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Kang, H. S.

Publications and source records attributed to Kang, H. S..

8 recordsLinked to original sources

Non-destructive Spatial Reconstruction of Plant Leaf Starch Using Reduced-Band SWIR Spectroscopy and Chemometric Modeling

1Non-structural carbohydrates (NSCs) are central to plant carbon allocation and physiological regulation, yet their quantification typically relies on destructive biochemical assays that lack spatial resolution. Here, we developed a shortwave infrared (SWIR) hyperspectral imaging workflow for non-destructive estimation and spatial reconstruction of starch-associated variation in strawberry leaves. The workflow combined automated hyperspectral segmentation, spectral preprocessing, Partial Least Squares Regression (PLSR), and constrained wavelength selection. Sample-level spectra extracted from 114 strawberry leaf samples grown across three different metabolic conditions were paired with destructive starch measurements and used to train models across the 900-1750 nm spectral range. A constrained greedy band-selection strategy revealed that predictive performance approached a plateau at approximately 12 wavelengths, indicating substantial spectral redundancy within the full hyperspectral dataset. The final reduced-band model achieved a cross-validated coefficient of determination (R2) of 0.771 {+/-} 0.066 and a root mean squared error (RMSE) of 0.743 {+/-} 0.098 mg g-1 fresh weight using repeated stratified 5-fold cross-validation. Pixel-wise application of the final model generated spatial starch-associated maps that preserved pronounced intra-leaf heterogeneity, including vein-associated spatial structure. These results demonstrate that starch-associated spectral information can be reconstructed from a constrained reduced-band SWIR framework while retaining sufficient predictive performance for spatial mapping. The identified wavelength reduction supports the feasibility of deployable multispectral systems for non-destructive carbohydrate sensing in plant phenotyping applications.

plant biology↗

GLIS3 is a key regulator of astrocyte differentiation in human neural stem cells

Astrocytes play a key role in neuronal homeostasis and in various neural disorders. The generation of astrocytes from neural progenitor cells (NPCs) and its functions are under a complex control of several signaling networks and transcription factors. In this study, we demonstrate that the transcription factor, GLIS similar 3 (GLIS3), which has been implicated in several neurodegenerative diseases, is highly expressed in astrocytes, and is required for the efficient differentiation of human NPCs into astrocytes. Loss of GLIS3 function greatly impairs astrocytes differentiation, resulting in reduced expression of astrocyte markers, whereas expression of exogenous GLIS3 restores the induction of astrocyte specific genes indicating a critical role for GLIS3 in astrocyte differentiation. Integrated transcriptomic and cistromic analyses revealed that GLIS3 directly regulates the transcription of several astrocyte-associated genes, including GFAP, SLC1A2, NFIA, and ATF3, in coordination with lineage-determining factors, such as STAT3, NFIA, and SOX9. We hypothesize that GLIS3 dysfunction disrupts this transcriptional network thereby contributing to astrocyte-associated neurological disorders. Identification of GLIS3 as a key regulator of astrocyte differentiation and gene expression will advance our understanding of its role in neurodegenerative diseases and may provide a new therapeutic target.

developmental biology↗

Cell wall charge gates iron availability in plant roots

Plants acquire essential mineral nutrients from the soil, yet these elements must first traverse the extracellular matrix of the root before reaching the cell surface. How the physical properties of this extracellular compartment influence nutrient distribution and availability remains poorly understood. In plants, this extracellular matrix is formed by the cell wall, which carries a dynamically regulated negative charge that can change during development and in response to environmental cues. Here we demonstrate that cell wall charge functions as a tunable electrostatic gate that determines how iron is partitioned between retention and bioavailability. This decoupling between iron abundance and availability reveals a fundamental tradeoff imposed by extracellular electrostatics. A mechanistic diffusion-binding model shows that increasing wall charge inherently enhances iron sequestration while limiting its mobility at the cell surface. Genetic perturbation of pectin de-methylesterification validates this principle in vivo. Moreover, iron limitation itself triggers active remodeling of cell wall charge, dynamically shifting the balance toward increased iron accessibility. Together, these findings identify the plant cell wall as an active regulator of nutrient homeostasis rather than a passive barrier. By dynamically modulating extracellular electrostatics, roots control iron partitioning and bioavailability, uncovering a new physical layer of regulation in plant mineral nutrition. One-Sentence SummaryThe plant cell wall operates as a tunable electrostatic gate that buffers and releases iron through spatially and environmentally regulated charge dynamics.

plant biology↗

The nuclear receptor ROR-alpha is a critical myogenic regulator of the cardiomyocyte transcriptome, including the alpha-1A adrenergic receptor

AimsWe recently found that the nuclear receptor retinoic acid-related orphan nuclear receptor alpha (ROR) protects against angiotensin II-induced cardiac hypertrophy and promotes cardiomyocyte mitophagy. The underlying molecular basis for these salutary effects remains unclear. MethodsWe used RNA microarrays to profile the cardiac transcriptomes of "staggerer" (RORsg/sg) mice that carry a naturally occurring mutation in the ligand-binding domain of ROR, resulting in a global loss-of-function genetic model. We then used genetic and pharmacologic loss-and-gain of function studies in cultured cardiomyocytes to ascertain whether ROR regulates transcription of Adra1a, the gene that encodes the alpha-1A-adrenergic receptor (1A-AR). ResultsThe absence of functional ROR results in broad transcriptional changes in the heart providing a likely molecular basis for the RORsg/sg cardiac phenotype. In vivo and in vitro studies confirmed that ROR directly regulates Adra1a transcription. This effect is enhanced by hypoxia. ConclusionsCollectively these findings position ROR as a previously unrecognized central regulator of the cardiac myogenic transcriptome and the first recognized transcriptional regulator of Adra1a in cardiomyocytes. Future studies will probe the contribution of ROR-mediated transcriptional regulation of Adra1a to both the response to cardiomyocyte injury and maintenance of circadian biology.

physiology↗

Reliability and accuracy of single-molecule FRET studies for characterization of structural dynamics and distances in proteins

Single-molecule FRET (smFRET) has become an established tool to study biomolecular structure and dynamics in vitro and in live cells. We performed a worldwide blind study involving 19 labs to assess the uncertainty of FRET experiments for proteins with respect to the measured FRET efficiency histograms, determination of distances, and the detection and quantification of structural dynamics. Using two protein systems that undergo distinct conformational changes, we obtained an uncertainty of the FRET efficiency of less than {+/-} 0.06, corresponding to an interdye distance precision of [≤] 0.2 nm and accuracy of [≤] 0.5 nm. We further discuss the limits for detecting distance fluctuations with sensitivity down to [lsim] 10% of the Forster distance and provide guidelines on how to detect potential dye perturbations. The ability of smFRET experiments to simultaneously measure distances and avoid averaging of conformational dynamics slower than the fluorescence lifetime is unique for dynamic structural biology.

biophysics↗

GLIS1 regulates trabecular meshwork function and intraocular pressure and is associated with glaucoma in humans

Chronically elevated intraocular pressure (IOP) is the major risk factor of primary open- angle glaucoma, a leading cause of blindness. Dysfunction of the trabecular meshwork (TM), which controls the outflow of aqueous humor (AqH) from the anterior chamber, is the major cause of elevated IOP. Here, we demonstrate that mice deficient in the Kruppel- like zinc finger transcriptional factor GLI-similar-1 (GLIS1) develop chronically elevated IOP. Magnetic resonance imaging and histopathological analysis reveal that deficiency in GLIS1 expression induces progressive degeneration of the TM, leading to inefficient AqH drainage from the anterior chamber and elevated IOP. Transcriptome and cistrome analyses identified several glaucoma- and extracellular matrix-associated genes as direct transcriptional targets of GLIS1. We also identified a significant association between GLIS1 variant rs941125 and glaucoma in humans (P=4.73x10-6), further supporting a role for GLIS1 into glaucoma etiology. Our study identifies GLIS1 as a critical regulator of TM function and maintenance, AqH dynamics, and IOP.

molecular biology↗

The nuclear receptor RORα preserves cardiomyocyte mitochondrial function by regulating mitophagy through caveolin-3

Preserving optimal mitochondrial function is critical in the heart, which is the most ATP-avid organ in the body. Recently, we showed that global deficiency of the nuclear receptor ROR in the "staggerer" (RORsg/sg) mouse exacerbates angiotensin II-induced cardiac hypertrophy and compromises cardiomyocyte mitochondrial function. The mechanisms underlying these observations have not been defined. Here we present evidence that ROR regulates cardiomyocyte mitophagy using pharmacological and genetic gain- and loss-of-function tools, including a novel cardiomyocyte-specific ROR knockout mouse. Cardiomyocyte ROR is upregulated by hypoxia and the loss of ROR blunts hypoxia-induced mitophagy and broadly compromises mitochondrial function. We show that ROR is a direct transcriptional regulator of the mitophagy mediator caveolin-3 in cardiomyocytes and that increased expression of ROR increases caveolin-3 abundance and enhances mitophagy. Knockdown of ROR impairs cardiomyocyte mitophagy, but this defect can be rescued by caveolin-3 overexpression. Collectively, these findings reveal a novel role for ROR in regulating mitophagy through caveolin-3 and expand our currently limited understanding of the mechanisms underlying ROR-mediated cardioprotection.

molecular biology↗

Prophage genomics reveals patterns in phage genome organization and replication

Temperate phage genomes are highly variable mosaic collections of genes that infect a bacterial host, integrate into the hosts genome or replicate as low copy number plasmids, and are regulated to switch from the lysogenic to lytic cycles to generate new virions and escape their host. Genomes from most Bacterial phyla contain at least one or more prophages. We updated our PhiSpy algorithm to improve detection of prophages and to provide a web-based framework for PhiSpy. We have used this algorithm to identify 36,488 prophage regions from 11,941 bacterial genomes, including almost 600 prophages with no known homology to any proteins. Transfer RNA genes were abundant in the prophages, many of which alleviate the limits of translation efficiency due to host codon bias and presumably enable phages to surpass the normal capacity of the hosts translation machinery. We identified integrase genes in 15,765 prophages (43% of the prophages). The integrase was routinely located at either end of the integrated phage genome, and was used to orient and align prophage genomes to reveal their underlying organization. The conserved genome alignments of phages recapitulate early, middle, and late gene order in transcriptional control of phage genes, and demonstrate that gene order, presumably selected by transcription timing and/or coordination among functional modules has been stably conserved throughout phage evolution.

biochemistry↗