bims-ginsta Biomed News
on Genome instability
Issue of 2026–05–17
35 papers selected by
Jinrong Hu, National University of Singapore



  1. Nat Cell Biol. 2026 May 14.
      During development, local mechanochemical cues within the cell microenvironment are translated into signalling pathways that drive cell fate decisions. Yet, as cells differentiate collectively, how global tissue-level properties shape these instructive cues remains unclear. Here we show that a tissue-scale rigidity transition guides patterning by tuning the length scales and timescales of morphogen signalling. By combining rigidity percolation theory, reaction-diffusion modelling, quantitative imaging and optogenetics in zebrafish, we uncover dynamical global tissue rigidity patterns that actively shape the Nodal morphogen gradient by locally changing its concentration and accelerating its signalling activity. In this self-generated mechanism, Nodal, besides instructing meso-endoderm fate specification, increases cell-cell adhesion strength via regulating planar cell polarity genes. Once the adhesion strength reaches a critical point, it triggers a rigidity transition which, in turn, induces the collapse of tissue porosity. The abrupt tissue reorganization negatively feeds back on Nodal signalling, impacting both its length scales, by restricting Nodal diffusivity, and its timescales, by speeding up the expression of its antagonist Lefty, thereby ensuring timely signal termination and robust patterning. Overall, we uncover a multiscale regulatory mechanism by which positional information and tissue material properties dynamically tune one another.
    DOI:  https://doi.org/10.1038/s41556-026-01954-4
  2. Sci Adv. 2026 May 15. 12(20): eaec3379
      The establishment of cell form, fate, and function during morphogenesis requires coordination between cell polarity and developmental cues. To achieve this, cells must establish polarity domains that are stable yet sensitive to guiding cues. Here, we show that Caenorhabditis elegans germline blastomeres use a time-varying polarization landscape to resolve this trade-off. Specifically, coupling the PAR polarity network to the oscillatory activity of cell cycle kinase CDK-1 ensures that newborn cells operate in a low feedback regime that lowers barriers to state switching, allowing spatial cues to induce and orient PAR protein asymmetries. As CDK-1 activity rises during mitosis, molecular feedback increases, reinforcing cue-induced asymmetries to yield robust and stable patterning of PAR polarity domains. Consistent with this model, we show that low CDK/feedback regimes destabilize PAR domains but are required for de novo polarization and polarity reorientation by cues. We propose that oscillatory networks represent a general mechanism for dynamically optimizing cellular decision-making landscapes, ensuring robust, signal-induced state switching during development.
    DOI:  https://doi.org/10.1126/sciadv.aec3379
  3. Nature. 2026 May 13.
      Cellular dormancy enables survival during prolonged nutrient limitation by reversibly suppressing protein synthesis1-4. How inactive eukaryotic ribosomes are reactivated when nutrients return remains unclear. Here, using high-resolution in situ cryo-electron tomography in Schizosaccharomyces pombe, we identify SNOR, an SBDS domain-containing ribosome-associated factor that binds at the peptidyl transferase centre and contacts the hypusinated loop of eIF5A during glucose depletion-induced dormancy. Rather than acting as a canonical hibernation factor, SNOR licenses dormant ribosomes for rapid translational restart. Upon glucose repletion, SNOR and eIF5A act together to promote efficient recovery of polysomes and exit from dormancy. These findings define a stress-responsive ribosome restart module that couples carbon-source limitation to surveillance of the ribosomal active site and reactivation of protein synthesis.
    DOI:  https://doi.org/10.1038/s41586-026-10530-7
  4. Mol Cell. 2026 May 12. pii: S1097-2765(26)00273-X. [Epub ahead of print]
      Variability in genome organization drives differential gene expression and shapes cellular diversity, yet whether transcription actively instructs genome structure and how this relationship is exploited in disease remains unclear. We show that transcription and cohesin direct the spatial positioning of lamina-associated domain (LAD) boundary genes. Transcriptional repression repositions LAD boundary genes to the nuclear lamina in a cohesin loop extrusion-dependent manner. Conversely, overactive cohesin is sufficient to reposition and silence LAD boundary genes, an effect counteracted by maintaining transcription. In Friedreich's ataxia, we demonstrate improper positioning of the pathogenically repressed LAD boundary gene FRATAXIN (FXN) at the nuclear periphery reflects an imbalance between transcription and cohesin dynamics. Importantly, modulating either transcription or cohesin activity restores FXN positioning and reactivates expression. Our findings establish transcription and cohesin as tunable molecular rheostats orchestrating LAD boundary spatial positioning and reveal how the flexible and dynamic nature of genome architecture is hijacked in disease.
    Keywords:  3D spatial positioning; FXN; Friedreich’s ataxia; LADs; cohesion; disease; genome organization; hiPSC; plasticity; transcription
    DOI:  https://doi.org/10.1016/j.molcel.2026.04.019
  5. Cell. 2026 May 08. pii: S0092-8674(26)00460-5. [Epub ahead of print]
      Human aging is characterized by complex structural and functional decline, but quantifying its heterogeneity and assessing biological age remain challenges. We present the mCAS (multicentric Chinese aging standardized cohort) developed from 2,019 Chinese individuals aged 18-91 years. Integrating high-dimensional clinical, physiological, and molecular-level data, we constructed a three-tiered aging framework: the core capacity clock (CC-clock) to quantify clinical physiological decline, the multimodal clock (MM-clock) with extensive parameter coverage and enhanced predictive precision, and organ-associated aging clocks. Cross-layer analysis demonstrates that plasma protein clocks not only capture chronological age but also serve as efficient proxies for systemic physiological capacity. Leveraging this framework for discovery, we identified the age-dependent accumulation of coagulation factors as a driver of multi-organ senescence and systemic inflammatory activation. This study provides a foundational framework that bridges molecular signatures with functional decline, identifies new biomarkers for aging assessment, and reveals a novel translational driver of aging.
    Keywords:  aging; aging clock; aging cohort; aging driver; biological age; coagulation factor; multimodal; systemic aging; vascular aging
    DOI:  https://doi.org/10.1016/j.cell.2026.04.025
  6. Nat Commun. 2026 May 11.
      During mitotic cell division, pliable interphase chromatin is transformed into stiff mitotic chromosomes able to withstand the pushing and pulling forces of the mitotic spindle. How the cell establishes this chromosome stiffness and the cellular consequences if this stiffness is disrupted, is unclear. Condensin complexes drive many of the structural changes in mitotic chromosomes. Here, we combine rapid protein depletion of Condensins I and II with live cell imaging and mechanical characterization of purified mitotic chromosomes to probe their role in mitotic chromosome mechanics. We show that Condensin I, but not Condensin II, is required to establish chromosome stiffness and chromatin elasticity, and yet is not required for maintaining these properties after chromosome formation. Nevertheless, metaphase depletion of Condensin I still leads to severe sister centromere cohesion defects. We propose that the chromatin loop network established by Condensin I is locked in place by an additional 'crosslinking' factor.
    DOI:  https://doi.org/10.1038/s41467-026-72825-7
  7. Nat Neurosci. 2026 May 12.
      Spatial transcriptomics has emerged as a transformative approach for in situ mapping of cellular heterogeneity and interactions, yet existing methods often compromise throughput, cost and tissue coverage. Here we introduce Imaging Reconstruction using Indexed Sequencing (IRISeq): an optics-free, cost-effective platform that leverages spatial interaction mapping by indexed sequencing to profile tissues at adjustable sizes and resolutions (5-50 µm). We applied IRISeq to map gene expression across more than 70 coronal sections from both adult and aged mouse brains, including wild-type and two lymphocyte-deficient models (Rag1 and Prkdc mutants) and generated more than 460,000 spatial transcriptome profiles. Our integrated analysis with 783,264 single-cell transcriptomes revealed region-specific aging signatures that are lymphocyte dependent, notably a downregulation of interferon signaling and inflammation in ventricular regions upon lymphocyte depletion, alongside mutant-specific upregulation of senescence pathways. Furthermore, lymphocyte deficiency was linked to preserved abundance of ependymal cells that line the brain's ventricles and to distinct microglial state dynamics, highlighting a key role for lymphocytes in driving inflammatory processes during brain aging. Overall, IRISeq provides a high-throughput and cost-effective solution for spatially resolved transcriptomic profiling, opening new avenues for elucidating region-specific cellular mechanisms underlying aging and identifying potential therapeutic targets to preserve brain homeostasis.
    DOI:  https://doi.org/10.1038/s41593-026-02293-1
  8. Nat Immunol. 2026 May 12.
      Intestinal stem cells (ISCs) are essential for sustaining epithelial renewal and barrier integrity, yet their role in orchestrating defense against enteric pathogens remains unclear. Here we identify a stem cell-intrinsic immune mechanism whereby Lgr5+ ISCs detect intracellular Salmonella enterica and activate an inflammasome-dependent differentiation program. Using fluorescent-labeled S. enterica, single-cell transcriptomics, fate mapping, organoid models, and genetic perturbations, we show that invaded ISCs undergo rapid reprogramming toward antimicrobial peptide-enriched Paneth cells via apoptosis-associated Speck-like protein containing a CARD (ASC, encoded by Pycard)-mediated inflammasome signaling. This fate switch enhances epithelial antimicrobial capacity and restricts pathogen persistence in the crypt. The response is Salmonella-specific and conserved in human intestinal organoids. Moreover, the invasion-associated transcriptional signature is enriched in ISCs from patients with Crohn's disease. Our findings reveal that ISCs act as active sensors of bacterial invasion and initiate epithelial remodeling through inflammasome signaling, highlighting stem cell plasticity as a frontline innate immune strategy.
    DOI:  https://doi.org/10.1038/s41590-026-02514-6
  9. Nucleic Acids Res. 2026 May 05. pii: gkag462. [Epub ahead of print]54(9):
      TOPBP1 is a scaffold protein with multiple functions in genome integrity. During mitosis, TOPBP1 is coordinating DNA repair and genome maintenance, thereby reducing carry-over of DNA damage to daughter cells. This function emerges as a critical backup pathway in BRCA-deficient cells, yet many aspects of TOPBP1 regulation during mitosis remain unclear. Mitotic kinases are involved in regulating genome maintenance pathways during mitosis. Indeed, TOPBP1 binds the mitotic kinase PLK1, but the molecular aspects as well as the functional significance of this is unclear. To address this, we here identify and characterize a conserved CDK1-primed binding site for PLK1 in TOPBP1. We show that mutation of this results in increased transmission of DNA damage to G1 daughter cells, deficient mitotic DNA repair synthesis, mislocalization of DNA polymerase θ, and increased frequency of anaphase bridges and micronucleation. Consistent with this, BRCA2 depleted cells are highly dependent on TOPBP1-PLK1 complex formation. Altogether, we reveal the molecular details of TOPBP1-PLK1 complex formation and address its role in genome maintenance during mitosis.
    DOI:  https://doi.org/10.1093/nar/gkag462
  10. Curr Biol. 2026 May 14. pii: S0960-9822(26)00518-X. [Epub ahead of print]
      Epithelial cells form barriers with specialized apical membranes facing the external environment or internal lumens, yet how interconnected epithelial tubular systems form from cystic epithelial primordia is poorly studied. At the boundaries of cystic epithelial primordia, apical surfaces must correctly align to yield functional connections within and between organs. Here, we use the digestive tract of the developing C. elegans embryo to define a crucial two-cell tissue, the rectal valve (vir) cells, that mediate the connection and apical alignment between the posterior intestine and the rectum. Vir cells migrate while attached to the rectal primordium to create an essential connection with the intestinal primordium and complete the digestive tract. Vir contact with the intestine, through E-cadherin signaling, is required for the intestinal apical surface to undergo a transition from a cyst with an inaccessible apical surface to an open tube that is competent to connect with neighboring tissues. Ablation of vir cell progenitor resulted in a lethal disconnection between the intestinal and rectal apical surfaces due to failure of this first step in apical accessibility. To resolve the final gap in apical continuity between the intestine and rectum, vir cells develop bipolar apical surfaces, each facing the neighboring tissue. The intestine-facing apical puncta in vir cells require intestinal E-cadherin signaling to form and accumulate as well as to correctly partition apical proteins within vir cells. Together these results establish E-cadherin-based signaling as the crucial factor aligning apical surfaces across primordia as epithelial cells from different germ layers form a vital connection.
    Keywords:  C. elegans; E-cadherin; endoderm; epithelial fusion; lumenogenesis; morphogenesis; tissue polarity; transitional epithelium
    DOI:  https://doi.org/10.1016/j.cub.2026.04.048
  11. Dev Cell. 2026 May 13. pii: S1534-5807(26)00123-1. [Epub ahead of print]61(5): 1146-1161.e8
      Mitochondrial DNA (mtDNA) exists in many copies per cell, with cell-to-cell variability in mutation load, which is known as heteroplasmy. Developmental and age-related expansion of heteroplasmic mtDNA mutations contributes to the pathogenesis of mitochondrial and neurodegenerative diseases. Here, we describe an approach for in situ sequence-specific detection of single mtDNA molecules (mtDNA-single-molecule fluorescent in situ hybridization [smFISH]). We apply this method to visualize and measure mtDNA and heteroplasmy levels in situ at single-cell resolution in whole-mount Drosophila tissue and cultured human cells. In Drosophila, we identify a somatic mtDNA bottleneck during neurogenesis. This amplifies heteroplasmy variability between neurons, as predicted by a mathematical bottleneck model, predisposing individual neurons to a high mutation load. However, both during neurogenesis and oogenesis, mtDNA segregation is accompanied by purifying selection, promoting wild-type (WT) over pathogenic mtDNA. mtDNA-smFISH thus elucidates how developmental cell-fate transitions, accompanied by changes in cell morphology, behavior, and metabolism, can shape the transmission and selection of deleterious mtDNA variants.
    Keywords:  Drosophila; bottleneck; heteroplasmy; mitochondria; mitochondrial DNA; mitochondrial disease; neurogenesis; oogenesis; purifying selection; single-molecule fluorescent in situ hybridization
    DOI:  https://doi.org/10.1016/j.devcel.2026.03.011
  12. Nat Commun. 2026 05 11. pii: 4228. [Epub ahead of print]17(1):
      The Polo-box domain (PBD) localizes Polo-like kinase 1 (PLK1) near mitotic substrates required for chromosome biorientation. Recent work on mitotic kinetochores showed PLK1 docking begins hierarchically at master docking motifs on BUB1 and CENP-U. Whether master docking motifs have common molecular features remains poorly understood. Presence on CENP-U of two neighbouring motifs generated by initial CDK1 priming and subsequent PLK1 phosphorylation led us to hypothesize PBD dimerization might be involved. Using biochemical, biophysical, and modelling approaches, we gathered strong evidence that CENP-U contains a single master docking motif. The motif is very high affinity and sufficient to form extensive interactions with the PBD, engaging multiple pockets on its surface without obvious added benefits from dimerization. Comparisons with motifs in BUB1, BUBR1, and PRC1 suggest commonalities of master PLK1 docking motifs. We discuss the implications of our observations for the mechanism of PLK1 activation.
    DOI:  https://doi.org/10.1038/s41467-026-73038-8
  13. Annu Rev Cancer Biol. 2026 Apr;10 19-38
      Somatic human cells contain a diploid genome consisting of 23 pairs of chromosomes. The maintenance of this diploid state is essential across all layers of biological organization, ranging from the physiology of individual cells to the proper regulation of tissue homeostasis and organismal development. Most cancer cells, however, harbor an aneuploid genome with an abnormal number of chromosomes, including whole and/or partial chromosome gains and losses. These alterations arise as a consequence of mitotic chromosome segregation errors and/or ongoing chromosomal instability (CIN). While aneuploidy usually imposes a fitness cost to nontransformed cells, certain recurrent aneuploidies confer adaptive advantages that are subjected to positive selection throughout tumorigenesis. In this review, we discuss how aneuploidy impacts cellular physiology, fitness, and adaptability in the context of cancer development. We also examine how the aneuploid state and CIN can create vulnerabilities that may be exploited for therapeutic intervention.
    Keywords:  aneuploidy; cancer genome; cell cycle; cell division; chromosomal instability; chromosome segregation
    DOI:  https://doi.org/10.1146/annurev-cancerbio-071124-101613
  14. Nat Commun. 2026 May 13.
      Targeted protein degradation harnesses endogenous cellular machinery to eliminate disease-causing proteins, yet achieving phenotype-specific degradation across diverse cell types remains challenging. Here we show that antibody-enriched biomolecular condensates formed by liquid-liquid phase separation function as intracellular protein degradation tools, combining cytosolic trafficking with direct proteasome recruitment for targeted substrate clearance. These nanoscale condensates incorporate a short proteasome-targeting motif into phase-separation precursors, preserve antibody activity, enable direct proteasome recruitment, and improve delivery uniformity. When loaded with a mutation-specific antibody, these condensates selectively degrade oncogenic KRAS G12V without affecting wild-type KRAS in heterozygous cells, and suppress tumor growth in a KRAS G12V xenograft model. This strategy provides a modular platform for intracellular protein degradation that can be readily adapted by exchanging antibodies, without requiring genetic modification of cellular system.
    DOI:  https://doi.org/10.1038/s41467-026-72967-8
  15. Genes Dev. 2026 May 15.
      By promoting replication through DNA lesions, translesion synthesis (TLS) DNA polymerases protect against chromosomal instability and tumorigenesis. However, it is not known whether TLS in mammalian cells operates in conjunction with the replisome or in postreplicational gaps and how that impacts genomic stability. Here we show that TLS in human cells operates in close coordination with the replisome and that ATR stabilizes the replisome at the stalled replication fork (RF). In ATR-inhibited cells, the CMG helicase and DNA synthesis components of the replisome disassemble from RFs stalled at DNA lesions, and the composition of TLS and DNA synthesis components and the ensuing TLS and replication mechanisms at the stalled RFs are altered drastically from those in ATR-proficient cells. These alterations include the lack of requirement for Rad18-dependent PCNA ubiquitination for TLS by Polη and primer synthesis by the newly identified PrimPol--PolA1/PolA2 Polα complex. These results reveal the coupling of TLS to DNA replication, thus providing a means for protection against chromosome instability.
    Keywords:  ATR; DNA repair; UV damage; fork stalling; translesion synthesis
    DOI:  https://doi.org/10.1101/gad.353474.125
  16. Nat Commun. 2026 May 13.
      Why some tumors respond to immunotherapy ("hot" tumors) while others remain resistant ("cold" tumors) is a central challenge in oncology. Elevated RAB5A-dependent endocytosis drives tissue fluidization during the transition to invasive breast carcinoma, but its immunological consequences are unclear. Here we show that RAB5A-driven fluidization induces a mechano-metabolic stress response that disrupts the AMPK-AKAP1-DRP1 mitochondrial fission pathway, causing mitochondrial elongation. RAB5A vesicles interact with hyperfused mitochondria and promote BAX/BAK-dependent pore formation, leading to limited mitochondrial outer membrane permeabilization. This sub-lethal event is amplified by palmitoylated GASDERMIN A oligomerization on mitochondria, establishing a positive feedback loop. The resulting release of mitochondrial DNA activates the cGAS-STING innate immune pathway and drives a hyperinflammatory state. Consequently, RAB5A-expressing tumors in immunocompetent mice grow more slowly, show increased immune infiltration, and display enhanced sensitivity to immune-checkpoint blockade in a BAX/BAK-, cGAS/STING-, and mtDNA-dependent manner. These findings connect mechanical stress, mitochondrial dynamics, and innate immunity, revealing strategies to potentiate antitumor immunotherapy.
    DOI:  https://doi.org/10.1038/s41467-026-71795-0
  17. bioRxiv. 2026 Feb 24. pii: 2026.02.23.706394. [Epub ahead of print]
      The development and maintenance of multicellular tissues requires that cell states be closely coupled to their local environment, including geometric and mechanical cues. However, studying this coupling in intact tissues has been challenging, because existing measurement technologies cannot simultaneously assess mechanical properties and molecularly defined cell states. To address this gap, we introduce the Unified Transcriptome and Mechanics Map (UTMM), a method for concurrent measurement of the transcriptome and cytoplasmic stiffness (high-frequency elastic modulus) within intact 3D multicellular structures. UTMM relies on two innovations: (1) a targeted in situ RNA sequencing approach for intact 3D embryos (3DISS), and (2) a strategy that leverages high-frequency intracellular organelle fluctuations to infer cell-level stiffness in vivo . We applied UTMM to mouse embryos from the zygote through the morula stage to characterize how RNA expression and cytoplasmic stiffness become coupled during early lineage specification. Our data reveal that, in the early morula, transcriptional and morphological distinctions emerge between trophectoderm and inner cell mass (ICM) lineages, coinciding with a gradual decrease in cytoplasmic stiffness (softening) across all cells from the 2-cell through morula stages. Furthermore, we observe that early lineage biases align with differential mechanical properties, reflecting distinct emerging developmental programs. When we delayed this softening process via mechanical perturbation, embryonic progression was impeded, highlighting the functional importance of coordinated mechanical and transcriptional changes. Together, these results demonstrate UTMM's ability to bridge molecular and mechanical dynamics in multicellular systems, providing a powerful framework for investigating how biomechanical cues shape cell fate decisions in intact tissues.
    One Sentence Summary: Joint 3D in situ quantification of spatial transcriptome and cytoplasm mechanics in preimplantation mammalian embryos.
    DOI:  https://doi.org/10.64898/2026.02.23.706394
  18. Cell. 2026 May 12. pii: S0092-8674(26)00463-0. [Epub ahead of print]
      Gene regulatory networks modulate the expression of the genome in response to signals and environmental conditions. Reconstructions of such networks can reveal the control principles cells use to maintain homeostasis and execute cell-state transitions. Here, we introduce a computational framework, dimension-scalable single-cell perturbation integration network (D-SPIN), that infers mechanistically interpretable and generative models of gene regulatory networks from single-cell mRNA-seq datasets collected across thousands of perturbation conditions. The models explain how perturbations modulate cell-state proportions by reconfiguring underlying regulatory interactions. Using large Perturb-seq and drug response datasets, D-SPIN models reveal key regulators of cell fate decisions and the coordination of distant cellular pathways in response to gene knockdowns and drug treatments, elucidate how combinations of immunomodulatory drugs induce combinatorial cell states through additive recruitment of gene expression programs, and simulate shifts in immune cell population structures across unobserved drug dosage combinations. D-SPIN provides a computational framework for revealing principles of cellular information processing and physiological control.
    Keywords:  D-SPIN; Perturb-seq; cell-state transition; drug combination; gene regulatory network; immunomodulatory drug; perturbation response; probabilistic graphical model; regulatory network inference; single-cell RNA sequencing
    DOI:  https://doi.org/10.1016/j.cell.2026.04.028
  19. Nature. 2026 May 13.
      Organ intrinsic nervous systems (OINSs) are critical components of the body-brain axis and coordinate visceral organ function with systemic physiological control1-7. Despite their importance, how these distinct neural architectures arise from a common neural crest cell origin has remained unclear. Here we present a systems-level, cross-organ analysis of OINS development, integrating lineage tracing, 3D imaging, single-cell transcriptomics and genetic perturbations across the heart, pancreas, intestine and lungs. We show that differences in neural crest cell migratory trajectories prefigure the spatial architecture of OINSs, laying the foundation for organ-specific patterning. By contrast, molecular identity emerges largely in response to local environments, indicating that extrinsic cues have a major instructive role. Using in vitro co-cultures, we demonstrate that organ-derived cues reprogramme intrinsic neurons towards organ-specific transcriptional profiles and direct neuronal differentiation, with extracellular matrix (ECM) contact as a central mediator. In vivo, ECM-integrin signalling supports neurogenesis of intrinsic cardiac neurons, and ECM crosslinking stabilizes their stereotyped ganglionic organization. Together, these findings reveal that OINS diversity arises through a dual logic: lineage programmes prefigure spatial frameworks, whereas organ-specific cues instruct final molecular identities and architectural precision. This work establishes a conceptual paradigm for how organs actively build their nervous systems, illuminating principles that underlie body-brain integration.
    DOI:  https://doi.org/10.1038/s41586-026-10490-y
  20. Nat Aging. 2026 May 14.
      Sarcopenia and the age-related decline in muscular strength and regenerative capacity contribute directly to loss of autonomy, greater risk for hospitalization and healthcare utilization. One contributing cellular phenotype associated with skeletal muscle aging is a loss in the function and number of resident muscle stem cells (MuSCs) or satellite cells. MuSC activation leads to dramatic changes in cellular architecture and metabolic reprogramming, including both mitochondrial biogenesis and increased glycolysis. Despite these changes to increase energy production, high energy demands may not be fully met during periods of MuSC activation. Here we used in vitro and in vivo approaches in mice to demonstrate the function of glutaminase for age-related changes in MuSC function. By combining fluorescence-activated cell sorting (FACS) isolation with metabolomics and stable isotope tracing, we show an age-related decline in reductive (counterclockwise) flux of glutamine through the tricarboxylic acid (TCA) cycle, a pathway by which MuSCs build cellular fatty acid stores as necessary biomass for MuSC function.
    DOI:  https://doi.org/10.1038/s43587-026-01120-3
  21. Cell. 2026 May 12. pii: S0092-8674(26)00461-7. [Epub ahead of print]
      Directed migration of immune and epithelial cells is critical for rapid responses to tissue injury or infection. Endogenous electric fields, generated by disruption of the transepithelial potential across the skin, are thought to guide cells to wound sites. However, how single cells detect these electrical cues remains unclear. We identified Galvanin (TMEM154), a poorly characterized single-pass transmembrane protein, as required for electric-field-guided migration of rapidly moving cells. Expression of Galvanin is sufficient to confer electric-field-guided migration on otherwise non-responsive epithelial cells. Upon electric-field exposure, Galvanin rapidly relocalizes to the anodal side of cells, and in human neutrophils, relocalization is immediately followed by changes in spatial patterns of cellular protrusion and retraction. These data suggest Galvanin acts as a direct sensor of the electric field, transducing spatial information about a cell's electrical environment to the intracellular migratory apparatus to support directed cell migration.
    Keywords:  CRISPR screen; Galvanin; TMEM154; biophysics; cell biology; directed cell migration; electrotaxis; functional genomics; galvanotaxis; neutrophils
    DOI:  https://doi.org/10.1016/j.cell.2026.04.026
  22. Sci Adv. 2026 May 15. 12(20): eaea4183
      Gap junction plaques (GJPs) enable direct intercellular communication and consist of connexin channels arranged into two-dimensional lattices. While structures of purified connexin channels have informed models of gating, they omit key intracellular regions and lack native context. Here, we use cryo-electron tomography and focused ion beam milling to determine the in situ structure of human connexin 43 (Cx43) GJPs in HEK293 cells at 14-Å resolution. We reveal a previously unresolved structural contribution of the large carboxyl-terminal domain to lateral channel-channel interactions that appear critical for plaque assembly. Coarse-grained molecular dynamics simulations suggest how lipids and cholesterol occupy the space between adjacent connexins. These findings resolve a decades-old question regarding gap junction organization and highlight a mechanistic function for the carboxyl-terminal domain, likely regulated by a helix-loop-helix motif. Our study provides a structural blueprint for understanding how connexin diversity and regulation shape tissue-level communication in health and disease.
    DOI:  https://doi.org/10.1126/sciadv.aea4183
  23. FASEB J. 2026 May 31. 40(10): e71888
      The metabolic regulation in embryos is distinct from that in somatic cells. Early mammalian embryos obtain nutrients from the maternal environment to fulfill the energy requirements of growth and development, and lactate is one of the major substrates of embryonic energy metabolism. To interrogate metabolic regulation during early embryogenesis, we transiently inhibited maternally supplied Lactate dehydrogenase B (LDHB) in early embryos, and found that inhibition led to developmental arrest during the 4- to 8-cell transition, reduced ATP levels, impaired mitochondrial readouts and a decreased NAD+/NADH ratio. Aspartate supplementation rescued developmental progression and restored the NAD+/NADH balance in a malate-aspartate shuttle (MAS)-dependent manner. Together, these data suggest that maternal LDHB is important during the 4- to 8-cell transition to maintain LDH-linked redox homeostasis, and that MAS activity contributes to redox restoration during the rescue. Our study highlights a link between metabolic flexibility, redox homeostasis, and developmental competence during mammalian preimplantation development.
    DOI:  https://doi.org/10.1096/fj.202601428R
  24. Neuron. 2026 May 13. pii: S0896-6273(26)00326-0. [Epub ahead of print]
      In many tissues, stem cells are found lining fluid-filled cavities, and their neighboring niche cells include cells with beating cilia. However, the role of mechanical forces created by cilia beating on stem cells remains elusive. We developed an approach to transiently inhibit the cilia beating of ependymal cells (ECs) lining the forebrain ventricle by injecting magnetic bead-coupled antibodies targeting EC cilia and then applying a magnetic field. We show that EC cilia beating enforces neural stem cell (NSC) quiescence through mechano-sensitive polycystin 1/2 (PKD1/2)- and transient receptor potential melastatin 3 (TRPM3)-mediated Ca2+ transients. Only a few hours of EC cilia beating inhibition triggered NSC activation in vivo. CRISPR-Cas9-mediated deletion of TRPM3 or PKD1/2 in NSCs phenocopied the effect of EC cilia beating inhibition, whereas pharmacological activation of TRPM3 rescued NSC quiescence in the absence of cilia beating. Our data reveal that mechanical forces generated by EC cilia beating regulate NSC quiescence/activation dynamics.
    Keywords:  Ca(2+) signaling; NSCs; PKD1/2; TRPM3; cilia beating; ependymal cells; imaging; mechanical forces; neural stem cells; subventricular zone
    DOI:  https://doi.org/10.1016/j.neuron.2026.04.031
  25. Cell. 2026 May 11. pii: S0092-8674(26)00457-5. [Epub ahead of print]
      Cell fate transitions are driven by regulatory circuitry, yet RNA velocity models cellular dynamics without explicitly accounting for gene regulatory interactions, limiting mechanistic insight. Conversely, gene regulatory network (GRN) inference methods largely neglect the dynamic nature of biological systems. To overcome this conceptual disconnect, we present RegVelo, a bottom-up, actionable, and interpretable deep learning framework that jointly models splicing kinetics and gene regulatory interactions. Across diverse biological systems, RegVelo provides reliable predictive power for terminal states, gene interactions, and perturbation simulations. By applying RegVelo to zebrafish neural crest development using full-length Smart-seq3 and shared gene expression and chromatin accessibility measurements, we delineate regulatory programs underlying fate specification. Guided by in silico perturbations and validated by CRISPR-Cas9 knockout and single-cell Perturb-seq, we establish tfec as an early driver and elf1 as a regulator of pigment cell fate. RegVelo establishes a quantitative framework for bridging gene regulation and cell fate decisions.
    Keywords:  cell fate decision; deep generative modeling; early drivers; gene regulatory network; in silico perturbation; in vivo Perturb-seq; mechanistic modeling; regulatory dynamics; transcriptional dynamics; zebrafish neural crest
    DOI:  https://doi.org/10.1016/j.cell.2026.04.022
  26. bioRxiv. 2026 Mar 01. pii: 2026.02.26.708310. [Epub ahead of print]
      Aging is marked by a decline in cellular functions accompanied by widespread changes in mRNA and protein abundance, yet whether aging broadly remodels subcellular protein localization and concentration-and why some proteins change while others remain stable-remains unclear. This gap matters because cellular function depends not only on expression levels but also on correct spatial organization. Using yeast replicative aging as a model, we built a robotic pipeline to enrich old cells from 5,661 strains, acquired 90 million single-cell 3D images, and applied machine learning to map proteome-wide changes in localization, concentration, and aggregation throughout aging. This age-resolved single-cell atlas uncovers widespread proteome remodeling and rewiring of protein interaction networks. Moreover, structural analysis reveals biophysical determinants of age-sensitive proteome remodeling across ages and species. Together, these results reveal a structure-encoded intrinsic principle underlying spatial proteome breakdown during aging and provide a resource to dissect mechanistic links among aging hallmarks.
    DOI:  https://doi.org/10.64898/2026.02.26.708310
  27. Nat Commun. 2026 May 13.
      Self-assortment of progenitor cells is critical for establishing distinct tissue identities during development, including segregation of the optic cup into the neural retina (NR) and ciliary margin (CM). Although Wnt signaling is required for CM specification, here we show that genetic ablation of β-catenin in the peripheral optic cup does not prevent formation of the CM-derived ciliary body and iris in adult mice. Mosaic analysis reveals that β-catenin-deficient cells are excluded from the CM due to a Wnt-dependent switch from P- to N-cadherin. This cadherin switch drives segregation of otherwise similar cells into distinct clusters, as supported by theoretical modeling and experimental manipulation of cadherin interactions. Consequently, wild-type cells are preferentially retained in the CM niche to support ciliary body formation, a process reversed by deletion of P- and N-cadherins. Together, these findings demonstrate that Wnt signaling can define tissue niches through passive cell competition.
    DOI:  https://doi.org/10.1038/s41467-026-72429-1
  28. J Cell Biol. 2026 Jul 06. pii: e202410019. [Epub ahead of print]225(7):
      The adhesive interactions of neutrophils with postcapillary venules during inflammation have been well studied. However, how neutrophils trigger molecular changes in endothelial cells (EC) during their extravasation requires further exploration. The endothelial actin-binding protein cortactin regulates endothelial contacts and neutrophil-endothelial interactions, but the associated mechanisms remain elusive. Hypothesizing that endothelial cortactin dynamics change during inflammation, using super-resolution confocal microscopy of inflamed mouse cremasteric venules and HUVEC, we report that neutrophil interaction with EC induces reduction in EC cortactin levels. This response was specifically mediated by neutrophil serine proteases, including cathepsin G, that were detected inside EC. The observed cortactin degradation was abolished after inhibition of serine proteases or blockade of neutrophil exocytosis. Finally, the endogenous serine protease inhibitor α1-antitrypsin suppressed cortactin degradation in vivo and reduced neutrophil adhesion and extravasation. Collectively, our data unveil a new mechanism by which neutrophils manipulate proteins inside EC to facilitate their extravasation.
    DOI:  https://doi.org/10.1083/jcb.202410019
  29. Proc Natl Acad Sci U S A. 2026 May 19. 123(20): e2602167123
      Transition toward senescence is a cellular response to various forms of stress. This phenomenon is evolutionarily conserved across species, from insects to humans. Senescent cells (SCs) permanently withdraw from the cell cycle and undergo physiological changes, notably the acquisition of a robust secretory activity characterized by the release of numerous molecules, including cytokines, chemokines, and metalloproteinases. Through this program, termed Senescence-Associated Secretory Phenotype, SCs communicate with and influence their microenvironment. In mammalian tissues, the number of SCs increases with age and their accumulation has been proposed to contribute to age-associated pathologies. Studies in vertebrate systems have demonstrated that new SCs can arise through paracrine signaling from preexisting SCs, a process that requires the activity of the Transforming Growth Factor β (TGF-β). We have investigated the occurrence of paracrine recruitment of SCs in the fruitfly Drosophila. Our results show that an initial stress event induces a primary wave of SCs, comprising approximately 10% of the cell population. Subsequently, a second wave of SCs emerges through paracrine signaling from the initial cohort, increasing the overall proportion of SCs to about 24%. The formation of this second wave is mediated by the growth factor Decapentaplegic (Dpp), a Drosophila ortholog of the TGF-β superfamily. Dpp activates a noncanonical signaling route in non-SCs, driving their conversion to a senescent state. This branch of the Dpp pathway engages components of the innate immune response. Collectively, these findings underscore the evolutionary conservation of senescence-associated signaling networks and suggest that paracrine amplification of senescence may play a role in tumorigenesis.
    Keywords:  Dpp; Drosophila; cellular senescence; immune response
    DOI:  https://doi.org/10.1073/pnas.2602167123
  30. Nat Cell Biol. 2026 May 12.
      Major advances over the past few decades have highlighted the complex regulation of RNA from transcription to nuclear export and from translation to decay. Despite the emerging cellular landscape of malleable and multifunctional RNA molecules, the role of RNA dysregulation in ageing, one of the most fundamental processes of human biology, is underappreciated. Here we focus on ageing-linked dysregulation of the mRNA life cycle. We summarize how RNA metabolism steadily deviates throughout ageing and senescence: in transcription, aged cells bias shorter genes at the expense of complex transcripts; in splicing, ageing-linked alternative exon usage is common; in translation, ribosomal collisions on mRNAs decouple transcriptional output from protein production; and in decay, aberrant RNAs accumulate due to poor degradation activity. We close by discussing how ageing-linked dysregulation of RNA biology can drive cellular stress and thus serve as a therapeutic target to reverse disease.
    DOI:  https://doi.org/10.1038/s41556-026-01946-4
  31. Nat Nanotechnol. 2026 May 14.
      The glycocalyx is a complex layer of glycosylated molecules that surrounds all cells in the human body. It is involved in regulating critical cellular processes, including immune response modulation, cell adhesion and host-pathogen interactions. Despite these insights, the functional relationship between the glycocalyx architecture and cellular state has remained elusive, largely due to the structural diversity of glycocalyx constituents and their nanoscale organization. Here we show that DNA-tagged lectin labelling and metabolic oligosaccharide engineering enable multiplexed super-resolution microscopy of the glycocalyx constituents, yielding an atlas of glycocalyx architecture with nanometre resolution. Quantitative analysis of the obtained nanoscale map of glycocalyx constituents facilitates the extraction of characteristic spatial relationships that accurately report on the cellular state. We demonstrate the capacity of our approach, which we term glycan atlassing, across cell and tissue types, ranging from cultured cell lines to primary immune cells, neurons and primary patient tissue. Glycan atlassing establishes a transformative strategy for investigating glycocalyx remodelling in development and disease, potentially enabling the development of glycocalyx-centred targets in diagnosis and therapy.
    DOI:  https://doi.org/10.1038/s41565-026-02151-y
  32. Nat Aging. 2026 May 12.
      Organs age at different rates, yet the protective mechanisms contributing to decelerated aging in certain tissues remain unclear. Applying cross-tissue comparisons to molecular readouts of aging, here we report that the intervertebral disc (IVD) ages slowly. We link the rate of aging to the persistently hypoxic environment of the IVD, and its unique ability to degrade hypoxia-inducible factor-1α (HIF-1α) in nucleus pulposus cells through optineurin-mediated selective autophagy, thereby uncoupling hypoxia from HIF-1α accumulation and limiting cellular stress. Further, we developed a small-molecule HIF-1α-targeting autophagy-tethering compound (HATC) to pharmacologically export the protective mechanism to other tissues. In aged mice, systemic weekly administration of HATC reduced HIF-1α levels across multiple organs, ameliorated a range of age-related pathologies and significantly extended both median (~14%) and maximum lifespan (~12%). These findings define a regulatory axis in which HIF-1α degradation under hypoxia contributes to longevity, and support HATC as a geroprotective strategy to improve healthspan.
    DOI:  https://doi.org/10.1038/s43587-026-01124-z
  33. Trends Neurosci. 2026 May 14. pii: S0166-2236(26)00077-9. [Epub ahead of print]
      Aging is the predominant risk factor for neurodegenerative diseases, yet the mechanisms linking biological aging to selective neuronal degeneration remain incompletely understood. Accumulating evidence indicates that aging progressively disrupts epigenetic regulation, manifested as increased epigenetic noise in DNA methylation, histone modifications, and chromatin accessibility, which undermines transcriptional precision and the stability of neuronal identity. Recent advances in single-cell and spatial epigenomics further suggest that these age-associated epigenetic alterations are not merely correlative but can actively shape neuronal vulnerability across brain regions and cell types. In this review, we synthesize emerging evidence showing how epigenetic noise contributes to selective neurodegeneration across Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease, and discuss emerging strategies aimed at stabilizing the aging neuronal epigenome.
    Keywords:  Alzheimer’s disease; Huntington’s disease; Parkinson’s disease; amyotrophic lateral sclerosis; frontotemporal dementia; neuroinflammation
    DOI:  https://doi.org/10.1016/j.tins.2026.04.006
  34. Nat Commun. 2026 05 12. pii: 4229. [Epub ahead of print]17(1):
      Endothelial cells lining the vessel network are indispensable for vascular transport but also provide paracrine signals controlling the behavior of nearby cell types. Pericytes are another essential component of the vessel wall, but little is known about their interactions with other cell populations during organ growth and patterning. Here, we use mouse genetics to address the function of three pericyte-derived factors in postnatal lung and brain. We find that inactivation of the gene for hepatocyte growth factor (HGF) or brain-derived neurotrophic factor (BDNF) in pericytes causes no overt alterations in postnatal brain but impairs lung development, which we attribute to defective interaction with AT2 epithelial cells and pulmonary endothelium, respectively. In contrast, pericyte expression of the growth factor Nodal is dispensable for lung morphogenesis but regulates vessel growth and barrier function in the postnatal brain through interactions with endothelial cells, astrocytes and microglia. Taken together, our findings establish that pericytes are a critical source of paracrine signals controlling morphogenetic processes in an organ-specific fashion.
    DOI:  https://doi.org/10.1038/s41467-026-71643-1
  35. Nat Commun. 2026 May 09.
      Collective cell migration is essential in various physiological processes, including embryonic development, wound healing, and cancer metastasis. However, the mechanisms by which individual cells achieve coordinated movement remain elusive. Here, we demonstrate that zonula occludens-1 (ZO-1), a scaffolding protein of tight junctions (TJs), dynamically translocates to form cell-extracellular matrix (ECM) adhesion complexes, podosomes, at the basal cell surface during migration. Extracellular signal-regulated kinase (ERK) activation triggers the translocation of ZO-1 to podosomes, where ZO-1 promotes invasive migration. ZO-1 also contributes to ERK activation dynamics within the cell collective, thereby influencing collective migratory behavior. In this work, we elucidate the dual roles of ZO-1 in coordinating intercellular signaling and invasive movement, providing insights into the mechanisms that integrate individual cell behaviors into a cohesive collective migration.
    DOI:  https://doi.org/10.1038/s41467-026-72840-8