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At least 19 recordsLinked to original sources
PubMed2026

A Real-Time Image-Based Co-Culture Assay to Quantify Tumor-Infiltrating Lymphocyte-Mediated Apoptotic Killing of Patient-Derived Tumor Organoids.

Understanding the functional capacity of tumor-infiltrating lymphocytes (TILs) to recognize and eliminate autologous tumor cells is central to advancing personalized immunotherapy. The goal of this method is to provide an image-based, live-cell imaging protocol that measures TIL-mediated, caspase-3-dependent apoptotic killing against patient-derived tumor organoids (PDTOs) in real time. This method integrates established procedures for isolation and expansion of PDTOs and TILs with a standardized three-dimensional co-culture system and automated fluorescence-based apoptosis detection. Tumor organoids are plated in imaging-compatible 96-well plates and labeled with a red tumor marker, while expanded TILs are added at defined effector-to-target ratios in the presence of a caspase-3 activated green fluorescent substrate. Co-cultures are imaged every 4 h using a live-cell analysis system to capture phase-contrast and dual-fluorescence channels. Quantitative image analysis identifies red-positive tumor structures and calculates the proportion of red/green double-positive apoptotic tumor objects over time. Appropriate technical and biological replicates are incorporated, along with baseline, spontaneous apoptosis, negative and positive killing controls to ensure assay rigor. By preserving tumor heterogeneity within the PDTOs' three-dimensional architecture while enabling longitudinal quantification, this protocol provides a physiologically relevant system for functionally profiling patient-specific tumor-TIL interactions and investigating immunomodulatory agents that augment anti-tumor immunity.

Humans↗
PubMed2025

Live-cell RNA imaging with the inactivated endonuclease Csy4 enables new insights into plant virus transport through plasmodesmata.

Plant-infecting viruses spread through their hosts by transporting their infectious genomes through intercellular nano-channels called plasmodesmata. This process is mediated by virus-encoded movement proteins. Whilst the sub-cellular localisations of movement proteins have been intensively studied, live-cell RNA imaging systems have so far not been able to detect viral genomes inside the plasmodesmata. Here, we describe a highly sensitive RNA live-cell reporter based on an enzymatically inactive form of the small bacterial endonuclease Csy4, which binds to its cognate stem-loop with picomolar affinity. This system allows imaging of plant viral RNA genomes inside plasmodesmata and shows that potato virus X RNA remains accessible within the channels and is therefore not fully encapsidated during movement. We also combine Csy4-based RNA-imaging with interspecies movement complementation to show that an unrelated movement protein from tobacco mosaic virus can recruit potato virus X replication complexes adjacent to plasmodesmata. Therefore, recruitment of potato virus X replicase is mediated non-specifically, likely by indirect coupling of movement proteins and viral replicase via the viral RNA or co-compartmentalisation, potentially contributing to transport specificity. Lastly, we show that a 'self-tracking' virus can express the Csy4-based reporter during the progress of infection. However, expression of the RNA-binding protein in cis interferes with viral movement by an unidentified mechanism when cognate stem-loops are present in the viral RNA.

Plasmodesmata↗
PubMed2026

From Static to Dynamic: Fluorescence Imaging Technology Advances Precise Embryo Evaluation.

Live-cell imaging technology has revolutionized our understanding of preimplantation embryonic development, shifting the field from static morphological descriptions to dynamic functional analyses. This has tremendously advanced the fields of in vitro fertilization (IVF) and embryonic development. At the heart of this transition lies the strategic application of fluorescent probes, which provide the requisite sensitivity and specificity to resolve complex biological events. This review provides a comprehensive overview of fluorescent probe-based strategies designed to address four cardinal questions in peri-implantation embryology: genomic stability, cell fate determination, tissue morphogenesis, and embryo-maternal interactions. We systematically evaluate the chemical design principles and imaging modalities of various probes, which range from small-molecule organic fluorophores to genetically encoded reporters and nanoparticle-based sensors. Furthermore, we discuss how these tools facilitate the real-time visualization of chromosomal aberrations, lineage segregation, biomechanical forces, and enzymatic activities within the delicate embryonic microenvironment. This review summarizes methodological strategies for selecting and developing optimal probes across diverse application contexts. By identifying current technical bottlenecks and proposing future directions, such as NIR-II imaging and noninvasive labeling, it aims to drive the translation of basic embryonic research into advanced reproductive medicine.

Humans↗
PubMed2025

Targeting Mitotic Exit in Malignant Cells.

In order to sustain genomic stability by correct DNA replication and mitosis and thus avoid malignant transformation of cells, the cell cycle is a strictly regulated process. Aberrant cell cycle regulation and defects in mitosis in malignant cells are targets of various cancer therapies. Cancer cells may survive antimitotic treatment due to mitotic slippage with a residual activity of the ubiquitin ligase anaphase-promoting complex (APC/C) and a continuous slow ubiquitin-proteasome-dependent cyclin B-degradation leading to mitotic exit. The combination of antimitotic chemotherapeutics with proteasome inhibitors to block cyclin B-proteolysis or with targeted inhibitors of the APC/C and the antiapoptotic protein Mcl-1 seems a promising approach to improve treatment response in different malignancies by enhancing mitotic arrest and apoptosis.The influence of conventional spindle poisons and new targeted substances and of their combinations on mitosis and apoptosis has not yet been conclusively clarified. Most models have been verified on cell lines whose biology may differ from that of tumors growing in vivo. To study the impact of various antimitotic substances on cell proliferation, especially detect onset of apoptosis depending on different cell cycle phases and thus to identify a possibly entity-dependent mechanism of those agents and their combinations, a combined approach with live-cell imaging and soft-agar colony assays in cultured patient-derived xenografts (PDX) was established.

Humans↗
PubMed2022

The evolutionary dynamics of extrachromosomal DNA in human cancers.

Oncogene amplification on extrachromosomal DNA (ecDNA) is a common event, driving aggressive tumor growth, drug resistance and shorter survival. Currently, the impact of nonchromosomal oncogene inheritance-random identity by descent-is poorly understood. Also unclear is the impact of ecDNA on somatic variation and selection. Here integrating theoretical models of random segregation, unbiased image analysis, CRISPR-based ecDNA tagging with live-cell imaging and CRISPR-C, we demonstrate that random ecDNA inheritance results in extensive intratumoral ecDNA copy number heterogeneity and rapid adaptation to metabolic stress and targeted treatment. Observed ecDNAs benefit host cell survival or growth and can change within a single cell cycle. ecDNA inheritance can predict, a priori, some of the aggressive features of ecDNA-containing cancers. These properties are facilitated by the ability of ecDNA to rapidly adapt genomes in a way that is not possible through chromosomal oncogene amplification. These results show how the nonchromosomal random inheritance pattern of ecDNA contributes to poor outcomes for patients with cancer.

Biological Evolution↗
PubMed2026

Imaging-Guided Omics Technologies for Resolving Rare Cancer States and Advancing Nanomedicine.

The ability to resolve rare and transient cellular states is critical for understanding metastasis, immune evasion, and therapy resistance in cancer, yet these dynamic processes often escape detection by conventional sequencing and imaging approaches. Recent advances at the interface of nanotechnology, high-resolution live-cell imaging, and single-cell/spatial multiomics methods have enabled functional profiling of cells with unprecedented precision within their native microenvironment. In this Mini-Review, we highlight emerging nanoscale platforms that couple real-time phenotypic imaging with molecular readouts, such as FUNseq and CIN-seq, to directly link functional heterogeneity to transcriptomic, proteomic, and epigenomic information. By integrating nanoscale optical imaging, microengineered perturbation tools, and AI-driven computational analysis, these technologies open up new avenues for dissecting rare metastatic, therapy-resistant, or immune-evasive subpopulations. We further discuss how these next-generation imaging-guided single-cell and spatial omics platforms not only advance fundamental cancer biology but also create opportunities to accelerate the development of nanomedicine applications.

Humans↗
PubMed2026

Evaluation of 3D Spheroids for AAV Transduction Studies.

Adeno-associated viruses (AAVs) are potent vectors used for gene delivery in gene therapy products. Their development requires in vitro systems that can reliably detect differences in vector design, serotype performance, regulatory element strength, and expression kinetics. These systems must also support applications such as potency assessment and vector optimization. Here, we describe a streamlined three-dimensional spheroid platform optimized for evaluating AAV potency, transgene expression kinetics, and serotype-specific transduction efficacy across diverse cell lines. Uniform spheroids are generated using ultra-low attachment plates and maintained under conditions that support stable architecture and long-term imaging. Following AAV transduction, fluorescent or luminescent readouts are monitored in real time using live-cell imaging systems. This enables quantitative assessment of reporter signal, dose responsiveness, regulatory element activity, and onset time through continuous kinetic imaging. The platform effectively discriminates between potent and weak vector genome designs and among multiple AAV serotypes. This method demonstrates robust performance across both slowly and rapidly dividing cell lines. These results establish its utility as a scalable and physiologically relevant system for preclinical gene therapy evaluation and development.

Dependovirus↗
PubMed2025

Core passive and facultative mTOR-mediated mechanisms coordinate mammalian protein synthesis and decay.

The maintenance of cellular homeostasis requires tight regulation of proteome concentration and composition. To achieve this, protein production and elimination must be robustly coordinated. However, the mechanistic basis of this coordination remains unclear. Here, we address this question using quantitative live-cell imaging, computational modeling, transcriptomics, and proteomics approaches. We found that protein decay rates systematically adapt to global alterations of protein synthesis rates. This adaptation is driven by a core passive mechanism supplemented by facultative changes in mechanistic/mammalian target of rapamycin (mTOR) signaling. Passive adaptation hinges on changes in the production rate of the machinery governing protein decay and allows for partial maintenance of the cellular proteome. Sustained changes in mTOR signaling provide an additional layer of adaptation unique to naive pluripotent stem cells, allowing for near-perfect maintenance of proteome composition. Our work unravels the mechanisms protecting the integrity of mammalian proteomes upon variations in protein synthesis rates. A record of this paper's transparent peer review process is included in the supplemental information.

TOR Serine-Threonine Kinases↗
PubMed2026

The TUBG meshwork is associated with centromere dynamics and micronuclear organization.

This study investigates how γ-tubulin and the centrosome contribute to interphase centromere dynamics and nuclear organization. Although classically associated with mitotic microtubule nucleation, here we show that γ-tubulin associates with chromatin and is enriched within centromere-defined volumes. Using live-cell imaging, immunofluorescence, and chromatin immunoprecipitation sequencing, we detect γ-tubulin-associated signal at satellite-rich, centromere-proximal chromatin. Reduced γ-tubulin levels are associated with increased centromere fluorescence intensity and reduced mobility, linking the γ-tubulin network to centromere organization. Under acute cisplatin-induced stress, centromere mobility increases, whereas centromere clustering is observed in separate fixed-cell analyses. Ser131 phosphorylation is associated with γ-tubulin self-assembly and centromere-related dynamics. Additionally, γ-tubulin accumulates in micronuclei, coinciding with increased replication-associated signal and DNA fluorescence. In primary clear cell renal cell carcinoma cells, stress is associated with higher γ-tubulin fluorescence intensity within centromere-defined volumes. Together, these findings support an association between the γ-tubulin meshwork and centromere organization, chromatin compartmentalization, and responses to genomic stress.

Centromere↗
PubMed2024

Transient Zn2+ deficiency induces replication stress and compromises daughter cell proliferation.

Cells must replicate their genome quickly and accurately, and they require metabolites and cofactors to do so. Ionic zinc (Zn2+) is an essential micronutrient that is required for hundreds of cellular processes, including DNA synthesis and adequate proliferation. Deficiency in this micronutrient impairs DNA synthesis and inhibits proliferation, but the mechanism is unknown. Using fluorescent reporters to track single cells via long-term live-cell imaging, we find that Zn2+ is required at the G1/S transition and during S phase for timely completion of S phase. A short pulse of Zn2+ deficiency impairs DNA synthesis and increases markers of replication stress. These markers of replication stress are reversed upon resupply of Zn2+. Finally, we find that if Zn2+ is chelated during the mother cell's S phase, daughter cells enter a transient quiescent state, maintained by sustained expression of p21, which disappears upon reentry into the cell cycle. In summary, short pulses of mild Zn2+ deficiency in S phase specifically induce replication stress, which causes downstream proliferation impairments in daughter cells.

Zinc↗
PubMed2026

Integrative modeling of the genome structure and dynamics in fission yeast.

Genome organization in the nucleus is highly structured and dynamic. Recent advances in genomic technology have enabled the measurement of genome-wide architecture and locus-specific motion, yielding contact maps and live-cell trajectories. However, these outcomes are derived from different modalities and are not directly comparable, with their quantitative integration being a key challenge. Here we establish a genome-wide live-cell imaging platform in fission yeast Schizosaccharomyces pombe, tracking 131 chromosomal loci, along with the spindle pole body (SPB) and nucleolus, to construct a quantitative map of locus dynamics. By integrating these dynamics with contact data through polymer modeling of Hi-C data, we build a physics-based "digital twin" of the S. pombe genome consistent with the spatiotemporal dynamics of interphase chromatin. We validate it against genome-wide mobility patterns and known architectural features, including centromere and telomere clustering. The model also identifies distinct dynamical regimes: centromere- and telomere-proximal loci relax within [Formula: see text]150 s, whereas the remaining loci relax within [Formula: see text]70 s. We measure semiperiodic dynamics of SPB motion, including a characteristic peak near 225 s and [Formula: see text] fluctuations. We use the model with SPB-directed forcing to show how these low-frequency components propagate through the genome to drive genome-wide chromatin displacements. Together, this predictive physics-based modeling framework integrates genome structure and dynamics to reveal how nuclear mechanical driving forces shape chromosome motion, linking mechanically driven chromatin responses to genome maintenance and regulation.

Schizosaccharomyces↗
PubMed2023

Transient Zn2+ deficiency induces replication stress and compromises daughter cell proliferation.

Cells must replicate their genome quickly and accurately, and they require metabolites and cofactors to do so. Ionic zinc (Zn2+) is an essential micronutrient that is required for hundreds of cellular processes, including DNA synthesis and adequate proliferation. Deficiency in this micronutrient impairs DNA synthesis and inhibits proliferation, but the mechanism is unknown. Using fluorescent reporters to track single cells via long-term live-cell imaging, we find that Zn2+ is required at the G1/S transition and during S-phase for timely completion of S-phase. A short pulse of Zn2+ deficiency impairs DNA synthesis and increases markers of replication stress. These markers of replication stress are reversed upon resupply of Zn2+. Finally, we find that if Zn2+ is removed during the mother cell's S-phase, daughter cells enter a transient quiescent state, maintained by sustained expression of p21, which disappears upon reentry into the cell cycle. In summary, short pulses of mild Zn2+ deficiency in S-phase specifically induce replication stress, which causes downstream proliferation impairments in daughter cells.

Biological sciences↗
PubMed2026

Anoxia tolerant DNA replication is supported by ATR kinase in the annual killifish Austrofundulus limnaeus.

Hypoxia and anoxia suppress cell proliferation due to an increase in replication stress and activation of DNA damage checkpoints. Embryos of the annual killifish Austrofundulus limnaeus tolerate prolonged anoxia, indicating improved genomic stability under oxygen starvation. We investigated the cell cycle regulation of the anoxia tolerant killifish embryonic cell line PSU-AL-WS40NE during anoxia. Live-cell imaging confirms continued proliferation of WS40NE cells for the first 24 h of anoxia with minimal cell death. Fluorescence imaging shows that cells accumulate in G1 after the first day in anoxia with a rapid entry into S phase upon reoxygenation. Pharmacological inhibition shows a reliance on ataxia telangiectasia and Rad3 related (ATR) signaling, suggesting that increased γH2AX levels are driven by replication stress instead of DNA damage. This conclusion is supported by a lack of induction of a G2 checkpoint, suggesting minimal DNA damage during anoxic exposure. Maintaining cellular proliferation during anoxia and accumulating cells in the G1 phase for extended anoxic exposure is likely one way that embryos of the killifish can survive prolonged anoxia, which provides insight into mechanisms that enable cells to proliferate under metabolic stress.

Animals↗
PubMed2026

Spindle Assembly Checkpoint Competency Determines Sensitivity to KIF18A Inhibition in Small-Cell Lung Cancer.

BACKGROUND: Small-cell lung cancer (SCLC) is characterized by pervasive chromosomal instability (CIN) and remains largely refractory to targeted therapies. KIF18A, a motor protein that regulates chromosome alignment during mitosis, has emerged as a selective dependency in CIN-high tumors. Whether this dependency extends to SCLC, a prototypical CIN-high cancer, has not been established, and biomarkers predicting response to KIF18A inhibition, currently in clinical trials, are lacking. METHODS: We integrated analyses of patient tumor datasets, neuroendocrine (NE) and non- NE SCLC cell lines, and functional perturbation models to define the determinants of response to KIF18A inhibition. Chromosomal instability metrics, transcriptional programs, mitotic dynamics, and spindle assembly checkpoint (SAC) function were assessed using genomic profiling, live-cell imaging, genetic perturbation, and pharmacologic inhibition. RESULTS: KIF18A expression was elevated in SCLC tumors and correlated with CIN-associated transcriptional programs, proliferative markers, and NE status; however, these features did not predict sensitivity to KIF18A inhibition. Instead, response was determined by the functional integrity of the SAC. SAC-proficient SCLC cells underwent sustained mitotic arrest followed by apoptotic cell death upon KIF18A inhibition, whereas SAC-defective cells failed to maintain checkpoint activation and survived. Mechanistically, resistant cells exhibited impaired kinetochore recruitment of core SAC components, including MAD1 and BUBR1. Importantly, transient induction of acute CIN through MPS1 inhibition partially restored sensitivity to KIF18A inhibition in resistant models. CONCLUSIONS: This study provides the first mechanistic characterization of KIF18A dependency in SCLC, identifying SAC competency as the primary determinant of response. These findings establish a biologically informed framework for patient stratification and rational combination strategies. TRANSLATIONAL RELEVANCE: Small-cell lung cancer (SCLC) is an aggressive malignancy with few effective targeted therapies and marked chromosomal instability. KIF18A has emerged as a potential therapeutic target in genomically unstable cancers, but biomarkers predicting response to KIF18A inhibition are lacking. We demonstrate that sensitivity to KIF18A inhibition in SCLC is determined not by KIF18A expression, neuroendocrine subtype, or baseline chromosomal instability, but by the functional integrity of the spindle assembly checkpoint (SAC). SCLC cells with intact SAC signaling undergo sustained mitotic arrest and apoptosis upon KIF18A inhibition, whereas SAC-defective cells bypass checkpoint activation and survive aberrant mitosis. Notably, transient induction of acute chromosomal instability through MPS1 inhibition partially restores sensitivity in resistant models. Together, these findings identify mitotic checkpoint competency as a mechanistic determinant and candidate predictive biomarker for KIF18A-targeted therapies, providing a biologically informed framework for patient stratification and rational combination strategies relevant to ongoing KIF18A inhibitor clinical trials.

Journal Article↗
PubMed2026

DENND3-p.R534S disrupts dyadic microdomain architecture to drive potentially pro-arrhythmic calcium and electrophysiologic instability.

AIMS: Inherited ventricular arrhythmias (VAs) frequently occur in the absence of pathogenic variants in canonical ion channel genes, suggesting alternative mechanisms of electrical instability. DENND3 is a guanine nucleotide exchange factor that regulates Rab GTPase-mediated trafficking, but its role in cardiac excitation-contraction coupling and membrane microdomain organization remains undefined. METHODS AND RESULTS: We studied induced pluripotent stem cell-derived cardiomyocytes generated from a CRISPR/CAS9-engineered ultra-rare DENND3-p.R534S variant-inserted line (previously identified in an idiopathic ventricular fibrillation pedigree) and matched isogenic controls. Multielectrode array recordings, live-cell calcium imaging, super-resolution imaging using expansion microscopy, and biochemical analyses were used to assess electrical activity, calcium handling, membrane architecture, and calcium release unit organization. Potentially therapeutic studies were performed using genetic and pharmacologic inhibition of Rab11b. DENND3-p.R534S induced pluripotent stem cell-derived cardiomyocytes exhibited multicellular electrical instability characterized by increased beat-to-beat variability, arrhythmic activity, conduction slowing, and prolonged excitation-contraction delay. These abnormalities were accompanied by heterogeneous and dyssynchronous calcium cycling despite preserved expression of major calcium-handling proteins. Super-resolution imaging revealed disruption of BIN1-dependent membrane architecture and nanoscale uncoupling of Cav1.2 and RyR2. Inhibition of Rab11b restored BIN1 organization, re-established dyadic coupling, normalized calcium cycling, and improved electrical stability. CONCLUSION: These findings support a model in which altered trafficking balance contributes to disruption of membrane microdomain organization, leading to dyadic uncoupling, calcium instability, and electrical dysfunction. Modulation of the Rab11b-mediated trafficking pathway restored structural and functional abnormalities, supporting the trafficking-associated pathway as a potential therapeutic target in DENND3-associated ventricular arrhythmia.

Myocytes, Cardiac↗
PubMed2026

CRISPR/Cas- and Argonaute-Based In Vivo Nucleic-Acid Imaging Technologies: Strategies, Challenges, and Perspectives.

Live-cell monitoring of sequence-specific nucleic acids is essential to understanding genome organization, RNA regulation, and disease progression. Clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated protein (Cas) and Argonaute (Ago) systems provide programmable, guide-directed recognition of DNA or RNA and are increasingly used as platforms for in vivo bioimaging. This review summarizes the structural and mechanistic features of representative CRISPR and Ago effectors and discusses design strategies for sensitive, specific, and multiplexed imaging of genomic loci, extrachromosomal DNA, and endogenous RNA in living cells. We compare the analytical performance and limitations of CRISPR- and Ago-based imaging, with particular emphasis on the major technical and biological challenges affecting their accuracy, applicability, and reliability. Finally, this review offers insights into developing high-resolution and user-friendly bioimaging platforms for fundamental biology and future translational applications.

CRISPR↗
PubMed2026

Trimeric autotransporter adhesins driving chain-like adhesion diversify surface colonization strategies in Shiga toxin-producing Escherichia coli.

Bacteria frequently colonize host and environmental surfaces under fluid flow. Chain-like adherence pattern (CLAP) is an EibG-mediated surface colonization phenotype of certain Shiga toxin-producing Escherichia coli (STEC) that lack the locus of enterocyte effacement (LEE). EibG, an immunoglobulin-binding trimeric autotransporter adhesin, drives CLAP, but the temporal dynamics and genetic diversity underlying chain formation remain unclear. Here, we use live-cell time-lapse imaging to show that chains arise from single cells that elongate and divide without separation. Under flow, chains resist detachment and undergo shear-dependent fragmentation at cell-cell junctions, releasing viable clonal units that disperse downstream. Comparative genomics reveals diversity among EibG-related adhesins and identifies distinct lineages, including chain-like adhesins (Cla) that mediate CLAP while lacking IgG binding. Screening of 1,354 genomes from England shows that claB is present in 95.6% of strains from major LEE-negative STEC serotypes, highlighting its epidemiological prevalence. Targeted mutagenesis demonstrates that chain formation and IgG binding are mediated by distinct structural domains, revealing the modular functional architecture of these adhesins. Furthermore, we show that EibG, ClaA, and ClaB confer robust resistance to complement-mediated killing. Collectively, these findings establish CLAP as a dynamic, surface-associated strategy of LEE-negative STEC and reveal diversification among adhesins that drive this behavior.

Bacterial Adhesion↗
PubMed2026

HoT auto-blinking probes enable real-time, super-resolution chromatin imaging in live cells and tissues.

Single-molecule localization microscopy (SMLM) enables visualization of chromatin architecture at nanoscale resolution. However, high-performance DNA probes suitable for SMLM in both live cells and tissues remain limited. We developed Hoechst-6-Carboxytetramethylrhodamine (6-TAMRA) derivative (HoT) probes-rhodamine-based derivatives conjugated to a Hoechst moiety-through structural fine-tuning of rhodamine spirocyclization. HoTs are self-assembling, auto-blinking probes with excellent photostability and high temporal resolution. They permeate live cells, enabling long-term, real-time nanoscopic chromatin imaging in live and fixed cells and in tissue sections. In live cells, we identified nanoscale features in the 3D organization of chromatin and quantified DNA fiber kinetics at high resolution. We quantified DNA compaction in single cells within retinal and colon cancer sections. OligoSTORM (stochastic optical reconstruction microscopy)-labeled gene loci can be visualized and measured within their HoT-labeled chromatin footprints. Our work provides powerful tools for investigating chromatin structure and functions in living cells and tissues, with applications ranging from cancer diagnosis to retinal regeneration.

Chromatin↗