Biology subjects

Jin, Y.

Publications and source records attributed to Jin, Y..

At least 55 records · Page 3Linked to original sources

bioRxiv2025

Graphene nanoedge electronics for monolithic and chronic recording of local microcircuits at neuronal density

High-density single-unit recording among closely spaced neurons over long durations is crucial for understanding the cellular-level functional architecture of the brain. Existing brain probes, however, either laterally sample neurons far more sparsely than neuronal density in the same cortical layer or suffer from long-term instability due to electrode modification, preventing precise neuron-to-neuron interrogation in local microcircuits. Here, we report a monolithic graphene-edge probe (NeuroEdge) that achieves single-unit recording at neuronal density (16 electrodes within 100 {micro}m diameter). We fabricate NeuroEdge using self-assembled reduced graphene oxide nanoflakes to form an electrochemically active tip consisting of exposed graphene nanoedges and electrolyte-filling nanotunnels, achieving an ultralow specific impedance of 20 M{Omega} {micro}m2. In vivo experiments over 5 months demonstrate recording at a high signal-to-noise ratio (>20 dB) and reliable interrogation of neighboring neurons. We also show that NeuroEdge can record from a single auditory cortical layer and reveal heterogeneities in the acoustic frequency response and dynamic connectivity among neighboring neurons. NeuroEdge provides a tool for precisely interrogating local microcircuits at the density of neurons in the brain.

bioengineering↗

bioRxiv2025

CDR-aware masked language models for pairedantibodies enable state-of-the-art bindingprediction

BackgroundTherapeutic antibodies are a leading class of biologics, yet their unique architecture poses challenges for computational modeling. Each antibody comprises paired heavy and light variable domains with conserved framework regions that maintain structure and hypervariable complementarity-determining regions (CDRs) that directly contact antigens. This functional asymmetry, where CDRs determine binding specificity while frameworks provide scaffolding, suggests that region-aware training strategies could yield superior representations. Existing protein language models treat all regions uniformly, potentially missing critical features present in CDRs. MethodsWe developed a region-aware pretraining strategy for paired variable domain sequences using two protein language models: a 3 billion parameter model (ESM2) and a compact 600 million parameter model (ESM C). We compared three masking approaches: uniform whole-chain masking, CDR-focused masking, and a hybrid strategy. Final models were trained on over 1.6 million paired antibody sequences and evaluated on binding affinity datasets with over 90,000 antibody variants across six antigens, including single-mutant panels and combinatorial libraries. ResultsHere we show that CDR-focused training produces embeddings with superior predictive performance for antibody-antigen binding. Our approach achieves up to 27% improvements in binding affinity prediction compared to benchmarked antibody models. Remarkably, training exclusively on paired sequences proves sufficient; pretraining on billions of unpaired sequences provides no measurable benefit. Our compact model matches or exceeds larger antibody-specific baselines. ConclusionsThese findings establish that prioritizing paired sequences with CDR-aware supervision over scale and complex training schemes achieves both computational efficiency and predictive accuracy, providing a practical framework for next generation antibody language models.

bioinformatics↗

bioRxiv2025

Integrated single-cell whole genome sequencing and spatial transcriptomics reveal latent intra-tumoral heterogeneity in ovarian cancer

The mortality rate of ovarian cancer remains disproportionately high compared to its incidence. This is partly due to a high level of intra-tumoral heterogeneity that promotes disease recurrence and treatment failure. In this study, we describe degrees of heterogeneity revealed by single-cell whole genome sequencing and spatial transcriptomics of five epithelial ovarian carcinomas. At the cellular level, we describe pseudo-diploid cells that match the malignant cell population in both somatic variant and copy number patterns. At the clonal and subclonal levels, we describe diversification associated with copy number gains and whole genome doubling. In multi-clonal samples, we infer evolutionary relationships from single cell copy number, loss of heterozygosity analysis, and somatic variant detection, and correlate these with tissue histology and gene expression programs. In one sample, we identify functionally consequential copy number alterations that contribute to molecular diversity, cell proliferation, and inflammation in a minor clone that persisted without major expansion alongside a more complex major clone. In another, we describe a complex evolutionary history including a spontaneous reversion of a driver mutation in a secondary clone, which correlated with a switch in oncogenic expression programs.

cancer biology↗

bioRxiv2025

Single-Neuron Encoding of Learnability in the Dorsal Anterior Cingulate Cortex

In natural environments, associations that indicate true learnable regularities are intermixed with those that arise from random and ultimately unlearnable relationships between events. To efficiently allocate cognitive resources and avoid inferring spurious patterns, organisms must distinguish learnable from unlearnable associations, but the mechanisms underlying this ability are not understood. We recently showed that monkeys performing a transitive inference task, while discovering the true hidden order in learnable image sets, also behaved to varying degrees as if they inferred subjective order in objectively random (unlearnable) image sets. Here, we show that the ability to detect learnability is encoded by neurons in the dorsal anterior cingulate cortex (dACC, area 24c). dACC neurons responded strongly after a decision outcome as reported in previous studies and, additionally, signaled whether a trial was from a learnable vs unlearnable set before outcome delivery, and showed interactions whereby their selectivity for the outcome (reward vs lack of reward) was stronger for learnable versus unlearnable sets. Learnability and interaction responses were independent of sensory or reward cues (which were equated for learnable and unlearnable sets) but their strength correlated with the monkeys ability to avoid inferring false order in unlearnable sets. The findings suggest that the dACC is part of a network that monitors learnability and enables animals to appropriately focus learning on true patterns while avoiding false inferences about spurious and random associations.

neuroscience↗

bioRxiv2025

Chemo-mechanotherapy of fibrosis: dynamic control of biological materials through tissue-architecture-dependent crosslink disruption

Extracellular matrix (ECM) stiffness drives cell fate, but tissues are nonlinear and difficult to modify chemically without harming patients. Here, we show that nonlinear mechanical responses of fibrous and porous tissues can be controlled by mechanically modulating crosslinks. Through integrated in vivo, in vitro, and computational approaches, we found that physiological dynamic stretching disrupts pathological advanced glycation end-product (AGE) crosslink-induced fibrogenesis in an architecture-dependent manner. This was effective in lung-like porous scaffolds but not in liver-like fibrous matrices, revealing a critical structure-property relationship. Computational and in vitro models established that this modulates cell-ECM feedback, and that controlling mechanical crosslinking modulates key nonlinearity of networked solids. This discovery inspired a non-invasive, "mechanotherapuetic" ventilation protocol, which reversed pulmonary fibrosis in mice by physically disrupting ECM pathological crosslinks. The therapeutic efficacy was further amplified when combined with pharmacological AGE inhibition. These findings establish design principles for dynamically reprogrammable biological materials and mechano-targeted therapies.

bioengineering↗

bioRxiv2025

Matrix metalloproteinase-3 promotes arteriovenous fistula failure by regulating FAK-AKT signaling

Objective- Surgically created upper extremity arteriovenous fistulae (AVF) are the preferred vascular access for patients requiring dialysis. It is estimated, however, that 50% of AVF fail within one year due to aggressive neointimal hyperplasia, which significantly increases morbidity and mortality. Matrix metalloproteinase-3 (MMP-3), also known as stromelysin-1, is a member of the metalloproteinase family that plays a critical role in the pathogenesis of many human disorders by degrading extracellular matrix and regulating molecular signaling pathways. The role of MMP- 3 in AVF neointimal failure has not been explored. Approach and Results- We observed that MMP-3 was induced in a time-dependent fashion by fetal bovine serum (FBS) and the growth factor PDGF-BB in cultured venous SMC. MMP-3 was also highly expressed in the neointimal SMCs of the outflow veins and the juxta-anastomotic area in an AVF mouse model, as well as in human AVF specimens. Knockdown of MMP-3 significantly suppressed venous SMC proliferation, whereas overexpression of MMP-3 facilitated cell growth in vitro. Importantly, deficiency of global and SMC-specific MMP-3 significantly reduced neointimal hyperplasia and improved patency after AVF creation. Mechanistic studies showed that MMP-3-mediated SMC proliferation and AVF neointimal hyperplasia were regulated via the FAK-AKT signaling pathway. Conclusions- These data suggest that MMP-3 is a key mediator of AVF neointimal failure. Targeting local MMP-3 activity may be a novel therapeutic strategy to prevent AVF neointimal failure and improve outcomes in patients requiring hemodialysis.

cell biology↗

bioRxiv2025

BIN1 deficiency leads to DNA damage and neuronal insulin resistance through ATM dysregulation

The major neuronal isoform of the AD risk gene BIN1 is specifically reduced in patients. In the present work, we demonstrate that BIN1 is necessary for intact insulin signaling and its loss leads to cellular-level insulin resistance. Persistently activated mTORC1 feedback inhibits the insulin signaling; meanwhile, ATM-dependent DNA Damage Response decreases the expression of multiple insulin signaling pathway members. Unexpectedly, nuclear ATM activation is accompanied by autophagic degradation of the cytoplasmic ATM, rendering neurons susceptible to oxidative stress, which predisposes oxidative DNA damage, DNA strand breaks, and ATM-dependent DNA Damage Response. Treating BIN1-deficient mice with rapamycin or liraglutide to improve the insulin response, or with the natural antioxidant alpha-lipoic acid to attenuate oxidative stress, both effectively preserved the spatial cognitive ability. Lastly, we reanalyzed a single-cell transcriptomic dataset from human neurons and identified positive correlations between levels of BIN1 and the insulin signaling, as well as neuronal activity. Together, this work revealed an ATM-centered mechanism that globally damages neuronal health in BIN1-deficient pyramidal neurons, which could be a driving force in the AD disease course.

cell biology↗

bioRxiv2025

SpaFoundation: a visual foundation model for spatial transcriptomics

Spatial transcriptomics (ST) has revolutionized biological research by enabling the joint profiling of gene expression and spatial context, along with histological images. However, current existing ST technologies remain high-cost and time-consuming, hindering their broader clinical applications. Although computational methods have been developed to infer gene expression directly from histology images, these methods still suffer from limited accuracy and spatial resolution due to insufficient training data and model capacity. Here, we introduce SpaFoundation, a large-scale histology foundation model designed to accurately predict spatial gene expression from tissue images. SpaFoundation employs a teacher-student Vision Transformer (ViT) architecture to learn generalizable histological representations by modeling potential dependencies among image patches. Notably, we incorporated self-distillation and masked image modeling (MIM) jointly to capture high-level semantic representations and fine-grained structural features, enriching spots representations. The model is pretrained on 1.79 million patches spanning 26 tissue types, with 80 million parameters. We validated SpaFoundation using 117 samples, demonstrating its flexibility across different spatial resolutions and superior performance in spatial gene expression prediction, as well as strong transferability to downstream tasks such as tumor detection and spatial domain clustering. Our results highlight the potential of large-scale foundation model to learn informative histological representations and underscore the benefits of domain-specific pretraining in extracting task-relevant representations, paving the way for foundation model-driven spatial gene expression inference. The implementation and pre-trained weights of SpaFoundation are publicly available at https://github.com/NingZhangCSUBio/SpaFoundation.

bioinformatics↗

bioRxiv2025

Spatiotemporal lineage mapping of tumor immune escape with eTRACER

The plasticity-first hypothesis posits that phenotypic plasticity emerges first in novel environments, followed by (epi)genetic changes that stabilize adaptive phenotypes. Whether tumor evolution follows this model, and how non-genetic mechanisms sustain long-term therapeutic resistance, remain unclear. Here, we develop eTRACER, an endogenously targeted, high-resolution and spatially-resolved CRISPR-Cas9 lineage-tracing system, to study tumor adaptation during longitudinal CD8+ T cell-mediated immunotherapy. Integrated clonal and single-cell transcriptomic analyses show that tumor immune evasion is governed by clonal state composition rather than clonal identity, arguing against selection from pre-existing genetic heterogeneity. Spatiotemporal lineage tracing reveals highly reversible state transitions prior to therapy, followed by consolidated epithelial-mesenchymal transition (EMT) during therapy. Single-cell multiomics identifies AP-1 as a key regulator of EMT stabilization and its inhibition enhances tumor sensitivity to immune killing. Together, these findings show that tumor plasticity precedes stable immune evasion, revealing an AP-1-centered mechanism underlying plasticity-first tumor evolution.

cancer biology↗

bioRxiv2025

Procrastination partly reflects an evolutionary byproduct of non-planning impulsivity

Procrastination has immediately visible repercussions on health and survival resilience, yet shows stably heritable and remains increasingly pervasive across human societies. Despite a paradox, this behavior is theoretically explained to represent a byproduct of evolutionary advantages underlying impulsivity, yet not deciphered well by scientific evidences. After adjusting psychometric endogeneity, we demonstrate the unique predictive roles of non-planning impulsivity (NPI) during late adolescence and early adulthood uniquely predicts procrastination in later adulthood in a twin cohort (N = 154). This association was further replicated in two independent cohorts (N = 327, N = 1,543). Using AE models, in conjunction of single-paper meta-analytic synthesis (N = 3,656 twin pairs), we observed significant shared genetic contributions underlying this NPI-procrastination association (rg = 0.51, 95% CI: 0.18 - 0.84). Beyond to the phenotypic heritability, employing a Genome-Wide-Association Study (GWAS), six NPI-procrastination overlapping SNPs are identified, functionally accounting for neural dysregulation. Thus, leveraging neurodevelopmental normative modelling (N = 37,407), online meta-analytic estimations (k = 198, loci = 5,855) and seed-based d mapping estimates (N = 893), cortical deviations in the left dorsolateral prefrontal cortex (DLPFC) - the brain region showing highest probabilistic overlap mapping NPI to procrastination, partly explains their shared genetic variants, but are substantially independent in genetic contribution. Mendelian Randomization analysis finally indicates causal roles of NPI and procrastination both, to DLPFC deviations. Our findings empirically clarified this theory that procrastination partly derives from NPI as an evolutionary byproduct indeed, but is still unique in neurogenetic entities. Brief summaryProcrastination is a puzzling human behavior that compromises survival-relevant outcomes yet remains both widespread and heritable. Although theorized as a byproduct of impulsivitys evolutionary advantages, empirical support for this account has been limited. Here, we provide converging evidence across psychometric, genetic, and neuroimaging modalities to show that non-planning impulsivity during late adolescence and early adulthood uniquely predicts later procrastination, and that the two traits share significant genetic overlap. We further identify specific genetic variants and morphological deviations in the DLPFC that link, but also partially dissociate, their biological pathways. These findings clarify the evolutionary and neurogenetic architecture of procrastination and underscore its partial derivation from impulsivity alongside distinct developmental origins.

neuroscience↗

bioRxiv2025

In vivo exposure of mixed microplastic particles in mice and its impacts on the murine gut microbiome and metabolome

Microplastics (MPs) are emerging environmental contaminants due to increasing global plastic production and waste. Microplastics, defined as plastic particles less than 5 mm in diameter, are formed through degradation of larger plastics via sunlight, weathering, and microbes. These plastic compounds are widely detected in water, soil, food, as well as human stool and blood. The gut microbiome, often referred to as our second genome, is important in human health and is the primary point of contact for orally ingested microplastics. To investigate the impact of ingested MPs on the gut microbiome and the metabolome, 8 weeks-old male and female C57/BL6 mice were orally gavaged mixed plastic (5 um) exposure consisting of polystyrene, polyethylene, and the biodegradable/biocompatible plastic, poly-(lactic-co-glycolic acid) twice a week for 4 weeks at 0, 2, or 4 mg/week (n = 8/group). Fecal pellets were collected for bacterial DNA extraction and metagenomic shotgun sequencing, and serum was subjected to targeted and untargeted metabolomics. MPs exposure resulted in significant sex-specific and dose-dependent changes to the gut microbiome composition along with substantial regulation of the predicted metabolic pathways. Untargeted metabolomics in serum showed that a low MPs dose displayed a more prominent effect on key metabolic pathways such as amino acid metabolism, mitochondrial function, and inflammation. Additionally, SCFA-targeted metabolomics showed significant changes in neuroprotective SCFAs levels in both sexes by MPs exposure. In conclusion, our study has demonstrated that microplastics dysregulate the gut microbiome and serum metabolome, providing critical insights into potential human disease risks associated with microplastic contamination.

pharmacology and toxicology↗

bioRxiv2025

Analysis of astrocyte progenitors derived from human induced pluripotent stem cells in vitro and following transplantation into the intact spinal cord.

Functional improvement following traumatic spinal cord injury (SCI) remains limited, therefore, it is necessary to develop therapeutic interventions such as cell transplantation to replace lost cells and promote connectivity. While transplantation typically focuses on neurons, it is important to include other neural cells, such as immature astrocytes, to provide a permissive environment, promote neuroprotection and regeneration, and ultimately restore connectivity. In this study, we leveraged cellular engineering using human induced pluripotent stem cells (hiPSCs) to generate astrocyte progenitor cells (hAPCs). We tested two hiPSC lines (WTC11 and KOLF2.1J) to characterize the fate of the hAPCs in vitro and following transplantation at the cervical level of the intact spinal cord for up to 3 weeks. Our results demonstrated efficient and consistent differentiation of the hiPSCs into hAPCs, their survival and integration with the adult spinal cord, with no signs of tumors, deleterious outcomes, and unexpected locations. The ability to survive and the absence of adverse effects indicate that hAPC transplantation could be a safe element of therapy in treating spinal cord injuries.

neuroscience↗

bioRxiv2025

TaPGS1 Driven Flavonol Accumulation Delays Endosperm Cellularization and Enlarges Wheat Grains

Flavonols play a crucial role in seed development by regulating multiple physiological processes, including seed coat pigmentation, dormancy, fertilization, and endosperm formation. Notably, flavonols influence the polar transport of auxin, thereby affecting seed growth dynamics. In our previous work, we found that overexpression of the wheat bHLH transcription factor TaPGS1 results in increased grain size; however, the underlying mechanism remained unclear. In this study, metabolomic and transcriptomic analyses of TaPGS1 overexpressing wheat lines revealed enhanced flavonol accumulation and upregulation of key flavonol biosynthetic genes. Further investigations suggested that flavonol accumulation in the seed coat may disrupt auxin transport, leading to localized auxin buildup, delayed endosperm cellularization, and an increase in endosperm cell number. These changes collectively contribute to grain enlargement. Our findings uncover a TaPGS1 flavonol regulatory module that links auxin distribution to endosperm development and seed size control in wheat.

plant biology↗

bioRxiv2025

Mapping neurogenetic characteristics of psychopathological procrastination using normative modeling in a prospective twin cohort

Procrastination, affecting over 70% global population, is pervasively incurring negative outcomes in human society. This has long been studied as a bad daily habit, but it loses in delineating neurogenetic substrates underlying its psychopathological phenotyping. Using a prospective twin adolescent cohort, we demonstrate moderate heritability of this subclinical condition - PPS. Neuroimaging normative modeling analysis, further reveals that neurodevelopmental deviations in nucleus accumbens during adolescence, are predictive of PPS in adulthood, while such deviations-PPS mappings were highly genetically shared. Beyond to regional anomalies, PPS-specific whole-brain deviation patterns, notably in the default mode network, are neurobiologically enriched with changes in cortical manifolds (gradients) and neurotransmitter systems. Integrating these neuroimaging markers with transcriptomic atlas, we capture significant PPS-specific neurogenetic signatures associated with molecular transport system, neuroimmune responses, and neuroinflammation, particularly in serotonergic and dopaminergic pathways. These findings shed light on the multisystem neurogenetic architecture underlying PPS, providing evidence to theoretically conceptualize this psychopathological phenotype as a subclinical "brain disorder". TeaserPsychopathological procrastination is not a bad daily habit solely, but a "brain disorder" associated with multiscale neurodevelopment.

neuroscience↗

bioRxiv2025

Spatiotemporal Single-Cell Analysis Reveals T Cell Clonal Dynamics and Phenotypic Plasticity in Human Graft-versus-Host Disease

Allogeneic hematopoietic cell transplantation (alloHCT) is curative for various hematologic diseases but often leads to acute graft-versus-host disease (GVHD), a potentially life-threatening complication. We leverage GVHD as a uniquely tractable disease model to dissect complex T-cell-mediated pathology in 27 alloHCT recipients. We integrate pre-transplant identification of alloreactive T-cells with longitudinal tracking across blood and gut, using mixed lymphocyte reaction-based clonal "fingerprinting", TCR clonotyping, single-cell RNA/TCR sequencing, and spatial transcriptomics. Using DecompTCR, a novel computational tool for longitudinal TCR analysis, we uncover clonal expansion programs linked to GVHD severity and TCR features. Multi-omics profiling of gut biopsies reveals enrichment and clonal expansion of CD8 effector and ZNF683(Hobit) resident memory T-cells, cytolytic remodeling of regulatory and unconventional T-cells, and localization of CD8 effector T-cells near intestinal stem cells in crypt loss regions. This framework defines dynamic immune circuit rewiring and phenotypic plasticity with implications for biomarkers and therapies. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=198 SRC="FIGDIR/small/655962v1_ufig1.gif" ALT="Figure 1"> View larger version (45K): org.highwire.dtl.DTLVardef@178b77dorg.highwire.dtl.DTLVardef@569226org.highwire.dtl.DTLVardef@1951281org.highwire.dtl.DTLVardef@1f1e046_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIPersistent expansion of diverse alloreactive T cell clones is a hallmark of severe GVHD C_LIO_LIDecompTCR reveals dynamic clonal expansion programs linked to GVHD severity and clinical outcome C_LIO_LICD8+ T cell clones exhibit phenotypic plasticity in vivo across intestinal tissue compartments in GVHD C_LIO_LIHigh-resolution spatial profiling shows CD8+ effector T cells localize near intestinal stem cell niches and drive epithelial injury in GVHD C_LI

systems biology↗

bioRxiv2025

Transposable elements drive species-specific and tissue-specific transcriptomes in human development

BackgroundTransposable elements (TEs) are an abundant and crucial regulatory resource in the human genome. Serving as alternative promoters, TEs can be reactivated and produce TE-initiated transcripts, which play importance roles in early development and differentiated tissues. However, the prevalence and function of TE-initiated transcription in human development are poorly characterized. ResultsWe identified 12,918 TE-initiated transcripts across 40 human body sites and embryonic stem cells. Among TE-initiated transcripts, 80% were activated in a tissue-specific manner. TEs with tissue-specific transcription factor binding motifs were enriched in particular tissues. Additionally, approximately half of TE-derived TSSs were primates-specific. Notably, 375 primates-specific TE-derived TSSs were found to create novel tissue-specific gene expression patterns during evolution. ConclusionsOur results characterize the global profile of TE-initiated transcription and enhance our understanding of TE contribution to the primate-specific gene regulatory networks in human development.

bioinformatics↗

bioRxiv2025

TEITbase: a database for transposable element (TE)-initiated transcripts in human cancers

Transposable elements (TEs) are abundant and play a crucial regulatory role in the human genome. Functioning as alternative promoters, TEs can be reactivated to produce TE-initiated transcripts. In cancer, TE-initiated transcription may upregulate oncogene expression and generate novel tumor-specific antigens, which could serve as potential targets for immunotherapy. However, there remains a lack of comprehensive databases that systematically investigate TE-initiated transcription in cancer. To address this gap, we developed a deep learning-based method and identified 38,995 TE-initiated transcripts across 33 cancer types from The Cancer Genome Atlas. Among these, 6,203 were tumor-specific expressed and strongly associated with the tumorigenesis. Using these annotations, we created TEITbase (http://teitbase.medbioinfo.org/), a user-friendly database that provides researchers with tools to conduct various downstream analyses and investigations for TE-initiated transcripts, including 546 novel onco-exaptation events. The establishment of TEITbase provides new insights into transcriptional reprogramming in cancers and enables further investigation into the potential roles of TE-initiated transcripts in cancer diagnostics and therapeutic strategies.

bioinformatics↗

bioRxiv2025

Discover the Maze-like Pathway for Glabridin Biosynthesis

Tailoring enzymes diversify plant metabolite scaffolds through complex, context-dependent modifications, generating maze-like biosynthetic networks that complicate metabolic pathway reconstruction. Here, we systematically deconstructed and reconstructed the biosynthetic network of glabridin, a valuable skin-whitening isoflavone from Glycyrrhiza. By integrating metabolic pathway mining with genome and 183 transcriptomes, we identified four functional routes among sixteen theoretical possibilities and uncovered a previously uncharacterized, ladder-like multi-route tailoring network. Reconstruction of such architecture in yeast revealed metabolic redundancy and interconnectivity confer unexpected robustness, enabling higher production efficiencies compared to a single-route design. Further modular engineering enabled the de novo biosynthesis of glabridin in yeast. Our work establishes a framework for reconstructing metabolic mazes and demonstrates that multi-route architectures can be harnessed to enhance the robustness and productivity of cell factories.

synthetic biology↗