hypersensitive response in a land plant

Active plant immune response involving programmed cell death called the hypersensitive response (HR) is elicited by microbial effectors delivered through the type III secretion system (T3SS). The marine bacterium Hahella chejuensis contains two T3SSs that are similar to those of animal pathogens, but elicited HR-like cell death in the land plant Nicotiana benthamiana, which was mediated by SGT1 and suppressed by AvrPto1. Thus, the land plant is capable of inducing the cell death in response to type III-secreted effectors of the marine bacterium it never have encountered, suggesting that plants may have evolved to cope with a potential threat posed by alien effectors. One-sentence summaryA marine bacterium Hahella chejuensis harboring functional type III secretion systems induced nonhost hypersensitive response in a land plant Nicotiana benthamiana, which was mediated by SGT1 and suppressed by AvrPto1.

plant biology↗

bioRxiv2022

Neuronal mitochondrial morphology is significantly affected by both fixative and oxygen level during perfusion

Neurons in the brain have a uniquely polarized structure consisting of multiple dendrites and a single axon generated from a cell body. Interestingly, intracellular mitochondria also show strikingly polarized morphologies along the dendrites and axons: in cortical pyramidal neurons (PNs) dendritic mitochondria have a long and tubular shape, while axonal mitochondria are small and circular. Mitochondria play important roles in each compartment of the neuron by generating ATP and buffering calcium, thereby affecting synaptic transmission and neuronal development. In addition, mitochondrial shape, and thereby function, is dynamically altered by environmental stresses such as oxidative stress, or in various neurodegenerative diseases including Alzheimers disease and Parkinsons disease. Although the importance of altered mitochondrial shape has been claimed by multiple studies, methods for studying this stress-sensitive organelle have not been standardized. Here we address the pertinent steps that influence mitochondrial morphology during experimental processes. We demonstrate that fixative solutions containing only paraformaldehyde (PFA), or that introduce hypoxic conditions during the procedure induce dramatic fragmentation of mitochondria both in vitro and in vivo. This disruption was not observed following the use of glutaraldehyde addition or oxygen supplementation, respectively. Finally, using pre-formed fibril -synuclein treated neurons, we show a difference between mitochondrial morphology when samples were fixed with PFA/glutaraldehyde or PFA/sucrose containing solutions, but not PFA alone. Our study provides optimized methods for examining mitochondrial morphology in neurons, and demonstrates that fixation conditions are critical when investigating the underlying cellular mechanisms involving mitochondria in physiological and neurodegenerative disease models.

neuroscience↗

bioRxiv2021

Whole-ExM: Expansion microscopy imaging of all anatomical structures of whole larval zebrafish

Nanoscale resolution imaging of whole vertebrates is required for a systematic understanding of human diseases, but this has yet to be realized. Expansion microscopy (ExM) is an attractive option for achieving this goal, but the expansion of whole vertebrates has not been demonstrated due to the difficulty of expanding hard body components. Here, we demonstrate whole-body ExM, which enables nanoscale resolution imaging of anatomical structures, proteins, and endogenous fluorescent proteins (FPs) of whole zebrafish larvae and mouse embryos by expanding them fourfold. We first show that post-digestion decalcification and digestion kinetics matching are critical steps in the expansion of whole vertebrates. Then, whole-body ExM is combined with the improved pan-protein labeling approach to demonstrate the three-dimensional super-resolution imaging of antibody- or FP-labeled structures and all major anatomical structures surrounding them. We also show that whole-body ExM enables visualization of the nanoscale details of neuronal structures across the entire body.

developmental biology↗

bioRxiv2018

MFF-dependent mitochondrial fission regulates presynaptic release and axon branching by limiting axonal mitochondria size

Neurons display extreme degrees of polarization, including compartment-specific organelle morphology. In cortical pyramidal neurons, dendritic mitochondria are long and tubular whereas axonal mitochondria display uniformly short length. Here, we explored the functional significance of maintaining small mitochondria for axonal development in vitro and in vivo. We report that the Drp1 receptor Mitochondrial fission factor (MFF) is required for determining the size of mitochondria entering the axon and then for maintenance of their size along the distal portions of the axon without affecting their trafficking properties, presynaptic capture, membrane potential or capacity for ATP production. Strikingly, this increase in presynaptic mitochondrial size upon MFF downregulation augments their capacity for Ca2+ ([Ca2+]m) uptake during neurotransmission, leading to reduced presynaptic [Ca2+]c accumulation, decreased presynaptic release and terminal axon branching. Our results uncover a novel mechanism controlling neurotransmitter release and axon branching through fission-dependent regulation of presynaptic mitochondrial size.

cell biology↗