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Biology subjects

Wu, Y.-H.

Publications and source records attributed to Wu, Y.-H..

12 recordsLinked to original sources

Designing enzymes for new-to-nature chemistry and non-natural substrates with AlphaProtein Novo

Creating highly active enzymes for arbitrary reactions is a transformative goal for the molecular sciences (1). Traditional protein engineering (2,3) is constrained by a reliance on existing natural starting points, which are often challenging to discover. De novo design offers the potential to overcome this by creating enzymes from first principles (4), but has yet to achieve practically relevant catalytic properties. Here we present AlphaProtein Novo (AP Novo), a machine-learning pipeline that demonstrates, for the first time, that de novo enzyme design can outperform natural sequence mining in addressing challenging chemistry. We used AP Novo to design new-to-nature nitrene transferases to synthesise the pharmacophore piperidine with unprecedented product selectivity, and to create enzymes that degrade the environmental toxin DEHP under conditions that denature natural enzymes. We also obtained state-of-the-art catalytic efficiencies on two well-studied model reactions, and through iterative design and analysis found that key enablers of success were mechanism-inspired metrics based on AlphaFold 3 predictions and sequence-ensemble-based scoring of designed backbones. Our results show that de novo design has become a powerful complement to natural enzyme diversity for discovering catalysts for a range of applications.

synthetic biology↗

Early dynamics of a neutrophil interferon program drive immunotherapy resistance and limit durable anti-tumor immunity

Despite the remarkable success of immune checkpoint blockade (ICB), durable clinical benefit remains limited to a subset of patients, highlighting the need for predictive biomarkers and new therapeutic targets. Here, we investigated the early immune dynamics associated with anti-PD1 responsiveness using longitudinal single-cell transcriptomics, spatial transcriptomics, and neutrophil-specific genetic perturbations in preclinical models of triple-negative breast cancer. We identified a conserved neutrophil interferon-stimulated gene (ISG) program that emerges before overt tumor divergence and predicts resistance to anti-PD1 therapy. Successful treatment was associated with an early reduction of IFN-responsive neutrophils in both blood and tumor tissues, whereas persistent neutrophil IFN signaling correlated with therapeutic resistance. Mechanistically, genetic disruption of either type I or type II interferon signaling in neutrophils enhanced anti-PD1 efficacy and promoted durable anti-tumor immune memory. Spatial analyses further revealed an inverse association between IFN-responsive neutrophils and tertiary lymphoid structure-enriched regions during effective therapy. Together, these findings identify IFN-responsive neutrophils as early determinants of immunotherapy outcome and establish dynamic neutrophil interferon programs as candidate blood-based biomarkers and therapeutic targets for cancer immunotherapy.

cancer biology↗

BioGeoSyn: a graphical software for reproducible biogeographic analyses and cross-clade synthesis of biogeographic events

O_LIHistorical biogeography increasingly looks beyond one clade at a time, pooling range-evolution and speciation events from lineages that share a region to ask whether the same geological and climatic events shaped them together. Despite the momentum behind this cross-clade synthesis, it still has no dedicated software. C_LIO_LIWe present BioGeoSyn, an open-source graphical application (with an equivalent scripting interface) that makes a complete, reproducible BioGeoBEARS analysis point- and-click: guided data upload and validation, model fitting and comparison, biogeographic stochastic mapping (BSM), and standardized tables, publication figures and a report. C_LIO_LIIts one novel capability is cross-clade synthesis. Once every clades events carry the same seven process labels and sit on a common time axis, BioGeoSyn integrates event rates through time, overall and region-resolved, across independently analysed clades, each carrying a 95% interval propagated from the stochastic maps, to reveal shared biogeographic pulses. C_LIO_LIBioGeoSyn lowers the barrier to reproducible historical biogeography for non-programmers and provides a ready-to-use route to multi-clade biogeographic-event synthesis. C_LI Data and code for peer reviewthe complete source code, the example data and the worked-example analyses are available to editors and reviewers at https://anonymous.4open.science/r/BioGeoSyn-696B/, an anonymised mirror of the development repository. An archived release is deposited in a public repository; its DOI is withheld here for double-blind review.

evolutionary biology↗

The Filterprep: A Simple and Efficient Approach for High-Yield, High-Purity Plasmid DNA Purification

Plasmid DNA purification remains a fundamental yet resource-intensive step in molecular biology and biotechnology. Conventional protocols often yield plasmids with suboptimal purity, while commercial kits, though efficient, are costly and use proprietary formulations that limit transparency and customization. Here, we present Filterprep, a hybrid method combining classical ethanol precipitation with a single spin-column cleanup step, enabling rapid recovery of high-purity plasmid DNA with yields notably higher than those obtained using commercial kits, in approximately 40 minutes. Filterprep offers a transparent, cost-effective, and scalable alternative, simplifying workflows and reducing hands-on time without compromising DNA quality. The purified plasmids are compatible with a variety of downstream applications, including mammalian cell transfection, protein expression, and reporter assays. With its balance of efficiency and practicality, Filterprep is well suited for high-throughput laboratories and resource-limited settings.

biochemistry↗

Predictive acoustical processing in human cortical layers

In our dynamic environments, predictive processing is vital for auditory perception and its associated behaviors. Predictive coding formalizes inferential processes by implementing them as information exchange across cortical layers and areas. With laminar-specific blood oxygenation level dependent we measured responses to a cascading oddball paradigm, to ground predictive auditory processes on the mesoscopic human cortical architecture. We show that the violation of predictions are potentially hierarchically organized and associated with responses in superficial layers of the planum polare and middle layers of the lateral temporal cortex. Moreover, we relate the updating of the brains internal model to changes in deep layers. Using a modeling approach, we derive putative changes in neural dynamics while accounting for draining effects. Our results support the role of temporal cortical architecture in the implementation of predictive coding and highlight the ability of laminar fMRI to investigate mesoscopic processes in a large extent of temporal areas.

neuroscience↗

Specificity Protein 1 is essential for the limb trajectory of ephrin-mediated spinal motor axons

The precise organization of neural circuits requires highly specific axon guidance, facilitated by cell-surface guidance receptors on axonal growth cones that help neurons reach their target destinations. Despite a limited repertoire of known guidance receptors and ligands, neural systems achieve complex axonal networks, suggesting that additional regulatory mechanisms exist. One proposed strategy is the co-expression of ligands and their receptors on the same axons, allowing modulation of receptor responsiveness to guidance cues. To investigate this mechanism, we studied the spinal lateral motor column (LMC) motor neurons, which make a binary axon pathfinding decision toward limb targets. We hypothesized that specificity protein 1 (Sp1), a transcription factor, regulates ephrin expression in LMC neurons, thereby modulating receptor functions via cis-attenuation to ensure accurate axonal pathfinding. Our results show that Sp1 is indeed expressed in LMC neurons during critical axonal extension periods. Manipulating Sp1 activity disrupted LMC axon trajectory selection, and RNA-Seq analysis indicated that Sp1 regulates genes associated with axon guidance, including ephrins. We found that Sp1 knockdown affected ephrin/Eph cis-binding and trans-signaling, highlighting Sp1s role in controlling axonal projections through ephrin gene regulation. Additionally, coactivators p300 and CBP are essential for Sp1s regulatory function. These findings identify Sp1 as a key transcription factor in LMC neurons, essential for ephrin expression and ephrin/Eph-mediated axon guidance, providing insights into the molecular mechanisms of neural circuit formation.

neuroscience↗

Unbiased metastatic niche-labeling identifies estrogen receptor-positive macrophages as a barrier of T cell infiltration during bone colonization

Microenvironment niches determine cellular fates of metastatic cancer cells. However, robust and unbiased approaches to identify niche components and their molecular profiles are lacking. We established Sortase A-Based Microenvironment Niche Tagging (SAMENT), which selectively labels cells encountered by cancer cells during metastatic colonization. SAMENT was applied to multiple cancer models colonizing the same organ and the same cancer to different organs. Common metastatic niche features include macrophage enrichment and T cell depletion. Macrophage niches are phenotypically diverse between different organs. In bone, macrophages express the estrogen receptor alpha (ER) and exhibit active ER signaling in male and female hosts. Conditional knockout of Esr1 in macrophages significantly retarded bone colonization by allowing T cell infiltration. ER expression was also discovered in human bone metastases of both genders. Collectively, we identified a unique population of ER+ macrophages in the metastatic niche and functionally tied ER signaling in macrophages to T cell exclusion during metastatic colonization. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=165 SRC="FIGDIR/small/593016v1_ufig1.gif" ALT="Figure 1"> View larger version (60K): org.highwire.dtl.DTLVardef@1cd65b6org.highwire.dtl.DTLVardef@1d099e2org.highwire.dtl.DTLVardef@26cd91org.highwire.dtl.DTLVardef@181f5f3_HPS_FORMAT_FIGEXP M_FIG C_FIG HIGHLIGHTSO_LISAMENT is a robust metastatic niche-labeling approach amenable to single-cell omics. C_LIO_LIMetastatic niches are typically enriched with macrophages and depleted of T cells. C_LIO_LIDirect interaction with cancer cells induces ER expression in niche macrophages. C_LIO_LIKnockout of Esr1 in macrophages allows T cell infiltration and retards bone colonization. C_LI

cancer biology↗

Single cell profiling of bone metastasis ecosystems from multiple cancer types reveals convergent and divergent mechanisms of bone colonization.

Bone represents congenial soil for metastatic seeds and is frequently affected by metastasis of multiple cancer types. The histological and molecular characteristics of bone metastases (BMs) are diverse but poorly understood. Herein, we performed single-cell RNA-seq on 34 BMs from 6 cancer types and identified 3 ecosystem archetypes characterized by enrichment of macrophages/osteoclasts (M{varphi}-OC), regulatory/exhausted T cells (Treg-Tex), and monocytes (Mono), respectively. Breast cancer BMs are mostly the M{varphi}-OC archetype driven by the osteolytic vicious cycle, whereas kidney cancers BMs mainly belong to the Treg-Tex archetype that lacks osteoclasts. Lung cancers BMs evenly distributed across all archetypes. Further analyses revealed parallel mechanisms of immunosuppression and bone remodeling. Elevated estrogen signaling distinguishes macrophages in the M{varphi}-OC subtype, which was investigated in a companion study. Together, we elucidated that divergent mechanisms toward bone colonization and that BMs of different origins can adopt the same mechanism through convergent evolution or adaptation. HIGHLIGHTSO_LIAnalyses of bone metastases from 6 cancer types revealed three immune archetypes. C_LIO_LIArchetypes diverge on immune trajectories, and features of tumor and stromal cells. C_LIO_LIDominant cell type in each archetype undergoes convergent evolution. C_LIO_LIRegulatory networks converge on osteoclasts and Tregs to drive archetype formation. C_LI Graphic Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=166 SRC="FIGDIR/small/593027v1_ufig1.gif" ALT="Figure 1"> View larger version (61K): org.highwire.dtl.DTLVardef@82cef6org.highwire.dtl.DTLVardef@1e1b021org.highwire.dtl.DTLVardef@1f2881eorg.highwire.dtl.DTLVardef@1c6874a_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Hydrogen Sulfide Coordinates Glucose Metabolism Switch through Destabilizing Tetrameric Pyruvate Kinase M2

Cancer cells reprogram their glucose metabolic pathway from oxidative phosphorylation toward aerobic glycolysis. Pyruvate kinase M2 (PKM2), which converts phosphoenolpyruvate (PEP) to pyruvate, is considered the rate-limiting enzyme involved in cancer glucose metabolism. By reducing PKM2 enzyme activity, cancer cells attain a greater fraction of glycolytic metabolites for macromolecule synthesis needed for rapid proliferation. Here we demonstrate that hydrogen sulfide (H2S) destabilizes PKM2 tetramer into dimer/monomer, leading to reduced PKM2 enzyme activity and an increase in the activation of nuclear transcriptional genes mediated by dimeric PKM2. Proteomic profiling of endogenous PKM2 reveals the occurrence of sulfhydration at cysteines, notably at cysteine 326. Blocking PKM2 sulfhydration at cysteine 326 through amino acid mutation stabilizes PKM2 tetramer and crystal structure further indicating that the tetramer organization of PKM2C326S is different from the currently known T or R states, revealing PKM2C326S as a newly identified form. The presence of a PKM2C326S mutant in cancer cells effectively rewires glucose metabolism to mitochondrial respiration, resulting in the significant inhibition of tumor growth. Collectively, PKM2 sulfhydration by H2S serves as a glucose metabolic rewiring mechanism in promoting tumorigenesis, and inhibition of PKM2 sulfhydration may be applied as a new therapeutic approach targeting cancer metabolism. One-Sentence SummaryH2S rewires glucose metabolism by destabilizing PKM2 tetramerization majorly through sulfhydration at cysteine 326 HighlightsO_LIH2S enhances PKM2 dissociation from tetramer to dimer to facilitate dimeric PKM2 nuclear translocation. C_LIO_LIH2S modifies PKM2 sulfhydration, notably at cysteine 326. C_LIO_LIThe crystal structure reveals PKM2C326S as a unique tetramer conformation. C_LIO_LIBlockage of PKM2 sulfhydration at C326 rewires cancer glucose metabolism and significantly inhibits tumor growth. C_LI

cancer biology↗

Chinese fir genome and the evolution of gymnosperms

Seed plants comprise angiosperms and gymnosperms. The latter includes gnetophytes, cycads, Ginkgo, and conifers. Conifers are distributed worldwide, with 630 species distributed across eight families and 70 genera. Their distinctiveness has triggered much debate on their origin, evolution, and phylogenetic placement among seed plants. To better understand the evolution of gymnosperms and their relation to other seed plants, we report here a high-quality genome sequence for a tree species, Chinese fir (Cunninghamia lanceolata), which has excellent timber quality and high aluminum adaptability and is a member of Cupressaceae with high levels of heterozygosity. We assembled an 11.24 Gb genome with a contig N50 value of 2.15 Mb and anchored the 10.89 Gb sequence to 11 chromosomes. Phylogenomic analyses showed that cycads sister to Ginkgo, which place to sister in all gymnosperm lineages, and Gnetales within conifers sister to Pinaceae. Whole-genome duplication (WGD) analysis showed that the ancestor of seed plants has differentiated into angiosperms and gymnosperms after having experienced a WGD event. The ancestor of extant gymnosperm has experienced a gymnosperm-specific WGD event and the extant angiosperms do not share a common WGD before their most recent common ancestor diverged into existing angiosperms lineages. Analysis of the MADS-box gene family of C. lanceolata revealed the developmental mechanism of the reproductive organs in C. lanceolata, which supported the (A)B(C) model of the development of gymnosperms reproductive organs. In addition, astringent seeds and shedding of whole branches (with withered leaves) might be a strategy of C. lanceolata that evolved during long-term adaptation to an aluminum-rich environment. The findings also reveal the molecular regulation mechanism of shade tolerance in C. lanceolata seedlings. Our results improve the resolution of ancestral genomic features within seed plants and the knowledge of genome evolution and diversification of gymnosperms.

genomics↗

Chemical-induced degradation of PreS2 mutant surface antigen reverses HBV- mediated hepatocarcinogenesis

Naturally evolved immune-escape PreS2 mutant is an oncogenic caveat of liver cirrhosis and hepatocellular carcinoma (HCC) during chronic hepatitis B virus (HBV) infection. Notably, PreS2 mutants is prevalent in above 50% of patients with HCC. Intrahepatic expression of PreS2 mutant large surface antigen (PreS2-LHBS) induces endoplasmic reticulum stress, mitochondria dysfunction, cytokinesis failure and subsequent chromosome hyperploidy. In this study, we ask if long-term inhibition of PreS2-LHBS may act to reverse HBV-mediated hepatocarcinogenesis. We set up a stability reporter platform and identified ABT199 as an inhibitor of PreS2-LHBS from a library of 1068 FDA-approved drugs. Treatment of ABT199 induced PreS2-LHBS degradation without affecting the general cell viability, as shown in hepatoma and immortalized hepatocyte cell lines. We found that ABT199 induced the recruitment of PreS2-LHBS to ring-shaped structures in close proximity to lysosomal marker Lamp1 and multivesicular body marker Rab7. Simultaneously, inhibitions of lysosomal degradation or microautophagy restored the expression of PreS2-LHBS. Specifically, a 24-hr treatment of ABT199 reduced DNA damages and cytokinesis failure induced by PreS2-LHBS. Persistent treatment of ABT199 for 3 weeks reversed chromosome hyperploidy in PreS2-LHBS cells and suppressed anchorage-independent growth of HBV-positive hepatoma cell line. Together, we showed that ABT199 provoked selective degradation of PreS2-LHBS through the induction of microautophagy, and a long-term treatment of ABT199 reversed oncogenic mechanisms induced by HBV. Our results indicate that long-term degradation of PreS2-LHBS may serve as a novel therapeutic strategy to constrain HBV-mediated hepatocarcinogenesis. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=66 SRC="FIGDIR/small/477454v1_ufig1.gif" ALT="Figure 1"> View larger version (16K): org.highwire.dtl.DTLVardef@1720c85org.highwire.dtl.DTLVardef@943121org.highwire.dtl.DTLVardef@1257a22org.highwire.dtl.DTLVardef@1756348_HPS_FORMAT_FIGEXP M_FIG C_FIG Author summaryHBV PreS2 mutant large surface antigen (PreS2-LHBS) is an oncoprotein that induces liver cirrhosis and liver cancer. This study identified ABT199 as a potential inhibitor of PreS2-LHBS. We found that ABT199 could trigger the degradation of PreS2-LHBS through the induction of microautophagy. Moreover, a long-term treatment of ABT199 significantly reversed LHBS-induced oncogenic events including DNA damage, mitotic failure, chromosome hyperploidy, and anchorage-independent growth. This study not only identifies a specific inhibitor of PreS2-LHBS but also highlights a plausible strategy to constrain HBV-mediated hepatocarcinogenesis through targeting the degradation of PreS2-LHBS.

microbiology↗

Aerobic glycolysis supports hepatitis B virus biosynthesis through interaction between viral surface antigen and pyruvate kinase isoform M2

As an intracellular pathogen, the reproduction of hepatitis B virus (HBV) depends on the occupancy of host metabolism machinery. Here we test a hypothesis if HBV may govern intracellular biosynthesis to achieve a productive reproduction. To test this hypothesis, we set up an affinity purification screen for host factors that interact with viral large surface antigen (LHBS). This identified pyruvate kinase isoform M2 (PKM2), a key regulator of glucose metabolism, as a binding partner of LHBS. We showed that the expression of LHBS affected oligomerization of PKM2 in hepatocytes, and thereby increased glucose consumption and lactate production, a phenomenon known as aerobic glycolysis. Interestingly, recovering PKM2 activity in hepatocytes by chemical activators, TEPP-46 or DASA-58, reduced biosynthesis of viral surface and core antigens. In addition, reduction of glycolysis by culturing in low-glucose condition or treatment with 2-deoxyglucose also decreased biosynthesis of viral surface antigen, without affecting general host proteins. Finally, TEPP-46 largely suppressed proliferation of LHBS-positive cells on 3-dimensional agarose plates, but showed no effect on the traditional 2-dimensional cell culture. Taken together, these results indicate that virus-induced metabolic switch may support de novo biosynthesis of HBV in hepatocytes. In addition, aerobic glycolysis is likely essential for LHBS-mediated oncogenesis. Accordingly, restriction of glucose metabolism may be considered as a novel strategy to restrain viral mediated biosynthesis and oncogenesis during chronic HBV infection. Author summaryChronic HBV infection is a life-long threat of patients, with a 25~40% increased risk of developing liver cirrhosis and cancer. Persistent expression of oncogenic viral products in the liver, especially LHBS, is an oncogenic caveat and resistant to current antiviral agents. Here we show that viral LHBS binds to host PKM2 and diminishes its kinase activity. This virus-host interaction induces metabolic switch from oxidative phosphorylation to aerobic glycolysis, with increased glucose consumption and lactate production. We show that such metabolic switch not only favors biosynthesis of HBV but also provokes hepatocarcinogenesis. Notably, restoration of PKM2 activity by chemical activators decreases expressions of viral products and largely suppresses virus-mediated hepatocarcinogenesis. This study highlights the importance of host metabolism in supporting viral biosynthesis and indicates a novel therapeutic approach to control chronic HBV infection via modulating host metabolic switch.

microbiology↗