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Biology subjects

Hu, Y.

Publications and source records attributed to Hu, Y..

At least 73 records · Page 4Linked to original sources

Midazolam suppresses glioma progression by attenuating neuronal activity and downregulating IGF1 signaling

Glioma is the most common primary malignant tumor of the brain, and accumulating evidence indicates that neuronal activity plays a pivotal role in tumor progression. In this study, neuronal activity is modulated in vitro using potassium chloride (KCl)-induced depolarization and midazolam (MDZ)-mediated suppression. MDZ is a neuronal activity modulation medication, commonly used for sedation, anxiolysis, and amnesia in clinics. After treatment, conditioned media derived from these neuronal cultures are subsequently co-cultured with glioma cells. EdU incorporation assays demonstrate that MDZ significantly inhibits glioma cell proliferation in vitro. Furthermore, an orthotopic xenograft glioma model is established to assess the anti-tumor efficacy of MDZ in vivo, as evaluated by tumor volume and Ki-67 immunostaining. Mechanistically, insulin-like growth factor 1 (IGF1) is identified as the neuronal-activity-regulated factor that promotes glioma growth through activation of the PI3K/AKT signaling pathway. Moreover, transcriptomic profiling of brain tissues reveals that MDZ attenuates neuronal activity and downregulates neuron-derived growth factors in both glioma and non-tumor regions, thereby exerting anti-tumor effects in vivo. Collectively, these findings demonstrate that MDZ suppresses glioma progression by suppressing neuronal activity and inhibiting neuron-derived trophic factors, providing new insights into the development of therapeutic strategies for glioma.

neuroscience↗

Repetitive extragenic palindrome (REP) elements are local, context-dependent, dual 3'UTR regulators in Escherichia coli

Repetitive extragenic palindromes (REPs) are the most abundant repetitive noncoding elements in the E. coli genome. Despite their abundance, the primary function of REPs has remained unclear. At different times, REPs have been proposed to contribute to chromosome organization, mRNA decay regulation, and transcription termination, among other functions. Here, we show that the model REP, REP325, does not measurably compact the chromosome but instead acts as a 3UTR-associated transcription regulator within the yjdMN operon, functioning both as a partially Rho-dependent terminator that limits transcription into the downstream yjdN gene and as an mRNA stabilizer that protects the upstream yjdM transcript from degradation. This dual role in controlling both transcriptional readthrough and susceptibility to decay provides a framework that reconciles several previously conflicting observations about REP function. Our genome-wide RNA-seq analysis further reveals that REPs with more canonical sequence and hairpin structures are more often associated with upstream-biased expression in tandem gene pairs, and that REPs positioned between convergent genes correlate with elevated expression of both genes. The large variance in expression patterns in both gene pair configurations is consistent with context-dependent termination and degradation blocking. Similarly, REPs do not uniformly affect mRNA half-lives. Because REP locations vary between E. coli strains, REPs likely contribute to regulatory diversity by tuning gene expression without altering protein-coding sequences or promoter regions, opening new avenues for modulating gene expression through REP-mediated transcription regulation.

biophysics↗

A single-nucleus multiome analysis of transcriptome and chromatin accessibility reveals cell-type-specific immune modulation for chronic cannabis use among people with HIV infection

As cannabis use continues to rise among people with HIV (PWH), understanding its impact on immune function in this population is becoming increasingly important. To provide new insights on how cannabis modulates immune function, we analyzed single-nucleus multi-omic profiles of peripheral blood mononuclear cells (PBMCs) from PWH to characterize the changes in gene expression and chromatin accessibility associated with chronic cannabis exposure. We identified numerous differentially expressed genes (DEGs) between cannabis users and non-users in each cell type, approximately half of which were unique to individual cell types. Changes in pro- and anti-inflammatory gene expression associated with cannabis use are dependent on cell lineage and type. We identified hundreds of differential chromatin accessibility regions in each cell type, including cis-regulatory elements correlated with cell-type-dependent DEGs (e.g. NFKBIA in CD4+ T cells and CCL3L1 in classical monocytes). Multiple cannabis-associated transcription factors (e.g., NFKB1, FOS, and TCF7) emerge as regulators of the differentially expressed inflammatory genes. Furthermore, cannabis altered the communication between classical monocytes and lymphocytes. These findings indicate that cannabis-induced immunomodulatory effects are profound, dynamic and complex among cell types and that transcriptional changes are regulated at least in part by epigenetic mechanisms.

genomics↗

RNA-binding is the essential biological function of the Drosophila protein Brat

Brain tumor (Brat) is a Drosophila TRIM-NHL protein required for embryogenesis and neural stem cell differentiation. Although structural and biochemical studies established that the Brat NHL domain specifically binds RNA, the in vivo requirement for this activity has not been directly tested. Here, we used structure-guided mutagenesis and genome engineering to determine whether RNA recognition is essential for Brat function during development. The direct interaction between Brats NHL domain and RNA containing Brat Binding Sites (BBS) can be abolished by alanine substitution of three separate residues on the NHL surface. We introduced these point mutations into the endogenous brat locus by CRISPR-mediated Scarless Gene Editing to generate three independent RNA-binding defective mutant (RBDmt) alleles. Complementation tests demonstrated that each allele behaves as a strong loss-of-function mutation: homozygotes and hemizygotes are inviable, and RBDmt alleles fail to complement classical brat null and hypomorphic alleles. Lethal phase analysis revealed death predominantly during late larval and pupal stages, consistent with known brat alleles. Consistent with the namesake brat phenotype, RBDmt larval brains exhibited widespread expression of neuroblast markers and a marked reduction of neuronal differentiation. In embryos, these alleles failed to complement female sterile brat alleles and recapitulated characteristic abdominal segmentation defects. Finally, RT-qPCR showed increased expression of endogenous Brat target mRNAs in mutant larvae, consistent with loss of Brat-mediated repression. Together, these results demonstrate that direct RNA binding is the essential molecular activity of Brat and that post-transcriptional regulation of Brat target mRNAs underlies its critical roles across development.

molecular biology↗

Sequence and structure of protein binding sites in RNA impact biomolecular condensates

Biomolecular condensates are central to subcellular compartmentalization. Although many condensates contain and regulate RNA, research has primarily focused on protein interactions. Here, we investigate RNA-protein interactions underlying cell cycle-regulating condensates in the multinucleate fungus Ashbya gossypii. These condensates form through interactions between G1 cyclin mRNA CLN3 and RNA-binding protein Whi3, which was predicted by homology to recognize a five-nucleotide motif repeated within the transcript. Natural variation in motif number in Ashbya strains led us to hypothesize that binding site valence may influence condensate properties. Using unbiased binding assays, we determined the preference of Ashbya Whi3 protein for specific primary RNA sequence and mutated individual Whi3-binding sites within CLN3 mRNA. Mutants exhibited distinct condensate properties despite having the same valence in terms of binding site number. Mutations altered the saturation concentration (Csat) and dense phase concentration of RNA and protein in cell-free reconstitution experiments. A subset of mutants, showed reduced number of condensates and deregulation of the cell cycle in cells. We also find that enhanced availability of single-stranded RNA can compensate for loss of binding sites. Together, these data indicate that differences in RNA protein binding-site context and not simply valence plays a critical role in determining condensate properties.

cell biology↗

Geoclimatic oscillations and ancient reciprocal adaptive introgression shape the evolutionary trajectories of threatened Coilia

Geoclimatic oscillations have repeatedly reshaped biodiversity, yet how ancient lineages persist and diversify through profound environmental upheavals remains a central question in evolutionary genomics. By integrating chromosome-level genome assemblies, population genomics, and transcriptomic data across the Coilia species complex, we reconstruct deep evolutionary histories of Coilia along the dynamic East Asian margins. Our analyses reveal divergences dating to the Miocene, coinciding with major tectonic and climatic transitions, including Tibetan Plateau uplift-linked reorganization of the Yangtze drainage toward the East China Sea, and the Middle Miocene Climatic Optimum. Despite long-term separation, we uncover evidence for ancient, reciprocal introgression among Coilia lineages, with gene flow confined to discrete genomic regions rather than distributed genome-wide. These introgressed regions are enriched for loci associated with immune function, vascular development, and osmoregulatory processes, and exhibit population genetic signatures consistent with positive selection. Temporal modelling indicates that this window of adaptive exchange preceded Pleistocene glacial intensification, after which gene flow became effectively restricted. Together, our results suggest that transiently permeable species boundaries historically acted as reservoirs of adaptive variation, shaping evolutionary trajectories and facilitating niche differentiation under repeated geoclimatic oscillations. This study highlights ancient adaptive introgression as an important evolutionary process contributing to the long-term persistence of threatened coastal fishes.

evolutionary biology↗

Functional and Structural Basis of Omicron BA.3.2.1 Spike

SARS-CoV-2 Omicron descendant BA.3.2, derived from BA.3 and carrying 39 additional spike substitutions, prompts concerns about altered fitness and antigenicity. Using BA.3.2.1 as a representative sublineage, we have engineered live-attenuated mNeonGreen SARS-CoV-2 encoding spikes from BA.3.2.1 and the JN.1-derived LP.8.1 and XEC, and benchmarked them against BA.3 and KP.3 in Calu-3 cells and primary human airway epithelium. BA.3.2.1 outcompetes BA.3 yet replicates more slowly than JN.1-descendants. Despite increased RBD-hACE2 affinity, BA.3.2.1 spike binds hACE2 less efficiently than LP.8.1, and shows the greatest resistance to neutralization by sera from KP.2/KP.3 infections. Cryo-EM reveals a predominantly closed, compact, asymmetric trimeric spike with a remodeled N-terminal domain, a distinct fusion-peptide-proximal region and altered N-glycosylation. BA.3.2.1 spike adopts a fine-tuned receptor-binding interface and shifted monoclonal-antibody footprints. These findings identify a trade-off between immune evasion and replication fitness driven by closed spike conformation, rationalizing BA.3.2s limited prevalence and underscoring the necessity for continued variant surveillance.

microbiology↗

ATG-18 drives longevity in an HLH-30-dependent manner

Enhancing autophagy increases lifespan and healthspan in animal models, yet the precise molecular mechanisms underlying these effects are not fully understood. Here we show that overexpression of the essential autophagic gene atg-18 extends the lifespan of C. elegans. We describe a previously unknown, pleiotropic mechanism by which atg-18 impacts lysosomes and extends lifespan through the transcription factor hlh-30, the master regulator of lysosomal biogenesis. We show that, under stress conditions, HLH-30 requires atg-18 for nuclear translocation. Furthermore, atg-18 overexpression broadly improves health and stress resilience yet paradoxically increases early-life susceptibility to lethal heat stress. In contrast, enhances heat-stress survival a loss-of-function of function mutation in atg-18 enhances heat-stress survival, uncovering a temporal-specific effect of atg-18. These finding suggest an ATG-18--HLH-30 autophagy--lysosome pathway that plays a key role in lifespan and healthspan. Bulleted main discoveriesO_LIATG-18 overexpression increases C. elegans lifespan and plays an important role in resilience against starvation and heat stress. C_LIO_LIATG-18 is required for nuclear translocation of HLH-30 C_LIO_LIHLH-30 is required for ATG-18--mediated lifespan extension C_LIO_LIATG-18 positively regulates lysosomal biogenesis, suggesting a novel role as a molecular coordinator between autophagy and the lysosomal network. C_LI

molecular biology↗

Real-paired single-cell/bulk RNA-seq benchmark and a practical protocol for accurate cell-type deconvolution in human BAL samples

BackgroundPseudo-bulk RNA-seq, generated by aggregating single-cell profiles, is widely used for benchmarking deconvolution methods because it globally approximates bulk transcriptomes and provides known cell-type proportions as ground truth. However, pseudo-bulk inherits single-cell specific measurement properties, and the extent to which these differ from real bulk RNA-seq remains difficult to quantify in the absence of paired data. In practice, deconvolution studies also commonly rely on large external single-cell references, yet the value of small, protocol-matched in-study references has not been systematically evaluated under real bulk conditions. These gaps motivate a paired benchmark that jointly examines pseudo-bulk fidelity, reference design, and their consequences for deconvolution accuracy. ResultsWe establish a fully paired benchmarking framework using split-sample, donor-matched bulk and single-cell RNA-seq (scRNA-seq) from human bronchoalveolar lavage (BAL). Embedded within a reverse five-fold cross-validation design and evaluated on real bulk RNA-seq data, this framework benchmarks 15 deconvolution algorithms published in 2013-2025 across 3 cell-type resolutions and 5 single-cell references, including three published BAL datasets, a harmonized lung BAL atlas, and an in-study reference derived from paired aliquots. We show that real bulk and matched pseudo-bulk profiles exhibit systematic gene-level differences, identifying 557 reproducibly discordant genes (|log2 FC| > 1, FDR< 0.05 by LIMMA), including cell-type informative features. These discrepancies reflect technology-specific effects and violate the linear mixing assumption underlying most deconvolution methods. We demonstrate that a protocol-matched in-study reference constructed from only six donors consistently outperforms substantially larger external references, with the advantage that increases at finer cell-type resolution. Moreover, paired samples enable the identification and selective removal of discordant genes, which further improves deconvolution accuracy for many algorithms, particularly in high-resolution settings. These findings are robust across methods, references, and evaluation criteria and extend beyond compositional accuracy to improving recovery of disease-associated cell-type differences in clinical applications. ConclusionsOur study provides the first fully paired benchmark of transcriptomic deconvolution on real bulk RNA-seq data of human BAL samples and demonstrates that reference design and data compatibility are as influential as algorithm choice. Beyond benchmarking, we introduce a practical and cost-effective protocol for deconvolution studies: generate single-cell data for a minimal subset of bulk samples (pilot pairing), use these data to construct an in-study reference and identify discordant genes, and apply the resulting insights to the full cohort. This strategy requires limited additional experimental effort yet yields substantial gains in accuracy and stability, offering actionable guidance for future bulk RNA-seq deconvolution studies across tissues and platforms. One-sentence summarySystematic benchmarking reveals pseudo-bulk biases and provides practical fixes for accurate RNA deconvolution.

bioinformatics↗

Spatial transcriptomics reveals organizational properties of mouse spinal cord and alterations in neuropathic pain

The spinal cord integrates diverse somatosensory inputs and executes motor outputs through anatomically and functionally distinct circuits. Here, we employed spatially resolved single-cell transcriptomic profiling of the adult mouse spinal cord to gain insights into the organizational logic of the spinal cord. Our results reveal distinct spatial and laminar distributions of neuronal subtypes, including axial level and sex-specific differences. Many neuronal subtypes exhibit close spatial proximity, implicating regionally specific patterns of connectivity and circuit functions. Additionally, neuronal subtypes within the dorsal horn exhibit a wide range of predicted cell-cell communication motifs, as assessed by the spatial distribution of neuropeptide-and other ligand-receptor pairs. Finally, we identified several neuronal subtypes with altered transcriptomic and predicted cell-cell communications in a model of neuropathic pain. This spatially resolved cellular and molecular map of the spinal cord will facilitate the decoding of circuit mechanisms underlying somatosensory and motor functions in health and disease.

neuroscience↗

A standardized atlas of human bronchoalveolar lavage cells built using scalable ensemble annotation and cross-study robust markers

BackgroundBronchoalveolar lavage (BAL) single-cell RNA sequencing (scRNA-seq) offers rich insights into pulmonary immune dynamics, yet consistent cell-type annotation remains elusive. Existing methods often rely on a single reference, risking inconsistency and domain shift across datasets. A BAL-specific, high-resolution annotation framework is critically needed. MethodsWe developed BAL-EA (BAL Ensemble Annotation), a BAL-centric automated annotation framework that integrates robust, cross-study marker discovery with ensemble machine learning. BAL-EA harmonizes BAL cell identities into a three-tier taxonomy (11 major lineages, 13 refined classes, 21 fine-grained subtypes) compatible with the Human Lung Cell Atlas (HLCA) while capturing lavage-enriched biology. Marker catalogues were derived via reproducibility-guided differential expression across at least 10 independent sub-studies, ensuring resilience to dataset-specific bias. Comparative benchmarking was performed against six leading annotation tools using independent BAL datasets. ResultsWe assembled the largest BAL scRNA-seq atlas to date, integrating more than 347,333 lung cells from HLCA, multiple public BAL datasets, and the largest inhouse BAL cohort ever reported (241,924 cells from 30 individuals). BAL-EA outperformed existing annotation tools, achieving balanced macro-F1 scores over 0.95 for key lineages such as alveolar macrophages (AM), non-alveolar macrophages, and epithelial cells. Application to Chronic Obstructive Pulmonary Disease (COPD) BAL samples revealed reproducible disease-associated shifts, including increased neutrophils and CCL2-positive macrophages alongside reduced AM in COPD patients, findings validated in independent COVID-19 BAL datasets. The released atlas includes harmonized multi-resolution annotations, robust marker panels, pretrained models. ConclusionsThis work contributes the most comprehensive BAL scRNA-seq atlas, introduces a novel BAL-specific annotation framework (BAL-EA), standardizes BAL taxonomy at three resolutions, and provides rigorously validated marker gene resources. Together, these advances deliver a powerful reference for reproducible BAL scRNA-seq analysis and lay the foundation for clinical and translational applications in respiratory disease research.

genomics↗

tBid mediated genetic ablation of connective tissue cells reveal their key regulatory function during limb regeneration in axolotls

Limb regeneration in adulthood is a fascinating phenomenon unique to salamanders, requiring precise coordination and interaction of various cell types. Connective tissue (CT) constitutes a major component of the limb and serves as the primary reservoir of positional information during regeneration. However, the direct evidence and the extent of CT in positional contribution remain limited. Here we develop an inducible Cre-LoxP-mediated tBid cell ablation system in axolotls and demonstrate efficient elimination of targeted muscle tissue and muscle stem cells through transient electroporation or genetic approach. Ablation of CT cells at early stages of regeneration results in delayed regeneration and loss of proximal limb segments (e.g., upper and lower limb), with minimal impact on hand differentiation. CT ablation during development yields similar defects as observed during regeneration, indicating an essential role for CT cells in determining the positional identity of developing and regenerating limb structures. Further scRNA-seq reveal a progressive proximal-to-distal transition among CT cells and identify distinct CT subtypes that contribute to proximal and distal segments. CT ablation results in reduction of the differentiated CT1--a subpopulation that maintains proximal identity throughout regeneration, and a delay of distal transformation in the proliferative CT1--a major CT subtypes showing progenitor property. These cellular shifts likely lead to the observed morphological deficits in regenerating limbs after CT ablation. Moreover, differentiated CT1 cells enhanced their interactions with surrounding cell types after CT ablation, to modulate adaptive proliferation in other populations, e.g., muscle stem cells. Our work establishes a tBid-based ablation strategy for functional studies of CT and other cell types in axolotls, and provides direct evidence demonstrating pivotal roles of CT cells in guiding positional memory and segmental patterning during organ regeneration.

molecular biology↗

Torsins Organize CLCC1 Assembly to Safeguard ER Bilayer and Lipid Homeostasis

The TMEM41B scramblase and its regulatory partner CLCC1 initiate lipid flux by equilibrating newly-synthesized phospholipids across the endoplasmic reticulum (ER) bilayer, a fundamental process required for diverse events ranging from membrane biogenesis to bulk lipid supply. Loss of CLCC1/TMEM41B causes ER bilayer imbalance, inducing giant ER-enclosed lipid droplets (geLDs) and driving rapid progression into severe MASH. Here we identify CLCC1 as the long-missing client of the lumenal Torsin ATPases, which selectively engage oligomerized CLCC1 at sites of ER bilayer imbalance. Hepatic TorsinA inactivation triggers geLD formation amid disrupted lipoprotein biogenesis and severe MASH, closely phenocopying CLCC1/TMEM41B deficiency. Mechanistically, Torsins act as foldases that drive CLCC1 oligomerization for its recruitment to imbalanced bilayers. Remarkably, ectopic CLCC1 expression reverses cellular and systemic lipid disorders arising from hepatic TorsinA deficiency. Hence, Torsin ATPases emerge as fundamental regulators that organizes CLCC1 and the downstream TMEM41B scramblase to govern lipid partitioning and membrane homeostasis.

cell biology↗

A high-throughput methods SNIPR-Nm reveals small RNA methylation ratio

Small RNAs regulate gene expression and genome stability, and their functions are shaped by 3'-terminal 2'-O-methylation (Nm). Although Nm is universal in plants and mainly marks animal piRNAs, recent evidence reveals Nm on mammalian miRNAs, highlighting broader regulatory roles. However, current sequencing underestimates Nm-modified RNAs due to ligation bias, and existing qPCR-based methods cannot simultaneously quantify abundance and modification, leaving Nm dynamics largely unexplored. We developed a unified enzymatic strategy that integrates poly(A) polymerase and a thermostable ligase to measure both small RNA abundance and 3'-end Nm status. Applied to mouse testis, it enables robust quantification of Nm ratios for piRNAs and miRNAs. Our method offers a versatile tool for dissecting small RNA methylation in development and disease.

genetics↗

Precise Control of Switchable Chimeric Antigen Receptor T Cells Allows Enhanced Safety and Less T Cell Exhaustion

BackgroundChimeric antigen receptor (CAR)-T cell therapies have achieved remarkable success in hematologic malignancies, yet their clinical utility remains limited by safety concerns, limited persistence, and T-cell exhaustion driven by continuous receptor signaling. While switchable CAR designs provide external control, many reported systems are irreversible, strictly binary, or compromise CAR-T potency. MethodsWe engineered an optimized chemically switchable CAR platform (CSN CAR) that pharmacologically regulates antigen engagement by controlling the surface expression of the full-length CAR. An NS3 protease module was embedded within the CAR construct to enable drug-dependent stabilization of intact CAR on T cells. Using engineered CAR-T cells, we quantified drug-controlled activation, cytotoxicity, and cytokine release against CD19+ tumor cells by flow cytometry and ELISA in vitro. We further screened clinically approved NS3/4A inhibitors in CAR-HEK and CAR-T cells to identify optimal small-molecule controllers. A chronic stimulation model was established to assess CAR-T persistence and exhaustion-associated phenotypes in vitro. ResultsCSN CAR-T cells enabled precise, dose-dependent regulation of CAR surface density, cytokine production, and cytotoxicity. In the OFF state, switchable CAR-T cells showed minimal basal activity, consistent with reduced antigen-driven activation and cytokine release in the absence of drug in the experimental conditions. Upon drug addition, intact surface CAR was detectable within 1 hour, reaching [~]80% of peak observed CAR expression by 4 hours. Reversible suppression of CAR expression enabled attenuation of cytotoxicity toward normal CD19+ B cells in vitro after target-cell reduction, supporting a potential strategy to mitigate prolonged on-target/off-tumor activity. Under chronic stimulation, switchable CAR-T cells exhibited reduced exhaustion-associated markers, more stable CAR expression, and preferential differentiation toward a central memory phenotype. ConclusionTogether, these findings establish CSN CAR as a reversible and tunable switchable CAR-T platform enabled by clinically approved NS3/4A inhibitors, supporting controllable modulation of CAR activity with potential applications for improving the precision and safety of CAR-T cell therapy.

cancer biology↗

From features to slice: parameter-cloud modeling of spatial transcriptomics for simulation and 3D interpolatory augmentation

Computational simulation and data augmentation of spatial transcriptomics (ST) are essential for quantitative benchmarking, reproducibility, and methodological innovation. Yet current models often lack flexibility in controlling spatial and transcriptional heterogeneity, fail to capture higher-order gene dependencies, and rarely extend to three-dimensional or alignment-aware contexts. Here we present FEAST, a computational infrastructure that models ST data within a parameter cloud - a latent manifold encoding gene-level mean, variance, and sparsity. By sampling and perturbing this manifold, FEAST generates high-fidelity synthetic slices with tunable spatial and transcriptional variation, enabling systematic evaluation of clustering, deconvolution, and spatial alignment algorithms. Beyond two dimensions, FEAST performs 3D parameter-cloud interpolation guided by optimal transport and benchmark alignment, reconstructing continuous tissue architectures while preserving molecular coherence. Together, these capabilities establish FEAST as a foundational platform for standardized benchmarking, data augmentation, and 3D reconstruction in spatial transcriptomics. The source code and tutorials for FEAST are publicly available at https://github.com/maiziezhoulab/FEAST, and can be installed via Pypi at https://pypi.org/project/FEAST-py/.

bioinformatics↗

Elucidation and engineering of arabinofuranosyltransferase to enable total de novo biosynthesis of paris saponins in yeast

Paris saponins (PSs) are structurally complex steroidal saponins that, due to their diverse glycosylation patterns, exhibit a range of significant pharmacological activities, including anti-tumor and antibacterial effects. However, incomplete characterization of the key enzymes responsible for glycosylation modifications has hindered their efficient heterologous biosynthesis. In this study, we reprogrammed the sugar donor specificity of a steroidal rhamnosyltransferase (UGT93M3) to enable the transfer of arabinofuranose (Araf). Through structural analysis, we identified key amino acid residues (368H/Q) that play an important role in determining Araf donor specificity. Guided by this insight, we successfully reconstructed the paris saponin I (PSI) biosynthetic pathway in Saccharomyces cerevisiae using engineered enzymes. To address challenges related to donor availability, we introduced UDP-sugar biosynthetic modules (UDP-Rha and UDP-Araf) into yeast. With this integrated platform, we were able to de novo produce a range of paris saponins, including diosgenin-3-O-glucosyl-(1[->]6)-glucoside (DGG), diosgenin-3-O-rhamnosyl(1[->]2) [glucosyl(1[->]6)]glucoside (DRGG) and paris saponin II. This work establishes a novel microbial platform for the sustainable production of paris saponins, particularly PSI, advancing the biosynthesis of steroidal glycosides and providing a potential strategy for the industrial-scale production of bioactive saponins. TeaserIn this study, we report the first complete de novo biosynthesis of four bioactive PSs, PSI, PSII, DGG and DRGG, in Saccharomyces cerevisiae from simple carbon source. Key advances include: (i) A single amino-acid switch (N368H) in the rhamnosyltransferase UGT93M3 endowed high-efficiency transfer of the rare five-membered arabinofuranose, solving a bottleneck in PS I biosynthesis; (ii) Elucidation of the molecular basis for sugar-donor specificity through AlphaFold3 docking and 300-ns molecular-dynamics simulations, revealing a histidine "latch" that stabilizes UDP-Araf in the catalytic pose; (iii) Construction of a 16-gene yeast chassis that integrates plant P450s, optimized glycosyltransferases, and de novo modules for UDP-rhamnose and UDP-arabinofuranose supply, achieving de novo microbial production of PS II, DGG, DRGG and PS I from glucose alone.

synthetic biology↗

Archaeal histone HTkC hypercompacts DNA

Histones are important organizers of chromatin in eukaryotes and archaea. In eukaryotes, the core histones assemble with DNA to form the octameric nucleosome. In archaea, histones form hypernucleosomes that are not restricted to an octameric histone core but can extend to variable lengths. We previously identified face-to-face (FtF) histones as a widely distributed group of archaeal histones that assemble into toroidal tetramer structures, distinct from nucleosomal histones. Here, we characterize the FtF histone HTkC from Thermococcus kodakarensis, which also encodes the canonical histones HTkA and HTkB. We show that HTkC wraps DNA around its toroidal tetramer and forms highly compact nucleoprotein complexes, achieving a level of compaction approximately twice that of hypernucleosomes. Consistent with a major chromatin-organizing role, htkC is among the most highly expressed genes in T. kodakarensis and its deletion leads to impaired growth. Together, these findings establish FtF histones as important organizers of archaeal chromatin alongside classical histones.

biochemistry↗