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Zhong, Q.

Publications and source records attributed to Zhong, Q..

At least 19 recordsLinked to original sources

U-Chrom: a unified framework for single-cell and spatial 3D genome data

Single-cell Hi-C, spatial Hi-C and chromatin tracing measure the same genomes in incompatible formats. ChromData, one data model, indexes all three by cell and genomic bin; an open-source toolkit, linked browser and 22-dataset atlas build on it. Applied to ten mouse brain datasets of all three assays, the same calls rank cell types alike by short- over long-range proximity, and contact-based reconstructions largely place cell-type differences where imaging does.

bioinformatics↗

De novo design of CR2 binder as vaccine scaffold

Efficient B cell activation during vaccine-induced humoral immunity relies on both B cell receptor (BCR) antigen recognition and synergistic signaling from co-receptors. Complement receptor 2 (CR2), the primary BCR co-receptor on B cells, lowers the activation threshold and amplifies downstream kinase signaling by orders of magnitude when engaged by complement fragment C3d decorated antigens. Targeting CR2 therefore represents a rational vaccine enhancement strategy, yet native C3d suffers from low affinity, poor stability, and manufacturing challenges. Here, we report the de novo design of a highly stable, high-affinity CR2 binder using deep learning driving protein design methods. Biophysical characterization, high-resolution cryoEM structural determination, and functional assays in vitro and in vivo confirm that the designed binder matches computational design models and specifically engages CR2 to boost B cell activation. When fused to antigen as a vaccine scaffold, the trimeric CR2 binder elicits robust humoral immune responses comparable to nanoparticle vaccines, while retaining the simplicity of single-chain protein production. Our work establishes a modular CR2 targeting vaccine scaffold platform with broad translational potential for next-generation protein vaccines.

immunology↗

A multi-scale structural and biophysical atlas of TCR-peptide-HLA recognition dynamics

Dynamic interactions between T cell receptor (TCR) and peptide-human leukocyte antigen (pHLA) complexes are central to peptide-specific immune recognition, influencing T cell activation and immune responses. While structural biology has provided valuable static structures of TCR-pHLA complexes, systematic datasets capturing their dynamic and interaction patterns remain limited. Here, we present DynaTPH, a curated structural dynamics dataset of human TCR-pHLA complexes. DynaTPH integrates TCR-pHLA structures, covering both HLA class I and class II complexes, and extends these static structural resources with standardized molecular dynamics simulations and derived biophysical properties. Through a multi-stage filtering procedure, we identified 256 representative complexes and performed standardized all-atom molecular dynamics simulations for each system, corresponding to a cumulative simulation time of 38.4 s. The dataset includes static structures, trajectories, corresponding frames, and derived physicochemical properties, including hydrogen bonds, intermolecular contacts, solvent accessibility, and backbone flexibility. By capturing the conformational flexibility and dynamic interaction patterns across diverse TCR-pHLA interfaces, DynaTPH extends static structural resources with multidimensional biophysical information. This dataset enables systematic investigation of TCR-pHLA recognition dynamics and supports applications in TCR engineering, vaccine design, and immune tolerance research and artificial intelligence-driven computational immunology.

molecular biology↗

The evolutionarily conserved APP-Spastin cooperation regulates endolysosomal homeostasis and apoptotic cell degradation

Efferocytosis, the recognition, engulfment, and degradation of apoptotic cells by phagocytes, is essential for tissue homeostasis and development, and its failure contributes to chronic inflammation and neurodegeneration. The amyloid precursor protein (APP), a central pathogenic factor in Alzheimers disease, retains physiological functions independent of amyloid production that remain poorly understood. Here, we identify a conserved, non-amyloidogenic role for APP in regulating apoptotic cell degradation via the endolysosomal pathway. Using Drosophila APPL as a model, structure-function analysis demonstrated that the intracellular internalization domain of APPL, but not its secreted ectodomain, is required for efficient apoptotic cell degradation. Immunoprecipitation coupled with mass spectrometry revealed a physical interaction between APPL and the microtubule severing ATPase Spastin, mediated by the microtubule-interacting and trafficking domain of Spastin. APPL interacts with Spastin on endosomal microtubules and modulates the dynamics of the Spastin-ESCRT-III complex, enabling Spastin to sever microtubules and promote endosomal tubule fission. Loss of APPL disrupts this process, causing aberrant endosomal tubulation and impaired lysosome biogenesis. Furthermore, it compromises the function of residual lysosomes, characterized by reduced acidity, diminished proteolytic activity, and increased lysosomal damage, which ultimately impairs the degradation of engulfed apoptotic cells. Critically, this phenotype is evolutionarily conserved in C. elegans and mice. Together, these findings establish a conserved APP-Spastin axis that regulates endolysosomal homeostasis and apoptotic cargo digestion. This reveals a critical non-amyloidogenic function of APP in maintaining tissue homeostasis through efficient efferocytosis, with broad implications for inflammatory and neurodegenerative disorders that warrant further investigation.

cell biology↗

Dormant Bacteria's Fatal Attraction to RNA Bacteriophages

Phages are the most abundant biological entities on Earth, yet RNA phages are strikingly scarce compared to their DNA counterparts--a long-standing mystery in phage biology. Here, we use dsRNA phage phiYY as a model to demonstrate that while RNA phages efficiently infect growing bacteria, they are gradually eliminated inside dormant bacteria through weak and time-dependent ROS-mediated damage. The RNA phages decline over days rather than through immediate clearance inside dormant bacteria. Accordingly, scavenging ROS with mannitol or overexpressing ROS degradation enzymes AhpB/TrxB2 rescues RNA phages from elimination. Crucially, because the underlying ROS-mediated RNA damage is minimal, RNA phage survival hinges on genomic redundancy. In single-phage infections, the lone RNA genome is highly vulnerable to cumulative damage and is eventually inactivated. In contrast, during co-infection by multiple RNA phages, the presence of multiple genome copies provides functional redundancy, thereby allowing a fraction of RNA phages to survive inside dormant bacteria. Given that most environmental bacteria are dormant and subject to heterogeneous phage infection, this copy number-dependent vulnerability offers a possible explanation for the scarcity, but not perish, of RNA phages in nature.

microbiology↗

PantheonOS: An Evolvable Multi-Agent Framework for Automatic Genomics Discovery

The convergence of large language model-powered autonomous agent systems and single-cell biology promises a paradigm shift in biomedical discovery. However, existing biological agent systems, building upon single-agent architectures, are narrowly specialized or overly general, limiting applications to routine analyses. We introduce PantheonOS (https://PantheonOS.stanford.edu), an evolvable, privacy-preserving multi-agent framework designed to reconcile generality with domain specificity. Critically, PantheonOS enables agentic code evolution, allowing evolving state-of-the-art batch correction and our reinforcement-learning augmented gene panel selection algorithms to achieve super-human performance. PantheonOS drives biological discoveries across systems: uncovering asymmetric paracrine Cer1-Nodal inhibition in proximal-distal axis formation of novel early mouse embryo 3D data; integrating human fetal heart multi-omics with whole-heart data to reveal molecular programs underpin heart diseases; and adaptively selecting virtual cell models to predict cardiac regulatory and perturbation effects. Together, PantheonOS points towards a future where scientific discoveries are increasingly driven by self-evolving AI systems across biology and beyond. Websitehttps://pantheonos.stanford.edu Ecosystemhttps://github.com/aristoteleo SummaryLarge language model-powered agent systems are driving a paradigm shift in scientific discovery by automating, scaling, and accelerating data analysis. This transformation is particularly profound in biology, where the rapid expansion of single-cell and spatial genomics has effectively reshaped the field into a data-intensive science. However, existing biological agent systems are typically constrained to single-agent designs, are narrowly specialized, or are overly general without sufficient domain expertise, limiting their applicability to routine or shallow analyses. Here, we introduce PantheonOS (https://pantheonos.stanford.edu), an evolvable, privacy-preserving, and general-purpose multi-agent framework designed to reconcile generality with deep domain specificity. PantheonOS provides an abstract, extensible architecture that enables customized agent composition and supports end-to-end single-cell and multi-omics analysis, spanning reinforcement-learning-augmented gene panel design, raw FASTQ processing, multimodal data integration, and three-dimensional spatial genomics reconstruction. Central to this framework, Pantheon-Evolve enables agentic code evolution, allowing the system to autonomously improve state-of-the-art batch-correction algorithms and new reinforcement-learning based gene panel design algorithms, achieving performance beyond manually designed baselines. We demonstrate the power of PantheonOS across multiple biological domains. In early mouse embryogenesis, PantheonOS automatically reconstructs three-dimensional spatial gene expression landscapes and resolves asymmetric Cer1 expression and paracrine Cer1-Nodal inhibition, revealing a robust proximal-distal axis at embryonic day six (E6.0). In human development, PantheonOS integrates fetal heart single-cell multi-omics with whole-heart 3D MERFISH+ data at post-conception week 12, uncovering spatially resolved molecular programs underlying heart disease ontogeny. Finally, an intelligent model-routing mechanism enables PantheonOS to adaptively select optimal virtual cell models across heterogeneous tasks, revealing minimal regulatory networks of cardiogenesis and predicting spatially resolved perturbation effects in the developing heart. Together, PantheonOS establishes a foundation for fully automated, evolvable, and domain-aware agentic analysis in genomics, and points toward a future in which scientific discovery is increasingly driven by self-improving AI systems across biology and beyond.

bioinformatics↗

Divergent phenotypic and functional roles of human T follicular helper cells from infancy to adulthood

Antibody responses to T-dependent antigens are suboptimal in young children, yet the evolution of T follicular helper cell (Tfh) function across the human lifespan remains poorly defined. Using human tonsils, a physiologically relevant and abundant source of Tfh, we investigated age-associated differences in their repertoire and functional programs. Pediatric tonsils were enriched for cytokine-expressing Tfh subsets with increased clonal diversity and phenotypic plasticity. However, in response to influenza antigens, they exhibited reduced Th1 polarization, diminished IL-21 production, and limited B cell help. Across ages, high neutralizing flu antibody responses were associated with robust Tfh1 activation, which was ICOS dependent in adults but not in children. Interestingly, Tfh depletion strategies revealed enhanced Tfh differentiation from distinct precursors in pediatric donors, yet antibody responses during early life were less reliant on Tfh help. Together, these findings define developmentally programmed differences in Tfh differentiation and function with implications for pediatric vaccine design.

immunology↗

Integrative Multi-Omics Analysis Identifies a Functional Enhancer Driving Tumorigenesis in Head and Neck Squamous Cell Carcinoma

Enhancer is a critical epigenetic feature in head and neck squamous cell carcinoma (HNSCC), yet the functional roles of individual enhancers remain poorly understood. Here, we conducted an integrative multi-omics analysis based on publicly available ATAC-seq, H3K27ac ChIP-seq, transcriptomic profiling, and genetic association datasets to systematically map HNSCC-associated enhancers and their target genes. Integrating ATAC-seq and H3K27ac ChIP-seq, we identified 20,362 enhancers and 18,040 enhancer-associated genes, highlighting widespread regulatory complexity. Functional characterization of the TERT-associated enhancer GH05J001312 (GRCh38/hg38: chr5:1312099-1317743) revealed strong transcriptional activity in HNSCC. CRISPR-mediated deletion of a core sequence significantly reduced TERT expression, impaired cellular proliferation in vitro, and suppressed tumor growth in vivo, confirming its role as a key cis-regulatory element. RNA-seq analysis of enhancer-edited cells uncovered 742 differentially expressed genes enriched in cancer-related pathways, including MAPK and IL-17 signaling, indicating a broad transcriptional impact. Collectively, our findings establish GH05J001312 as a functional enhancer driving oncogenic programs in HNSCC and suggest enhancer-targeted strategies as a potential therapeutic avenue.

cancer biology↗

Structural mechanism of Necrocide 1 activation of human TRPM4 that triggers necrosis by sodium overload

The small molecule Necrocide 1 (NC1) constitutively activates human TRPM4, triggering Na influx and leading to necrotic cell death, a process termed Necrosis by Sodium Overload (NECSO). NC1 activation is specific to human TRPM4 and does not affect most of the other mammalian TRPM4 orthologs. Here, we elucidate the molecular mechanism underlying NC1 activation and its species-specific selectivity for human TRPM4 using a combination of single-particle cryo-EM, electrophysiology, and cell death assays. We identify the NC1-binding site and the key molecular determinants responsible for channel activation. In addition, we explain the insensitivity of mouse TRPM4 to NC1 and pinpoint specific residues that define NC1 specificity for human TRPM4. Given the upregulation of TRPM4 in various human cancers, our mechanistic insights into NC1 activation and specificity provide a framework for the potential development of cancer therapeutics targeting TRPM4-mediated necrosis.

biophysics↗

An octadecameric O-glucosyltransferase generates diversity in antibody epitopes on variant surface antigens in African trypanosomes

Immune evasion in many pathogens relies on sequence variation to generate antigenic diversity. African trypanosomes use an additional strategy where O-glucosylation of variant surface glycoproteins (VSGs) alters antibody epitopes and influences infection outcome, but the responsible enzyme remained elusive. Here, we show that an expression-site-associated gene (ESAG3), which is co-transcribed with the active VSG, encodes an O-glucosyltransferase required for VSG3 O-glycosylation in vivo. ESAG3 depletion abolishes VSG3 O-glycosylation and recognition of live trypanosomes by an O-glycan-dependent monoclonal antibody, while complementation restores both. ESAG3 has strict UDP-glucose donor specificity and modifies serine/threonine residues within VSG3 peptides in vitro. Cryo-electron microscopy at 3.4 Angstrom resolution reveals that ESAG3 forms a homo-octadecameric ring with C3 symmetry, an architecture not previously observed among glycosyltransferases. Structure-guided mutagenesis shows that disruption of ESAG3 inter-subunit interfaces reduces higher-order assembly, enhances substrate conversion, and alters VSG glycoform composition. Furthermore, we show that VSG3 O-glycan occupancy correlates with susceptibility to complement-mediated trypanolysis in an antibody-dependent manner, establishing that ESAG3-mediated O-glucosylation shapes both antibody specificity and the functional outcome of the host response.

microbiology↗

A tonsil organoid model reveals Epstein-Barr virus infected germinal center B cell states during primary infection

Epstein-Barr virus (EBV) colonizes secondary lymphoid tissues to establish persistent infection and is strongly associated with malignancy and autoimmunity. Our understanding of EBV infection biology is hindered by a lack of models that capture infected B cell activity in the lymphoid tissue microenvironment. We therefore developed an EBV human tonsil organoid model to evaluate key B cell states and antiviral responses, including after primary infection. EBV promoted B cell differentiation into germinal center (GC)-like phenotypes and transcriptomic analyses highlighted numerous B cell transcriptional programs unique to EBV-infected cells. B cell receptor repertoire analysis revealed that most EBV-infected B cells underwent class switching but only rarely participated in somatic hypermutation. CD4 T cells, highly activated by organoid infection, limited EBV+ B cell outgrowth. Our findings demonstrate human tonsil organoids as a physiologically relevant model to investigate key aspects of EBV immunity and pathogenesis.

immunology↗

Single-cell transcriptomic atlas reveals that vascular tissues orchestrate cell fate transitions to initiate adventitious root formation in tomato

O_LIAdventitious root (AR) formation enables vegetative propagation critical for agriculture, conservation, and breeding, yet the cellular basis of AR competence in crop species remains poorly characterized. Most mechanistic studies rely on Arabidopsis, which exhibits constrained AR capacity compared to species dependent on clonal propagation. C_LIO_LIWe constructed a single-cell transcriptomic atlas of tomato (Solanum lycopersicum) AR development comprising 7,920 cells across 12 cell types. Regulatory networks were inferred using hdWGCNA and MINI-EX, validated by RNA in situ hybridization and qPCR. Cross-dataset integration with shoot-borne root initiation data enabled developmental staging, while SATURN-based integration of 118,730 vascular cells from eight species permitted evolutionary comparison. C_LIO_LICytoTRACE analysis revealed that vascular tissues--root stele and phloem--possess the highest developmental potential, supporting a model of latent stem cell-like identity rather than dedifferentiation-based reprogramming. Network analysis identified LEA3 as a central hub gene constitutively expressed throughout AR development, regulated by the DOF transcription factor DOF11. Cross-species integration demonstrated that tomato AR-initiating cells share transcriptomic similarity with woody dicots (Liriodendron, r = 0.46; Eucalyptus, r = 0.42) but not Arabidopsis (r = -0.02), with LEA3-containing macrogene weights highest in basal angiosperms and woody species. C_LIO_LIOur findings establish the DOF11-LEA3 axis as a conserved vascular identity module and suggest that AR competence represents an ancestral program retained in species with active cambial dynamics. These results reframe Arabidopsis as a derived rather than representative model for AR biology and identify molecular targets for enhancing vegetative propagation. C_LI

plant biology↗

Machine Learning-Driven Discovery of Synergistic Protein Interactions Identifies ATL3 as a Putative Biomarker for Cancer Drug Response

BackgroundResistance to targeted molecular therapies--both primary and acquired--remains a major obstacle to effective cancer treatment. Despite extensive research, the molecular determinants of treatment resistance are still incompletely understood, underscoring the need to identify robust resistance drivers to improve therapeutic outcomes. Recently, the ProCan and Wellcome Sanger Institute released the worlds largest pan-cancer proteomic dataset to date, comprising 949 cancer cell lines treated with 625 anti-cancer agents. Despite progress in identifying single protein markers, scalable methods for detecting synergistic protein interactions driving drug susceptibility remain limited. Machine learning models such as random forests may offer a robust framework for capturing non-linear protein interactions across diverse cancer types. ResultsOur study presents synerOmics, a scalable framework for identifying putative synergistic protein interactions by leveraging parent-child co-occurrences in random forest regression trees to reduce the interaction search space. We validated our approach using simulated data and two independent cancer proteomic datasets, identifying both pan-cancer and breast cancer-specific markers associated with drug susceptibility. Synergistic interactions that consistently replicated across datasets were enriched for endoplasmic reticulum stress pathways. Notably, shared targets included established sensitivity markers for tyrosine kinase inhibitors (TKIs) and revealed a resistance-associated network centred on ATL3, which demonstrated both prognostic and predictive relevance. ConclusionsApplying synerOmics to the largest cancer cell line proteomic dataset to date, we identified ATL3 as a strong candidate biomarker for lapatinib resistance in breast cancer, with superior predictive performance compared to the current gold standard sensitivity biomarker, ERBB2. HighlightsO_LIWe present a machine learning framework for drug response biomarker discovery, leveraging the largest proteomic cancer cell line dataset, ProCan-DepMapSanger C_LIO_LIATL3 is proposed as a candidate predictive biomarker for lapatinib resistance in breast cancer C_LIO_LIElevated expression of a novel resistance-conferring subcluster centered on ATL3 is associated with poor prognosis across 11 TCGA cancer types C_LIO_LIBaseline drug resistance may be broadly driven by stress pathways, with ER stress and protein ATL3 implicated in ER-phagy in response to TKIs. C_LI

cancer biology↗

GBP1 recruitment to actin-rich pedestals induced by extracellular Gram-negative bacteria promotes pyroptosis.

The IFN{gamma}-induced GTPase guanylate binding protein 1 (GBP1) binds to lipopolysaccharide (LPS) on cytosolic Gram-negative bacteria and promotes pyroptosis via the recruitment and activation of caspase-4 on the bacterial outer membrane. Enteropathogenic and enterohaemorrhagic Escherichia coli (EPEC and EHEC, respectively) are extracellular pathogens that also induce LPS-and caspase-4-dependent pyroptosis. However, whether GBP1 is involved in this process remains unknown. EPEC and EHEC adhere intimately to intestinal epithelial cells via avid interactions between the bacterial adhesin Intimin and Tir (Translocated intimin receptor), a type 3 secretion system effector protein. Intimin-mediated clustering of Tir triggers actin polymerisation, leading to pedestal-like structures at bacterial attachment sites. Here we show that GBP1 is recruited to actin-rich pedestals in human cells infected with EPEC and EHEC in vitro and mouse colonocytes infected with the EPEC-like murine pathogen Citrobacter rodentium in vivo. GBP1-dependent caspase-4 trafficking to these sites leads to pyroptosis and IL-18 release. GBP1 mutants defective in LPS coatomer formation also localised to EPEC pedestals, pointing to LPS-independent mobilisation of GBP1 by actin polymerisation induced by extracellular A/E pathogens. To further dissect the underlying mechanism, we engineered a chimeric receptor (Fc{gamma}R-Tir) by combining the intracellular signalling domain of Tir and the extracellular ligand-binding domain of the Fc{gamma} receptor. Clustering of Fc{gamma}R-Tir with IgG-coated beads produced sterile actin-rich pedestals that were sufficient to recruit GBP1 independently of bacteria. Our findings reveal that cytosolic GBP1 is mobilised to sites of pathogen-induced actin remodelling independently of LPS. We establish that GBP1 not only operates as a pattern-recognition receptor but also orchestrates effector-triggered immunity against pathogens that hijack the actin cytoskeleton. 175-word AbstractThe IFN{gamma}-induced GTPase guanylate binding protein 1 (GBP1) binds to lipopolysaccharide (LPS) on cytosolic Gram-negative bacteria and promotes pyroptosis via the recruitment and activation of caspase-4 on the bacterial outer membrane. Enteropathogenic and enterohaemorrhagic Escherichia coli (EPEC and EHEC, respectively) are extracellular pathogens that adhere to host cells and stimulate dense actin polymerisation underneath their attachment sites, generating structures called actin-rich pedestals. Here we show that GBP1 traffics to actin-rich pedestals in human cells infected with EPEC and EHEC in vitro and mouse colonocytes infected with the EPEC-like murine pathogen Citrobacter rodentium in vivo. GBP1 promotes caspase-4 recruitment to actin-rich pedestals, leading to pyroptosis and IL-18 release. GBP1 mutants defective in LPS coatomer formation also localised to EPEC pedestals. Our novel assay that mimics pathogenic effector activity revealed GBP1 recruitment to sterile actin polymerisation sites. We conclude that cytosolic GBP1 is mobilised to sites of pathogen-induced actin remodelling independently of LPS. Our study establishes that GBP1 not only operates as a pattern-recognition receptor but also orchestrates effector-triggered immunity against pathogens that hijack the actin cytoskeleton.

immunology↗

Multimodal profiling of proinflammatory protease activity identifies caspase-1 as a target for lung cancer interception

The systemic inhibition of IL-1b, a key mediator of pulmonary inflammation, has been shown to reduce the incidence of lung cancer in patients in years following treatment, but knowledge gaps surrounding its activation and role in the tumor microenvironment are hindering approaches for cancer interception. We developed a suite of activity-based technologies to probe inflammation in early lung cancer and identified a translational target candidate. We designed probes sensitive to various IL-1b-activating proteases and applied them to a murine model of inflammatory lung cancer, Kras/Trp53-mutant with SIINFEKL expression (KPS). Our nanosensors revealed reduced cleavage of a caspase-1 reporter in the lungs of KPS mice treated with IL-1b antibody, as well as elevated caspase-1 expression and activity in naive tumor tissue sections, highlighting the importance of caspase-1 processing of IL-1b during cancer development. We conducted a pre-clinical trial of a novel combination intervention by administering both IL-1b blockade and caspase-1 inhibition shortly after tumor induction. Following treatment, we observed significant reduction in lung cancer formation, including complete ablation of tumor incidence in nearly 20% of KPS mice. Our approach to understand the interplay of protease activity and cytokine activation supports development of new strategies to mitigate inflammation and intercept lung cancer progression.

bioengineering↗

Analysis of duplication and possible sub-functionalization of wing gene network components in pea aphids

A fundamental focus of evolutionary-developmental biology is uncovering the genetic mechanisms responsible for the gain and loss of characters. One approach to this question is to investigate changes in the coordinated expression of a group of genes important for the development of a character of interest (a gene regulatory network). Here we consider the possibility that modifications to the wing gene regulatory network (wGRN), as defined by work primarily done in Drosophila melanogaster, were involved in the evolution of wing dimorphisms of the pea aphid (Acyrthosiphon pisum). We hypothesize that this may have occurred via changes in expression levels or duplication followed by sub-functionalization of wGRN components. To test this, we annotated members of the wGRN in the pea aphid genome and assessed their expression levels in first and third nymphal instars of winged and wingless morphs of males and asexual females. We find that only two of the 32 assessed genes exhibit morph-biased expression. We also find that three wing genes (apterous (ap), warts (wts), and decapentaplegic (dpp)) have undergone gene duplication. In each case, the resulting paralogs show signs of functional divergence, exhibiting either sex-, morph-, or stage-specific expression. Two gene duplicates, wts2 and dpp3, are of particular interest with respect to wing dimorphism, as they exhibit a wingless male-specific isoform and wingless male-biased expression, respectively. These results supplement our understanding of trends in developmental gene network evolution, such as side-stepping pleiotropic constraint via duplication and sub-functionalization, underlying the emergence of novel phenotypes.

evolutionary biology↗

Ancient DNA Reveals Hominoid Evolution: Intermediate DNA Sequences and Advances in Molecular Paleontology

AbstractFossils and ancient crude pottery vessels function as physical "DNA containers," preserving oriDNA (original, in situ DNA) and accumulating eDNA (environmental DNA) over time. Ancient DNA (aDNA) serves as molecular fossils, chronicling evolutionaryhistory. Using "nano-affinitybead technology", we extracted and sequenced DNAfrom Lycoptera fossils in the Jehol region and a "round-bellied jar (Jar)" from the Erlitou period in Guangwu Town, yielding 236,545 primate sequences from the fossils and 86,908 from the pottery. We observed that the AFF value of DNA sequences negatively corre lates with species divergence time1, offering a quantitative measure of DNA preservation and host divergence. Some fragments distinct from modern genomic sequences, termed "intermediate DNAsequences" (IDS), have been identified. Many IDS exhibit an upper age limit, preserving characteristics of the last common ancestor (LCA) of the Hominidae and offering molecular insights into "Darwins puzzle". Among IDS, the SRRA subtype (Sequence Reversal and Rearrangement), identified in mRNA-coding exonic sequences, arises from the incorporation of a complementary antisense strand upstream of the sense strand, either adjacent to it or separated bya sequence interval. This introduces a novel post-transcriptional regulatory mechanism at the mRNA level, driven by SRRA, which presets hairpin structures and Indels in the UTR or CDS of exonic sequences, modulating gene variation. We propose: "SRRAs played a critical trial-and-error role in early Hominidae evolution, facilitating adaptive genomic changes, with some SRRA sequences later excised from exons", positioning SRRAas an evolutionary "genetic switch". Additionally, seven species -specific fragments (SSFs) of non-human primates (NHPs) linked to Asian Homo erectus were identified in the fossils, and pottery DNA reveale d sequences from tropical species (e.g., zebrass, oil palms), providing evidence of climate-driven local extinction and supporting paleo-ecological and paleo-environmental reconstruction. This method of analyzing aDNA from non-skeletal materials opens new avenues in paleontology, archaeology, and geology, guiding the tracing of ancient migration patterns and fossil searches. DNAfragments preserved within "DNA containers " exhibit an "old-few, new-many" turnover pattern, with many aDNA fragments displaying non-deamination. This evidence challenges prevailing perspectives, the authenticity criteria for aDNA, and the capabilities and scope of the traditional research method, necessitating a thorough reevaluation of the relevant knowledge framework. Furthermore, this study opens new opportunities for frontier research.

paleontology↗

Tff2 marks gastric corpus progenitors that give rise to pyloric metaplasia/SPEM following injury

In BriefTu et al. show that Tff2+ corpus isthmus cells are TA progenitors, and they, not chief cells, are the primary source of SPEM following injury. Upon Kras mutation, these progenitors directly progress to dysplasia, bypassing metaplasia, highlighting them as a potential origin of gastric cancer. HighlightsO_LITff2+ corpus cells are TA progenitors that give rise to secretory cells. C_LIO_LITff2+ progenitors, not chief cells, are the primary source of SPEM after injury. C_LIO_LIKras-mutant Tff2+ progenitors progress directly to dysplasia, bypassing metaplasia. C_LIO_LIMulti-omics analysis reveals distinct trajectories for SPEM and gastric cancer. C_LI O_FIG O_LINKSMALLFIG WIDTH=191 HEIGHT=200 SRC="FIGDIR/small/647847v1_ufig1.gif" ALT="Figure 1"> View larger version (46K): org.highwire.dtl.DTLVardef@48a2d1org.highwire.dtl.DTLVardef@b96642org.highwire.dtl.DTLVardef@1e89a4dorg.highwire.dtl.DTLVardef@1ea6a86_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstractC_FLOATNO C_FIG Pyloric metaplasia, also known as spasmolytic polypeptide-expressing metaplasia (SPEM), arises in the corpus in response to oxyntic atrophy, but its origin and role in gastric cancer remain poorly understood. Using Tff2-CreERT knockin mice, we identified highly proliferative Tff2+ progenitors in the corpus isthmus that give rise to multiple secretory lineages, including chief cells. While lacking long-term self-renewal ability, Tff2+ corpus progenitors rapidly expand to form short-term SPEM following acute injury or loss of chief cells. Genetic ablation of Tff2+ progenitors abrogated SPEM formation, while genetic ablation of GIF+ chief cells enhanced SPEM formation from Tff2+ progenitors. In response to H. pylori infection, Tff2+ progenitors progressed first to metaplasia and then later to dysplasia. Interestingly, induction of KrasG12D mutations in Tff2+ progenitors facilitated direct progression to dysplasia in part through the acquisition of stem cell-like properties. In contrast, Kras-mutated SPEM and chief cells were not able to progress to dysplasia. Tff2 mRNA was downregulated in isthmus cells during progression to dysplasia. Single-cell RNA sequencing and spatial transcriptomics of human tissues revealed distinct differentiation trajectories for SPEM and gastric cancer. These findings challenge the conventional interpretation of the stepwise progression through metaplasia and instead identify Tff2+ progenitor cells as potential cells of origin for SPEM and possibly for gastric cancer.

cell biology↗