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Liu, K.

Publications and source records attributed to Liu, K..

At least 109 records · Page 6Linked to original sources

Intelligent Design of Escherichia coli Terminators

Terminators are specific nucleotide sequences located at the 3 end of a gene and contain transcription termination information. As a fundamental genetic regulatory element, terminators play a crucial role in the design of gene circuits. Accurately characterizing terminator strength is essential for improving the precision of gene circuit designs. Experimental characterization of terminator strength is time-consuming and labor-intensive; therefore, there is a need to develop computational tools capable of accurately predicting terminator strength. Current prediction methods do not fully consider sequence or thermodynamic information related to terminators, lacking robust models for accurate prediction. Meanwhile, deep generative models have demonstrated tremendous potential in the design of biological sequences and are expected to be applied to terminator sequence design. This study focuses on intelligent design of Escherichia coli terminators and primarily conducts the following research: (1) To construct an intrinsic terminator strength prediction model for E. coli, this study extracts sequence features and thermodynamic features from E. coli intrinsic terminators. Machine learning models based on the selected features achieved a prediction performance of R2 = 0.72. (2) This study employs a generative adversarial network (GAN) to learn from intrinsic terminator sequence training data and generate terminator sequences. Evaluation reveals that the generated terminators exhibit similar data distributions to intrinsic terminators, demonstrating the reliability of GAN-generated terminator sequences. (3) This study uses the constructed terminator strength prediction model to screen for strong terminators from the generated set. Experimental verification shows that among the 18 selected terminators, 72% exhibit termination efficiencies greater than 90%, confirming the reliability of the intelligent design approach for E. coli terminators. In sum, this study constructs a terminator strength prediction model and a terminator generation model for E. coli, providing model support for terminator design in gene circuits. This enhances the modularity of biological component design and promotes the development of synthetic biology.

synthetic biology↗

Diammonium glycyrrhizinate injection promotes zebrafish angiogenesis through the mTOR/HIF-1 signaling pathway

(1) BackgroundGlycyrrhizic acid (GA) is the main component of the traditional Chinese medicine Glycyrrhiza glabra. Many GA preparations in the pharmaceutical market have good efficacy in hepatoprotection and the treatment of liver diseases. However, the pro-angiogenic effects for GA-based agents have not been researched specifically. The aim of this study was to investigate the pro-angiogenic activity of GA preparations commonly used in clinical practice and screen the representative angiogenesis promotor to further elucidate the mechanism of action (2) MethodsA zebrafish vascular injury model induced by PTK787 was used to assess the pro-angiogenic effect of GA preparations. The pro-angiogenic activity of diammonium glycyrrhizinate injection (DGI) was further systematically evaluated by detecting the growth of the intersegmental vessels (ISVs) and subintestinal vein vessels (SIVs) in zebrafish. The underlying mechanism of action for DGI was explored by transcriptomics analysis and RT-qPCR validation; (3) ResultsThe results showed that magnesium isoglycyrrhizinate injection (MII), DGI, compound glycyrrhizinate tablets (CGT), and diammonium glycyrrhizinate enteric-coated capsules (DGEC) could demonstrate significantly pro-angiogenic effects. Among them, DGI exhibited the strongest activity. Transcriptomic analysis showed that the pro-angiogenic activity of DGI was closely associated with the mTOR signaling pathway. RT-qPCR results indicated that the expression levels of key genes of the mTOR/HIF- pathway were significantly upregulated in DGI-treated zebrafish relative to the PTK787 group; (4) ConclusionsGA preparations have an obvious pro-angiogenic effect, in which DGI can exert particularly strong activity by activating the mTOR/HIF-1 signaling pathway. This study broadens the clinical application of GA agents and provides new insights into the pharmacodynamics and potential mechanisms of DGI as a candidate agent for treating ischemic diseases

pharmacology and toxicology↗

Structural and Functional Insights into GGCX-FIX Interaction: Implications for Vitamin K-Dependent Bleeding Disorders

Gamma-carboxylation, catalyzed by {gamma}-glutamyl carboxylase (GGCX), is a critical post-translational modification essential for the biological activity of vitamin K-dependent proteins (VKDPs). Mutations in GGCX, depending on their specific location, result in vitamin K-dependent coagulation factor deficiency type 1 (VKCFD1), which encompasses a broad spectrum of clinical manifestations ranging from mild to severe, including bleeding disorders, osteoporosis, and vascular calcification. The limited knowledge of GGCXs structure and functional regions hinders our understanding of the consequences of GGCX mutations and the treatment for VKCFD1. This study aimed to identify key functional regions of GGCX and their interactions with VKDPs to better elucidate the molecular mechanisms underlying these diverse clinical symptoms. Using AlphaFold 3 and molecular dynamics simulations, we developed a complex binding model of GGCX, FIX, and reduced vitamin K, which revealed critical regions and residues involved in their interaction. Site-directed mutagenesis and cell-based assays further validated the model, confirming that multisite and regional cooperative binding of FIX to GGCX plays a key role in modulating {gamma}-carboxylation efficiency. Additionally, novel residues (I296, M303, M401, M402) were identified as essential for GGCXs dual enzymatic activities: carboxylation and vitamin K epoxidation. We further demonstrated that the spatial proximity of these active sites supports the hypothesis that GGCXs carboxylation and vitamin K epoxidation centers are interconnected, ensuring the efficient coupling of these processes. Our GGCX-FIX binding and carboxylation model aligns with known pathogenic GGCX mutations, providing valuable insights into the molecular basis of coagulation disorders caused by GGCX mutants.

pathology↗

Biological function and mechanism of flpL gene in regulating pathogenicity of Aeromonas hydrophila

Aeromonas hydrophila is human-animal commensal bacterium that seriously threatens the development of aquaculture and human health. Type IV pili (T4P) are essential for bacterial physiological function. The relationship between the molecular mechanism of flpL gene affiliated to T4P and the pathogenicity is still unclear. In the research, A. hydrophila with a genetically stable deletion of flpL gene ({Delta}flpL) was constructed. The median lethal dose of {Delta}flpL for Crucian carp was 4.87 times higher compared to wild-type strain, suggesting that {Delta}flpL significantly reduced pathogenicity. The attenuation may be attributed to a reduced capacity for biofilm formation and downregulation of the expression levels of virulence-related genes in {Delta}flpL. Meanwhile, the significant increase in swimming capacity and adhesion can be related to the upregulation of flpC, tapM, tapB and tapP genes. In conclusion, flpL gene plays essential role in the pathogenicity, adhesion, motility, and capacity for biofilm formation in A. hydrophila. The research aims to clarify the pathogenesis of A. hydrophila, and lay the foundation for developing live attenuated vaccines through the targeted modification flpL gene.

microbiology↗

CHD3 regulates BMP signalling response during cranial neural crest cell specification

CHD3 is a component of the NuRD chromatin remodeling complex. Pathogenic CHD3 variants cause Snijders Blok-Campeau Syndrome, a neurodevelopmental disorder with variable features including developmental delays, intellectual disability, speech/language difficulties, and craniofacial anomalies. To unveil the role of CHD3 in craniofacial development, we differentiated CHD3-KO induced pluripotent stem cells into cranial neural crest cells (CNCCs). CHD3 expression is low in wild-type iPSCs and neuroectoderm, but upregulated during CNCC specification, where it opens the chromatin at BMP-responsive enhancers, to allow binding of DLX5 and other factors. CHD3 loss leads to repression of BMP target genes and an imbalance between BMP and Wnt signalling, ultimately resulting in aberrant mesodermal fate. Consequently, CNCC specification fails, replaced by early-mesoderm identity, which can be partially rescued by titrating Wnt levels. Our findings highlight a novel role for CHD3 as a pivotal regulator of BMP signalling, essential for proper neural crest specification and craniofacial development.

developmental biology↗

Leopard Cats Occupied Human Settlements in China for 3,500 years before the Arrival of Domestic cats in 600-900 CE around the Tang Dynasty

The earliest cats in human settlements in China were not domestic cats (Felis catus), but native leopard cats (Prionailurus bengalensis). To trace when and how domestic cats arrived in East Asia, we analyzed 22 feline bones from 14 sites across China spanning 5,000 years. Nuclear and mitochondrial genomes revealed that leopard cats began occupying anthropogenic scenes around 5,400 years ago and last appeared in 150 CE. Following several centuries gap of archeological feline remains, the first known domestic cat (706-883 CE) in China was identified in Shaanxi during the Tang Dynasty. Genomic analysis suggested a white or partially white coat and a link to a contemporaneous domestic cat from Kazakhstan, indicating a likely dispersal route via the Silk Road. The two felids once independently occupied ancient anthropogenic environments in China but followed divergent paths and reached different destinations in human-animal interactions.

evolutionary biology↗

YTHDF3 promotes the progression of gastric cancer by activating Wnt/β-catenin signaling pathway via targeting NEK7

Gastric cancer (GC) is a widespread and deadly malignancy among global digestive tract tumors, alarmingly ranked the fifth most common cancer in terms of incidence and mortality. This study used immunohistochemistry and RT-qPCR to reveal a significant upregulation of YTHDF3 expression in GC tissues compared with that of adjacent normal tissues. This increased expression of YTHDF3 was closely associated with the incidence of lymph node metastasis and the progression to more advanced TNM stages. In vitro experiments demonstrated that YTHDF3 was crucial in promoting the aggressive characteristics of GC cells by enhancing their ability to proliferate, migrate, and invade, while simultaneously inhibiting apoptosis. The role of YTHDF3 in the progression of GC was further confirmed using the BALB/c nude mice subcutaneous tumor model, which showed a slowed tumor growth after YTHDF3 knockdown. This study further confirmed through Co-IF RIP-qPCR, western blotting, and rescue studies that YTHDF3 promotes GC progression by targeting NEK7 to regulate the Wnt/{beta}-catenin signaling pathway. In conclusion, our pivotal findings highlight the YTHDF3/NEK7/Wnt/{beta}-catenin axis as a promising and accessible therapeutic target for the development of new treatments aimed at improving clinical outcome of patients with GC.

cancer biology↗

High-dose DFMO alters protein translation in neuroblastoma

DFMO has been studied as a cancer therapeutic at doses ranging from 500-9,000 mg/m2/day. Lower doses are favored for cancer prevention studies while higher doses, often with chemotherapy, are studied in refractory cancers. DFMO inhibits the rate-limiting enzyme in polyamine synthesis, ornithine decarboxylase (ODC), an oncogene transcriptionally regulated by MYC. MYC genes are the principal oncogenic drivers of neuroblastoma, and ODC1 is co-amplified in a subset with dismal outcome, so DFMO is a rational therapeutic candidate. Low-dose DFMO has now been FDA-approved for high-risk patients though the mechanisms for its anti-tumor activity, and the exposures required to elicit them, remain obscure. We sought to define biomarkers of activity across exposures achieved in the clinic with low through high-dose DFMO. Polyamines support protein translation by providing spermidine, which is essential to hypusinate (and activate) the elongation factor, eIF5A. Selective binding of polyamines with tRNA and rRNA provide eIF5A-independent mechanisms of translation support. We show that low-dose DFMO does not extend survival in mouse models in vivo nor alter translation biomarkers in vitro. High-dose DFMO consistently extends survival in neuroblastoma models, and, in a subset of neuroblastoma cell lines, inhibits eIF5A hypusination and global translation at achievable concentrations. However, the concentration required to engage these changes across many cell lines exceeded that achievable even with high-dose DFMO. No correlation was seen among MYCN and/or ODC1 copy number and sensitivity to DFMO. Combining high-dose DFMO with additional agents to further deplete tumor polyamines may be necessary to fully engage polyamine-depletion effects on tumors, and more granular measures of translation, including codon-resolution ribosome profiling, may be required to define these effects. STATEMENT OF TRANSLATIONAL RELEVANCELow-dose DFMO is approved by the FDA for the treatment of neuroblastoma. The depletion of tumor polyamines has been shown to have activity against tumors with activated MYC signaling, like neuroblastoma, yet the degree of polyamine depletion required, the mechanisms by which this impedes tumor progression, and the DFMO exposures required to enable these are poorly understood. Here we evaluate alterations in protein translation as putative mechanisms for DFMO activity. Translation biomarkers and colony formation can be inhibited by DFMO in vitro at exposures achievable in vivo with high-dose DFMO. Similarly, high-dose DFMO, but not low-dose DFMO, extends neuroblastoma-prone mouse survival. These findings support studying DFMO at higher doses and in therapeutic combinations that further augment polyamine depletion within tumors.

cancer biology↗

TOGGLE identifies fate and function process within a single type of mature cell through single-cell transcriptomics

Cells that appear transcriptionally identical can maintain vastly different functions or fates--an enduring blind spot in single-cell transcriptomics. Here we introduce TOGGLE, a self-supervised graph diffusion framework that delineates fine-grained functional heterogeneity within phenotypically stable cell populations. By combining deep diffusion learning with reinforcement-guided clustering and a BERT-inspired masking strategy, TOGGLE reconstructs hidden trajectories of cell fate without prior labels or temporal information. Applied across multiple single-cell RNA-seq datasets, TOGGLE achieves up to 90 % accuracy in unsupervised fate prediction, surpassing existing trajectory algorithms such as WOT and Cospar. It distinguishes ferroptotic, apoptotic, and intermediate neuronal states in ischemic stroke, with predictions experimentally validated in animal models. In neural stem cells TOGGLE reveals epigenetic memory of metabolic activity, linking local DNA demethylation and chromatin accessibility to mitochondrial RNA expression. We further introduce the Graph Diffusion Functional Map, which isolates subtle RNA functional groupings otherwise obscured by conventional dimensionality reduction. TOGGLE thus establishes a generalizable framework for mapping functional identity and epigenetic dynamics at single-cell resolution, providing new insights into cellular memory, regeneration, and disease mechanisms. Biographical NoteChens guidance comes from Dr. Alex P. Carll. Another mentor is Dr. Lu Cai, one of the contributors to the standardization of autophagy detection methods, whose research on criteria for identifying diabetes induced apoptosis has been included in numerous clinical guidelines. Professor Jinwen Ge is a State Council Special Allowance Expert of China. He has been involved in formulating medical standards for integrated traditional Chinese and Western medicine in China and has participated in developing retrieval/indexing norms for journals in the field of integrated traditional Chinese and Western medicine. Code and Data availabilityThe raw data for the hematopoiesis dataset can be accessed at the Gene Expression Omnibus database with accession number GSE140802, the reprogramming dataset with accession number GSE99915, the e-cigarette aerosol inhalation on mouse cardiac tissue with accession number GSE183614, the rat myocardial infarction dataset with accession number GSE253768, the ischemic stroke dataset with accession number GSE232429, and the adult NSC lineage dataset with accession number GSE209656 and GSE211786. All codes and guide page & analyzed data are full open available at: https://github.com/FullBlackWolf/TOGGLE?tab=readme-ov-file https://fullblackwolf.github.io/TOGGLE/ Key points(1) Previous studies have primarily focused on distinguishing cell types and different cellular subpopulations, whereas our tool is designed to identify subtle functional differences among highly similar cell states. For example, in Test2, it first isolates neurons undergoing cell death, then further differentiates early, intermediate, and late death stages, and separates ferroptosis from apoptosis as two major categories. Notably, ferroptosis and apoptosis share a large number of molecular pathways, making this task highly challenging. In addition, in Test4, our method discriminates fibroblasts with distinct immune-communication patterns, even though they do not show prominent separation or temporal progression on conventional UMAP plots. (2) We developed an innovative Graph Diffusion Functional Map that significantly reduces noise, resulting in clearer visualization of RNA functional groupings and enabling the detection of subtle functional differences in high-dimensional data. This provides a novel tool for pathway discovery. For instance, in Test4, we found that the KEGG inflammatory response pathway was most strongly activated in young mice, suggesting that e-cigarette exposure exerts more severe effects on immature cardiac tissue. (3) We implemented a novel trajectory-tracking strategy capable of distinguishing early, intermediate, and late stages of cellular programming, which we refer to as functional lineage tracing. In Test3, we successfully separated nearly indistinguishable aNSC and qNSC populations and further uncovered their methylation-regulated transcriptional programs, demonstrating that local DNA demethylation activates genes involved in cell proliferation and energy metabolism, thereby regulating the activation of quiescent neurons. (4) In the testing dataset, it was found that local DNA demethylation activates the expression of genes associated with cell proliferation and energy metabolism, thereby regulating the activation of quiescent neurons. Neuronal ferroptosis in ischemic stroke may be linked to the high expression of ferroptosis driver genes such as Ctsb, Mtdh, Ndrg1, Smad7, Cd82, and Acsl1.

bioinformatics↗

Single-cell analysis reveals distinct immune characteristics of hepatocellular carcinoma in HBV-positive versus HBV-negative cases

Infection with the Hepatitis B virus (HBV) is a key risk factor for Hepatocellular carcinoma (HCC) development and progression. It is widely recognized that immunopathological mechanisms are pivotal in developing HBV-related HCC. Nevertheless, the specific mechanisms by which HBV-induced modifications within the tumor microenvironment (TME) contribute to HCC pathogenesis are still not well understood. Here, we utilized single-cell RNA sequencing to analyze and compare the immune landscapes between HBV-positive and HBV-negative HCC. We discovered that HBV infection significantly modifies the immune cell makeup and state, and leads to the suppression and exhaustion of T cells within the TME. Specifically, an increase in SLC4A10+ CD8+ T cells and IFITM3+ macrophages was observed, along with the upregulation of the gene SLC35F1 in various immune cell subtypes. These findings offer valuable insights into the alteration of the immunological microenvironment in HCC associated with HBV infection, suggesting possible targets for immunotherapeutic intervention.

bioinformatics↗

Agent-based modeling reveals impacts of cell adhesion and matrix remodeling on cancer collective cell migration phenotypes

Understanding the phenotypic transitions of cancer cells is crucial for elucidating tumor progression mechanisms, particularly the transition from a non-invasive spheroid phenotype to an invasive network phenotype. We developed an agent-based model (ABM) using Compucell3D, an open-source biological simulation software, to investigate how varying biophysical and biochemical parameters influence emerging properties of cellular communities, including cell growth, division, and migration. Our focus was on cell-cell contact adhesion and matrix remodeling effects on cancer cell migration. We simplified enzymatic remodeling of the extracellular matrix and the subsequent enhancements to cellular chemotaxis or durotaxis as a combined effect of localized cellular secretion of a chemoattractant. By varying the chemoattractant secretion rate and contact adhesion energy, we simulated their effects on cellular behavior and driving the transition from a spheroid phenotype to a network phenotype. The model serves as a digital twin for 3D cancer cell culture, simulating cancer cell growth, division, and invasion over 1 week, validated against published data. The simulations track the emergent morphological and collective phenotype changes using key metrics such as cell circularity and invasion. Our findings indicate that increased chemoattractant secretion enhances the invasiveness of the collective cells, promoting the transition to a network phenotype. Additionally, changing cell-cell contact energy from a strong cell-cell adhesion to a weak cell-cell adhesion affects the compactness of the spheroids, resulting in lower circularity and increased collective cell invasion. Our work advances the understanding of tumor progression by providing insights into the biophysical mechanisms behind invasive cancer cell phenotypic transitions.

biophysics↗

Benchmarking AI Models for In Silico Gene Perturbation of Cells

Understanding perturbations at the single-cell level is essential for unraveling cellular mechanisms and their implications in health and disease. The growing availability of biological data has driven the development of a variety of in silico perturbation methods designed for single-cell analysis, which offer a means to address many inherent limitations of experimental approaches. However, these computational methods are often tailored to specific scenarios and validated on limited datasets and metrics, making their evaluation and comparison challenging. In this work, we introduce a comprehensive benchmarking framework to systematically evaluate in silico perturbation methods across four key scenarios: predicting effects of unseen perturbations in known cell types, predicting effects of observed perturbations in unseen cell types, zero-shot transfer to bulk RNA-seq of cell lines, and application to real-world biological cases. For each scenario, we curated diverse and abundant datasets, standardizing them into flexible formats to enable efficient analysis. Additionally, we developed multiple metrics tailored to each scenario, facilitating a thorough and comparative evaluation of these methods. Our benchmarking study assessed 10 methods, ranging from linear baselines to advanced machine learning approaches, across these scenarios. While some methods demonstrated surprising efficacy in specific contexts, significant challenges remain, particularly in zero-shot predictions and the modeling of complex biological processes. This work provides a valuable resource for evaluating and improving in silico perturbation methods, serving as a foundation for bridging computational predictions with experimental validation and real-world biological applications.

bioinformatics↗

ITGB4 promotes the progression of colorectal cancer by activating Wnt/β-catenin signaling pathway via targeting EZR

ObjectivesColorectal cancer (CRC) is a major cause of cancer-related mortality worldwide. Integrin beta 4 (ITGB4) has been previously identified as being overexpressed in CRC; however, its precise oncogenic mechanism remains unclear. The present study aimed to elucidate the functional role of ITGB4 in CRC progression and identify its downstream molecular effectors to provide new insights for targeted therapy. MethodsThe biological functions of ITGB4 were investigated in CRC cell lines (SW480 and HCT116) using a series of in vitro assays, including CCK-8, colony formation, Transwell migration and invasion, and flow cytometry for apoptosis following ITGB4 knockdown. An in vivo xenograft mouse model was used to evaluate the effect of ITGB4 on tumor growth. Downstream targets were screened using RNA sequencing (RNA-seq) and validated by co-immunoprecipitation and co-immunofluorescence. The underlying signaling pathway was investigated by Western blotting and functional rescue experiments. ResultsKnockdown of ITGB4 significantly suppressed CRC cell proliferation, migration, and invasion, while promoting apoptosis in vitro. Similarly, silencing ITGB4 markedly inhibited tumor growth in the in vivo xenograft model. RNA-seq analysis identified Ezrin (EZR) as a key downstream target of ITGB4, and a direct protein-protein interaction was confirmed between them. Mechanistically, ITGB4 knockdown decreased the expression of EZR at both the mRNA and protein levels. ITGB4 was demonstrated to exert its pro-tumorigenic effects through the regulation of EZR, which subsequently activated the Wnt/{beta}-catenin signaling pathway. Interestingly, EZR overexpression partially restored ITGB4 levels, suggesting a potential positive feedback loop via Wnt/{beta}-catenin signaling that further amplifies this oncogenic axis. Notably, the malignant phenotypes suppressed by ITGB4 silencing were significantly rescued by the overexpression of EZR. ConclusionThe present study identified a novel ITGB4/EZR/Wnt/{beta}-catenin signaling axis in colorectal cancer. ITGB4 promotes CRC progression by modulating EZR expression and subsequently activating the Wnt/{beta}-catenin pathway. These findings highlight ITGB4 as a potential prognostic biomarker and a promising therapeutic target for CRC.

molecular biology↗

Response of Serum-isolated Extracellular Vesicles to Focused Ultrasound Blood-Brain Barrier Opening

The blood-brain barrier (BBB) limits drug delivery to the brain and the movement of neurological biomarkers between the brain and blood. Focused ultrasound-mediated blood-brain barrier opening (FUS-BBBO) noninvasively opens the BBB, allowing increased molecular transport to and from the brain parenchyma. Despite being initially developed as a drug delivery method, FUS-BBBO has shown promise both as a neuroimmunotherapeutic modality, and as a way of improving neurological disease diagnosis via amplification of disease biomarker circulation. Recently, the role of extracellular vesicles (EVs) in modulating the neuroimmune system and in improving biomarker detection has sparked research interest. However, despite their potential role in modulating FUS-BBBO-induced neuroimmunotherapy and their ability to improve biomarker specificity after treatment, the EV response to FUS-BBBO had not been extensively characterized prior to this study. In this study, we investigated the effect of FUS-BBBO on EV concentration and content in the serum of mice and Alzheimers Disease (AD) patients. We observed a 164% increase in murine EV concentration one hour after treatment, as well as an increase in EV RNA associated with FUS-BBBO neuroimmunotherapy. Patient EV concentration also increased one hour after treatment and was dependent on the volume of BBB opening three days post-treatment. Furthermore, EV isolation was found to significantly enhance the amplification of AD biomarker detection by FUS-BBBO. Overall, we present the first evidence of altered murine and AD patient EV concentration and content in response to FUS-BBBO, providing evidence of EVs role within FUS-BBBO neuroimmunotherapy as well as their utility in improving FUS-BBBO biomarker amplification.

bioengineering↗

Pyruvate Kinase Directly Generates GTP in Glycolysis, Supporting Growth and Contributing to Guanosine Toxicity

Guanosine triphosphate (GTP) is essential for macromolecular biosynthesis, and its intracellular levels are tightly regulated in bacteria. Loss of the alarmone (p)ppGpp disrupts GTP regulation in Bacillus subtilis, causing cell death in the presence of exogenous guanosine and underscoring the critical importance of GTP homeostasis. To investigate the basis of guanosine toxicity, we performed a genetic selection for spontaneous mutations that suppress this effect, uncovering an unexpected link between GTP synthesis and glycolysis. In particular, we identified suppressor mutations in pyk, which encodes pyruvate kinase, a glycolytic enzyme. Metabolomic analysis revealed that inactivating pyruvate kinase prevents guanosine toxicity by reducing GTP levels. Although traditionally associated with ATP generation via substrate-level phosphorylation, B. subtilis pyruvate kinase in vitro was found to produce GTP and UTP approximately ten and three times more efficiently than ATP, respectively. This efficient GTP/UTP synthesis extends to Enterococcus faecalis and Listeria monocytogenes, challenging the conventional understanding of pyruvate kinase's primary role in ATP production. These findings support a model in which glycolysis directly contributes to GTP synthesis, fueling energy-demanding processes such as protein translation. Finally, we observed a synergistic essentiality of the {Delta}ndk {Delta}pyk double mutant specifically on glucose, indicating that pyruvate kinase and nucleoside diphosphate kinase are the major contributors of NTP production and complement each other during glycolysis. Our work highlights the critical role of nucleotide selectivity in pyruvate kinase and its broader implications in cellular physiology.

microbiology↗

Deficiency of DDI2 suppresses liver cancer progression byworsening cell survival conditions

The levels of reactive oxygen species (ROS) and the extent of ensuing DNA damage significantly influence cancer initiation and progression. Of crucial importance, the aspartate protease DDI2 has been proposed to play a pivotal role in monitoring intracellular ROS levels (to trigger oxidative eustress or distress), as well as in the oxidative DNA damage repair, through redox homeostasis-determining factor Nrf1 (encoded by NFE2L1). However, the specific role of DDI2 in the multi-step process resulting in the development and progression of liver cancer remains elusive to date. In the present study, we employed the CRISPR/Cas9 gene editing system to create two nuanced lines of DDI2 knockout (i.e., DDI2-/- and DDI2insG/-) from liver cancer cells. Subsequent experiments indicate that the knockout of DDI2 leads to increased ROS levels in hepatoma cells by downregulating two major antioxidant transcription factors Nrf1 and Nrf2 (encoded by NFE2L2), exacerbating endogenous DNA damages caused by ROS and not-yet-identified factors, thereby inhibiting cell proliferation and promoting apoptosis, and ultimately hindering in vivo malignant growth of xenograft tumor cells. Conversely, the restoration of DDI2 expression reverses the accumulation of ROS and associated DNA damage caused by DDI2 knockout, eliminating the subsequent inhibitory effects of DDI2 deficiency on both in vitro and in vivo growth of liver cancer cells. Collectively, these findings demonstrate that DDI2 deficiency impedes liver tumor growth by disrupting its survival environment, suggesting that DDI2 may serve as a novel therapeutic target for anti-cancer strategies aimed at modulating ROS or DNA damage processes.

cancer biology↗

Modernizing histopathological analysis: a fully automated workflow for the digital image analysis of the intestinal microcolony survival assay

BackgroundManual analysis of histopathological images is often not only time-consuming and painstaking but also prone to error from subjective evaluation criteria and human error. To address these issues, we created a fully automated workflow to enumerate jejunal crypts in a microcolony survival assay to quantify gastrointestinal damage from radiation. Methods and MaterialsAfter abdominal irradiation of mice, jejuna were obtained and prepared on histopathologic slides, and crypts were counted manually by trained individuals. The automated workflow (AW) involved obtaining images of jejunal slices from the irradiated mice, followed by cropping and normalizing the individual slice images for resolution and color; using deep learning-based semantic image segmentation to detect crypts on each slice; using a tailored algorithm to enumerate the crypts; and tabulating and saving the results. A graphical user interface (GUI) was developed to allow users to review and correct the automated results. ResultsCrypts counted manually exhibited a mean absolute percent deviation of (34 {+/-} 26)% between individuals vs the group mean across counters, which was reduced to (11 {+/-} 6)% across the 3 most-experienced counters. The AW processed a sample image dataset from 60 mice in a few hours and required only a few minutes of active user effort. AW counts deviated from experts mean counts by (10 {+/-} 8)%. The AW thereby allowed rapid, automated evaluation of the microcolony survival assay with accuracy comparable to that of trained experts and without subjective inter-observer variation. HighlightsO_LIWe fully automated the digital image analysis of a microcolony survival assay C_LIO_LIAnalyzing 540 images takes a few hours with only minutes of active user effort C_LIO_LIThe automated workflow (AW) is just as accurate as trained experts C_LIO_LIThe AW eliminates subjective inter-observer variation and human error C_LIO_LIHuman review possible with built-in graphical user interface C_LI Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=81 SRC="FIGDIR/small/627578v1_ufig1.gif" ALT="Figure 1"> View larger version (40K): org.highwire.dtl.DTLVardef@4d178eorg.highwire.dtl.DTLVardef@1457d39org.highwire.dtl.DTLVardef@120644eorg.highwire.dtl.DTLVardef@1996992_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Synthetic ratio computation for programming population composition and multicellular morphology

Recent advancements in genetic engineering have provided diverse tools for artificially synthesizing population diversity in both prokaryotic and eukaryotic systems. However, achieving precise control over the ratios of multiple cell types within a population derived from a single founder remains a significant challenge. In this study, we introduce a suite of recombinase-mediated genetic devices designed to achieve accurate population ratio control, enabling the distribution of distinct functionalities across multiple cell types. We systematically evaluated key parameters influencing recombination efficiency and developed data-driven models to reliably predict binary differentiation outcomes. Using these devices, we implemented parallel and series circuit topologies to create user-defined, complex cell fate branching programs. These branching devices facilitated the autonomous differentiation of precision fermentation consortia from a single founder strain, optimizing cell-type ratios for applications such as pigmentation and cellulose degradation. Beyond biomanufacturing, we engineered multicellular aggregates with genetically encoded morphologies by coordinating self-organization through cell adhesion molecules (CAMs). Our work provides a comprehensive characterization of recombinase-based cell fate branching mechanisms and introduces a novel approach for the bottom-up, high-resolution construction of synthetic consortia and multicellular assemblies.

synthetic biology↗