bims-ginsta Biomed News
on Genome instability
Issue of 2026–01–25
27 papers selected by
Jinrong Hu, National University of Singapore



  1. Nat Commun. 2026 Jan 23.
      The skin exhibits extraordinary plasticity, enabling it to adapt to mechanical changes in the environment. While transient deformations are accommodated without lasting structural effects, sustained mechanical stress induces durable tissue changes. To investigate if these responses are mediated by shifts in epidermal stem cell fate, we employed two-photon intravital imaging to visualize epidermal cells in live skin subjected to acute mechanical forces. Mechanical force triggered the formation of intracellular "stress" vesicles within epidermal stem cells that filled with extracellular fluid and progressively enlarged, deforming the nucleus. Lineage tracing analyses revealed that the extent of nuclear deformation can predict cell fate outcomes. Moreover, mechanical stress caused sustained elevation of intracellular calcium in basal epidermal stem cells, and conditional deletion of the mechanosensitive ion channel Piezo1 disrupted calcium dynamics and increased stress vesicle formation. Using human skin xenografts, we demonstrated that stress vesicles are conserved in mammalian skin. Together, these findings identify stress vesicles as key mediators linking mechanical stress, calcium signaling, and epidermal stem cell fate.
    DOI:  https://doi.org/10.1038/s41467-026-68294-7
  2. Genome Biol. 2026 Jan 20.
       BACKGROUND: Transposable elements (TEs) occupy nearly half of the human genome and play diverse biological roles. Despite their abundance, the extent to which TEs contribute to three-dimensional (3D) genome structure remains unclear.
    RESULTS: To investigate this, we generate a modified Hi-C analysis pipeline to probe TE-associated chromatin interactions. Our analysis reveals that TE sequences are responsible for 3D genome structure in interphase nuclei. This phenomenon is mediated by the recruitment of specific epigenetic/transcription factors to TEs, which both promote and impair chromatin contacts. We computationally identified known factors positively associated with chromatin contacts (CTCF, RAD21, SMC3) and chromatin contact impairing proteins (RNF2). Additionally, we identiy potential novel factors (SMARCA4, MAFK), which, when knocked down, lead to decreased chromatin contacts and loops at and between TEs. Notably, SMARCA4 knockdown selectively reduce short-range contacts, highlighting its role in maintaining 3D genome structure through TE binding.
    CONCLUSIONS: Overall, our findings demonstrate that TEs are crucial determinants of 3D genome organization in mammalian cells.
    Keywords:  3D genome; BAF complex; Epigenetics; SMARCA4; Transcription factors; Transposable elements
    DOI:  https://doi.org/10.1186/s13059-026-03945-y
  3. Nature. 2026 Jan 21.
      Plasticity-the ability of cells to undergo phenotypic transitions-drives cancer progression and therapy resistance1-3. Recent studies have suggested that plasticity in solid tumours is concentrated in a minority subset of cancer cells4-6, yet functional studies examining this high-plasticity cell state (HPCS) in situ are lacking. Here we develop mouse models enabling the detection, longitudinal lineage tracing and ablation of the HPCS in autochthonous lung tumours in vivo. Lineage tracing reveals that the HPCS cells possess a high capacity for cell state transitions, giving rise to both early neoplastic (differentiated) and progressed lung cancer cell states in situ. Longitudinal lineage tracing using secreted luciferases reveals that HPCS-derived cells have a high capacity for growth compared with bulk cancer cells or another cancer cell state with features of differentiated lung epithelium. Ablation of HPCS cells in early neoplasias abrogates benign-to-malignant transition, whereas ablation in established tumours by suicide gene or chimeric antigen receptor (CAR) T cells robustly reduces tumour burden. We further demonstrate that the HPCS gives rise to therapy-resistant cell states, whereas HPCS ablation suppresses resistance to chemotherapy and oncoprotein-targeted therapy. Notably, an HPCS-like state is ubiquitous in regenerating epithelia and in carcinomas of multiple other tissues, revealing a convergence of plasticity programs. Our work establishes the HPCS as a critical hub enabling reciprocal transitions between cancer cell states. Targeting the HPCS in lung cancer and in other carcinomas may suppress cancer progression and eradicate treatment resistance.
    DOI:  https://doi.org/10.1038/s41586-025-09985-x
  4. Mol Cell. 2026 Jan 19. pii: S1097-2765(25)01021-4. [Epub ahead of print]
      Natural proteins often form intricate multidomain, oligomeric architectures. This presents a prima facie challenge to cellular homeostasis, as topologically complex proteins seldom refold efficiently in vitro. Here, we show that the efficient folding and assembly of the five-domain homotetramer β-galactosidase is obligatorily coupled to its synthesis on the ribosome, and we define the underlying mechanisms. During refolding from a denaturant, maturation of the catalytic domain is frustrated. Assembly outpaces monomer folding, and non-native oligomers accumulate. Efficient de novo folding is characterized by segmental domain folding, shaped by the binding of a nascent amphipathic helix to a cryptic pocket on uL23 on the ribosome surface. Homomer assembly also initiates cotranslationally via recruitment of a full-length subunit to the nascent polypeptide, and the failure to do so results in misassembly. Our results reveal how the ribosome can dictate the timing of folding and assembly to enable efficient biogenesis of a topologically complex protein.
    Keywords:  cotranslational folding; protein assembly; protein folding; ribosome
    DOI:  https://doi.org/10.1016/j.molcel.2025.12.022
  5. Development. 2026 Jan 20. pii: dev.204549. [Epub ahead of print]
      During development, spatial-temporally patterned tissue-level stresses and mechanical properties create diverse tissue shapes. To understand the mechanics of small-scale embryonic tissues, precisely controlled sensors and actuators are needed. Previously, we reported a control-based approach named tissue force microscopy (TiFM1.0), which combines dynamic positioning and imaging of an inserted cantilever probe to directly measure and impose forces in early avian embryos. Here we present an upgraded system (TiFM2.0) that utilises interferometer positioning to minimise probe holder footprint, enhancing accessibility and imaging signal. This new design enables a double-probe configuration for bidirectional stretching, compression and stress propagation experiments. As proof-of-concept, we showcase a variety of examples of TiFM2.0 applications in chicken and zebrafish embryos, including the characterization of mechanical heterogeneities important for the morphogenesis of the chicken posterior body axis. We also present simplified designs and protocols for the replication of TiFM systems with minimal custom engineering for developmental biology labs.
    Keywords:  Body axis; Embryo; Force; Morphogenesis; Rheological property; Tissue mechanics
    DOI:  https://doi.org/10.1242/dev.204549
  6. Cancer Res. 2026 Jan 22.
      Whole genome doubling (WGD) is a frequent event in cancer evolution associated with chromosomal instability, metastasis, and poor prognosis. While the genomic consequences of WGD are well documented, non-genetic alterations that accompany WGD, such as changes to cell and nuclear size, may also play an important role in tetraploid (4N) cancer cell physiology. Here, we showed that cell and nuclear volume do not always scale with DNA content after WGD in cancer cells, resulting in 4N cells that differ in size. Small size was associated with enhanced cell fitness, mitotic fidelity, and tumorigenicity in 4N cancer cells and with poor patient survival in WGD-positive human cancers. Overall, these results suggest that cell and nuclear size may contribute to the tumorigenic potential of 4N cancer cells and could be an important prognostic marker in human tumors that undergo WGD.
    DOI:  https://doi.org/10.1158/0008-5472.CAN-24-3718
  7. Cell Stem Cell. 2026 Jan 21. pii: S1934-5909(25)00457-6. [Epub ahead of print]
      Organoids derived from pluripotent stem cells have emerged as powerful models to study human development. To investigate signaling pathways regulating human pancreas differentiation and morphogenesis, we developed a high-content, image-based screen and quantitative multivariate analysis pipelines robust to heterogeneity to extract single-cell and organoid features using pancreatic progenitor organoids. Here, we identified 54 compounds affecting cell identity and/or morphological landscape. Focusing on one family of compounds, we found that glycogen synthase kinase 3α/β (GSK3A/B) inhibition via wingless/int-1 (WNT) signaling has a reversible effect on cell identity, repressing pancreatic progenitor markers and inducing a poised state in progenitors transitioning to acinar cells. We show that additional fibroblast growth factor (FGF) repression enables further differentiation of acinar cells, recapitulating pancreatic acinar morphogenesis and function. The ability to produce acinar cells is valuable for future studies on pancreatic exocrine function and cancer initiation in humans, as acinar cells are thought to be an important cell of origin for pancreatic adenocarcinoma.
    Keywords:  WNT; acinar differentiation; high-content drug screening; human pancreas organoids; image analysis; organoid morphology; pancreas development
    DOI:  https://doi.org/10.1016/j.stem.2025.12.023
  8. J Clin Invest. 2026 Jan 22. pii: e192225. [Epub ahead of print]
      Transitions of cancer cells between distinct cell states, which are typically driven by transcription reprogramming, fuel tumor plasticity, metastasis, and therapeutic resistance. Whether the transitions between cell states can be therapeutically targeted remains unknown. Here, using the epithelial-to-mesenchymal transition (EMT) as a model, we show that the transcription reprogramming during a cell-state transition induces genomic instability through R-loops and transcription-replication conflicts, and the cell-state transition cannot occur without the ATR kinase, a key regulator of the replication stress response. ATR inhibition during EMT not only increases transcription- and replication-dependent genomic instability but also disrupts transcription reprogramming. Unexpectedly, ATR inhibition elevates R-loop-associated DNA damage at the SNAI1 gene, a key driver of the transcription reprogramming during EMT, triggering ATM- and Polycomb-mediated transcription repression of SNAI1. Beyond SNAI1, ATR also suppresses R-loops and antagonizes repressive chromatin at a subset of EMT genes. Importantly, inhibition of ATR in tumors undergoing EMT reduces tumor growth and metastasis, suggesting that ATR inhibition eliminates cancer cells in transition. Thus, during EMT, ATR not only protects genome integrity but also enables transcription reprogramming, revealing that ATR is a safeguard of cell-state transitions and a target to suppress tumor plasticity.
    Keywords:  Cancer; Cell biology; Oncology
    DOI:  https://doi.org/10.1172/JCI192225
  9. J Cell Biol. 2026 Feb 02. pii: e202502087. [Epub ahead of print]225(2):
      The cyclin-dependent kinase subunit CKS remains poorly understood. We found that Caenorhabditis elegans CKS-1 and its partner CDK-1 co-localized to the cytosol, chromosomes, and spindle structures throughout cell division. Nevertheless, CKS-1 was required well after CDK-1, during oocyte meiosis I metaphase, which was prolonged in cks-1 mutants. Anaphase A precedes anaphase B in C. elegans oocytes, and while delayed in onset, chromosomes in cks-1 mutants separated normally during meiosis I anaphase A but failed to separate further and instead rapidly transitioned into meiosis II prometaphase, skipping anaphase B. The anaphase A to B transition also was defective during meiosis II. Furthermore, meiosis I anaphase B required that CKS-1 be bound to CDK-1 and have a functional anion pocket. Finally, our results suggest that CKS-1 promotes anaphase onset during meiosis I through securin destruction and during meiosis II through cyclin B1 destruction, and that both securin and cyclin B3 have positive roles independent of their destruction during meiosis II.
    DOI:  https://doi.org/10.1083/jcb.202502087
  10. J Cell Biol. 2026 Mar 02. pii: e202507211. [Epub ahead of print]225(3):
      Collective cell migration is essential for development and tissue homeostasis and plays a central role in pathological processes such as tumor metastasis. While extensively studied in epithelial cells, collective migration is also observed in mesenchymal cells, though the mechanistic similarities and differences between these modes remain unclear. Here, we use neural crest (NC) cells to investigate collective chemotaxis in epithelial and mesenchymal states within the same lineage. Mesenchymal NC clusters migrate collectively toward the chemoattractant SDF-1 through rear-directed contractility of supracellular actomyosin cables and polarized front-edge protrusions. In contrast, epithelial NC cells exhibit polarized cryptic protrusions and increased active Rac1 localization at E-cadherin-mediated junctions. During epithelial chemotaxis, traction forces originate from internal cell-cell junctions, whereas in mesenchymal clusters, they remain peripheral. Our findings reveal that mesenchymal collective chemotaxis relies on supracellular force coordination, while epithelial chemotaxis depends on force generation by individual cells within the collective.
    DOI:  https://doi.org/10.1083/jcb.202507211
  11. Nat Mater. 2026 Jan 19.
      Biological processes are regulated by chemical and mechanical signals, yet how these signalling modalities interact remains poorly understood. Here we identify a crosstalk between tissue stiffness and long-range chemical signalling in the developing Xenopus laevis brain. Targeted knockdown of the mechanosensitive ion channel Piezo1 in retinal ganglion cells or in the brain tissue surrounding retinal ganglion cells causes pathfinding errors in vivo. In the brain parenchyma, Piezo1 downregulation decreases the expression of the diffusive long-range chemical guidance cues Semaphorin3A (Sema3A) and Slit1, which instruct turning responses in distant cells. Furthermore, Piezo1 knockdown results in tissue softening due to reduced expression of the adhesion proteins NCAM1 and N-cadherin. Targeted depletion of NCAM1 and N-cadherin similarly reduces tissue stiffness and Sema3A expression. Conversely, increasing environmental stiffness ex vivo enhances tissue-level force generation and Slit1 and Sema3A expression. Finally, in vivo stiffening of soft brain regions induces ectopic Sema3A production via a Piezo1-dependent mechanism. Overall, these findings demonstrate that tissue mechanics locally modulates the availability of diffusive, long-range chemical signals, thus influencing cell function at sites distant from the mechanical cue.
    DOI:  https://doi.org/10.1038/s41563-025-02463-9
  12. Nat Aging. 2026 Jan 22.
      Cardiac aging is a major driver of cardiovascular diseases and associated mortality, yet its therapeutic options are limited. While long interspersed nuclear element-1 (LINE-1) retrotransposons are known to drive cellular senescence, their role in cardiac aging is poorly defined. Here we showed that LINE-1 expression increased in the heart with age. To investigate their role in cardiac aging, we generated cardiomyocyte-specific Mov10-knockout mice, which failed to suppress LINE-1. These mice developed LINE-1 derepression, cardiac dysfunction and premature cardiac aging by 3 months of age, accompanied by cGAS-STING activation. Pharmacological inhibition of LINE-1 reverse transcription (with 3TC) or STING (with H-151) suppressed cGAS-STING activation and attenuated senescence in Mov10-knockout H9C2 cells. Notably, both inhibitors improved cardiac function and reduced cardiac inflammation and senescence phenotypes in naturally aged mice. Together, our findings establish LINE-1 as a driver of cardiac aging via cGAS-STING activation, highlighting LINE-1 and its downstream effectors as therapeutic targets for age-related cardiac dysfunction.
    DOI:  https://doi.org/10.1038/s43587-025-01056-0
  13. Cell. 2026 Jan 16. pii: S0092-8674(25)01374-1. [Epub ahead of print]
      Essential for eukaryotes, multiple copies of the exocyst complex tether each secretory vesicle to the plasma membrane (PM) in constitutive exocytosis. The exocyst higher-order structure (ExHOS) that coordinates the action of these multiple exocysts remains unexplored. We integrated particle tracking, super-resolution microscopy, and cryo-electron tomography to time-resolve the continuum conformational landscape of the ExHOS and to functionally annotate its different conformations. We found that 7 exocysts form a flexible ring-shaped ExHOS that tethers vesicles at <45 nm from the PM. The ExHOS rapidly expands while pulling the vesicle toward the PM in a stepwise mechanism comprising three metastable states at 27, 18, and 5 nm from the PM. After fusion, Sec18 mediates the disassembly of the stationary ExHOS, a function that controls the rate of exocytosis. By resolving biophysical principles in situ, we reconstructed the spatiotemporal dynamics of the multimeric architecture controlling vesicle tethering in exocytosis.
    Keywords:  Sec18; constitutive exocytosis; cryo-electron tomography; exocyst; exocyst higher-order structure; in situ structural biology; metastable states; particle tracking; single molecule localization microscopy; vesicle tethering
    DOI:  https://doi.org/10.1016/j.cell.2025.11.038
  14. bioRxiv. 2025 Dec 11. pii: 2025.12.09.693231. [Epub ahead of print]
    Human Genome Structural Variation Consortium
      Centromeres are essential for accurate chromosome segregation during cell division, yet their highly repetitive sequence has historically hindered their complete assembly and characterization. Consequently, the full spectrum of centromere diversity across individuals, populations, and evolutionary contexts remains largely unexplored. Here, we address this gap in knowledge by assembling and characterizing 2,110 complete human centromeres from a diverse cohort of individuals representing 5 continental and 28 population groups. By developing a novel suite of bioinformatic tools tailored for centromeric regions, we uncover previously unknown variation within centromeres, including 226 novel centromere haplotypes and 1,870 new α-satellite higher-order repeat (HOR) variants. We find that mobile element insertions are present in 30% of centromeres, with chromosome 16 harboring Alu elements within the kinetochore site at an 11-fold higher frequency than expected. While most centromeres have a single kinetochore site, 6% of them have di-kinetochores, and <<1% have tri-kinetochores, which we confirm with long-read CENP-A CUT&RUN, DiMeLo-seq, and multi-generational inheritance. We further show that the position of the kinetochore is not random and is, instead, closely associated with the underlying sequence and structure of the centromere. To understand the nature of evolutionary change, we compared 2,110 complete human centromeres to 5,747 complete centromeres recently assembled from the Human Pangenome Reference Consortium. We show that centromeres have a >50-fold variation in mutation rate, with the most rapidly mutating centromeres on chromosome 1 and the slowest mutating centromeres on chromosome Y. Additionally, a subset of centromeres show evidence of introgression from archaic hominins, shaping their sequence, structure, and evolutionary history. We validate these centromere mutation rates in a four-generation family, spanning 28 family members and 483 accurately assembled centromeres, and show that the kinetochore site is the most rapidly mutating region in the centromere, with twofold more single-nucleotide variants than the rest of the centromeric α-satellite HOR array on average. We propose a model that reveals an 'arms race' between centromeric sequence and proteins, with frequent mutations within the site of the kinetochore that lead to changes in genetic and epigenetic landscapes and, ultimately, rapid evolution of these critically important regions.
    DOI:  https://doi.org/10.64898/2025.12.09.693231
  15. Nat Chem Biol. 2026 Jan 20.
      Mammalian cells receive signaling instructions through interactions on their surfaces. Proteoglycans are critical to these interactions, carrying long glycosaminoglycans that recruit signaling molecules. Biosynthetic redundancy in the first glycosylation step by two xylosyltransferases XT1/2 complicates annotation of proteoglycans. Here we develop a chemical genetic strategy that manipulates the glycan attachment site of cellular proteoglycans. Through a bump-and-hole tactic, we engineer the two isoenzymes XT1 and XT2 to specifically transfer the chemically tagged xylose analog 6AzGlc to target proteins. The tag contains a bioorthogonal functionality, allowing to visualize and profile target proteins in mammalian cells. Unlike xylose analogs, 6AzGlc is amenable to cellular nucleotide-sugar biosynthesis, establishing the XT1/2 bump-and-hole tactic in cells. The approach allows pinpointing glycosylation sites by mass spectrometry and exploiting the chemical handle to manufacture proteoglycans with defined glycosaminoglycan chains for cellular applications. Engineered XT enzymes permit an orthogonal view into proteoglycan biology through conventional techniques in biochemistry.
    DOI:  https://doi.org/10.1038/s41589-025-02113-w
  16. Curr Biol. 2026 Jan 16. pii: S0960-9822(25)01632-X. [Epub ahead of print]
      Epithelial sheet integrity is established by adherent contacts that form between cells at the interface between their apical and basolateral domains. Although cell contacts are reinforced by actomyosin contractility, which generates tension that propagates across the apical surface, how epithelial cells tune tension to reinforce junctions without compromising their physical barrier properties remains unclear. Herein, we report that Sperm Flagellar 1 (Spef1) is a microvillar component enriched in the apical domain and terminal web of enterocytes that prevents actomyosin hypercontractility. The loss of function of Spef1 in Caco-2 BBE cells induced invaginations of the apical domain at tricellular contacts, with a redistribution of the tricellular and tight junction components. These changes were driven by an increase in the NM2A:NM2C heavy chain ratio, which elevated tension throughout the apical surface and ultimately compromised barrier function. These findings highlight Spef1 as a microvillar resident that tunes actomyosin contractility across the apical surface to a level appropriate for junctional reinforcement and maintenance of epithelial function.
    Keywords:  barrier function; cell contractility; microvilli; tight junctions
    DOI:  https://doi.org/10.1016/j.cub.2025.12.011
  17. Nature. 2026 Jan 21.
      Neurodegenerative diseases affect 1 in 12 people globally and remain incurable. Central to their pathogenesis is a loss of neuronal protein maintenance and the accumulation of protein aggregates with ageing1,2. Here we engineered bioorthogonal tools3 that enabled us to tag the nascent neuronal proteome and study its turnover with ageing, its propensity to aggregate and its interaction with microglia. We show that neuronal protein half-life approximately doubles on average between 4-month-old and 24-month-old mice, with the stability of individual proteins differing among brain regions. Furthermore, we describe the aged neuronal 'aggregome', which encompasses 1,726 proteins, nearly half of which show reduced degradation with age. The aggregome includes well-known proteins linked to diseases and numerous proteins previously not associated with neurodegeneration. Notably, we demonstrate that neuronal proteins accumulate in aged microglia, with 54% also displaying reduced degradation and/or aggregation with age. Among these proteins, synaptic proteins are highly enriched, which suggests that there is a cascade of events that emerge from impaired synaptic protein turnover and aggregation to the disposal of these proteins, possibly through microglial engulfment of synapses. These findings reveal the substantial loss of neuronal proteome maintenance with ageing, which could be causal for age-related synapse loss and cognitive decline.
    DOI:  https://doi.org/10.1038/s41586-025-09987-9
  18. Development. 2026 Jan 15. pii: dev204789. [Epub ahead of print]153(2):
      Spatial regulation of Notch signaling is crucial for tissue patterning, yet how compartment-specific activation thresholds are set remains unclear. Here, we identify Kuzbanian (Kuz) expression as a key spatially controlled determinant in the Drosophila midgut. Kuz is suppressed in the copper cell region by BMP signaling and induced by EGFR activity in adjacent compartments, directly explaining regional differences in Notch activation. Strikingly, elevated Kuz expression alone is sufficient to cleave Notch and trigger ligand-independent signaling. cis-Delta potently inhibits this non-canonical activation, establishing it as a key safeguard. Furthermore, high Kuz levels enable trans-Delta ligands on neighboring cells to overcome cis-inhibition. These findings support a model in which spatially defined Kuz expression sets a proteolytic threshold that determines the outcome of competition between cis-inhibition and trans-activation. Our findings reposition Kuz/ADAM10 as a crucial spatial regulator of Notch signaling, providing a new framework for understanding signal integration in vivo.
    Keywords:   Drosophila ; ADAM10; Kuzbanian; Ligand-independent Notch activation; Midgut; Notch cis-inhibition; S2 cleavage
    DOI:  https://doi.org/10.1242/dev.204789
  19. Dev Cell. 2026 Jan 19. pii: S1534-5807(25)00772-5. [Epub ahead of print]
      The mesothelium is a squamous monolayer that ensheathes internal organs and lines the body cavities. Aside from facilitating tissue sliding, its additional functions remain poorly understood. Here, we study the mesothelium through investigating myelin regulatory factor (Myrf), a transcription factor expressed in the mesothelium and a top mutated gene in congenital diaphragmatic hernia (CDH), a developmental disorder that affects the lung and diaphragm. In mice, inactivation of Myrf early in embryogenesis resulted in CDH and defective mesothelium specification, compromising its role as a signaling center for lung growth. Inactivation after mesothelium specification led to additional defects, including enhanced differentiation into various mesenchymal cell types, causing a striking accumulation of elastin-expressing smooth muscle/myofibroblasts encasing the lung, mimicking pleuroparenchymal fibroelastosis (PPFE), a rare adult lung condition. Compound mutants demonstrate that MYRF functions synergistically with YAP/TAZ in mesothelium differentiation. Together, these findings highlight the complex role of the mesothelium in development and disease.
    Keywords:  Hippo signaling; MYRF; TAZ; YAP; congenital diaphragmatic hernia; lung; mesothelium; mesothelium-to-mesenchyme transition; pleuroparenchymal fibroelastosis
    DOI:  https://doi.org/10.1016/j.devcel.2025.12.011
  20. J Cell Biol. 2026 Mar 02. pii: e202504025. [Epub ahead of print]225(3):
      Cell migration and cytoskeletal remodeling are energetically demanding processes. Reorganizing the cytoskeleton requires ATP to fuel the actomyosin complex, enabling cells to adhere to and migrate through a matrix. While it is known that energy is required for cell migration, the mechanism by which cell-extracellular matrix adhesion influences cell energetics is unclear. Here, we investigated the relationship between cell-extracellular matrix adhesion and cellular metabolic state with a focus on vinculin given its role in connecting the cytoskeleton to focal adhesions and extracellular space. Knocking out vinculin increases the metabolic activity in cells and results in fast, frequent Rho kinase activity-dependent changes in cell shape and protrusions. The cellular protrusion dynamics and bioenergetics are interrelated processes, as stimulating RhoA/Rho kinase activity increases dynamic blebbing protrusions and energy production, and inhibiting metabolism decreases the frequency of blebbing cell protrusions. This link between cell-extracellular matrix adhesion and bioenergetics provides a novel basis by which cellular metabolism and cell migration could be controlled.
    DOI:  https://doi.org/10.1083/jcb.202504025
  21. Aging Cell. 2026 Feb;25(2): e70386
      Calorie restriction (CR) is a robust intervention for improving metabolic health and delaying obesity and age-related diseases, yet its translational utility is limited by adherence challenges and diminished effectiveness later in life. Dietary protein restriction (DPR), which reduces dietary protein without decreasing total caloric intake, has emerged as a promising alternative, yet its cardioprotective potential in the context of obesity and aging remains poorly understood. Here, we demonstrate that DPR mitigates obesity-induced cardiac remodeling and inflammaging by activating the AMPK-ULK1 signaling axis and enhancing mitochondrial quality control. In middle-aged male mice with high-fat diet-induced obesity, 4 months of DPR attenuated cardiac hypertrophy and normalized heart failure markers, independently of FGF21 signaling. Transcriptomic and protein analyses revealed that DPR suppressed the activation of the cGAS-STING pathway, reduced mitochondrial DNA release into the cytosol, and blunted expression of pro-inflammatory mediators, including IRF3 and IFN-γ. DPR also restored mitochondrial dynamics, enhanced mitophagy, and maintained ATP content despite reduced respiratory capacity. Mechanistically, DPR increased AMPK-dependent ULK1 phosphorylation while suppressing mTOR signaling, thereby promoting mitochondrial turnover. These effects were confirmed in cardiomyocytes, where AMPK knockdown abrogated ULK1 activation and mitophagy under conditions of low amino acid availability. Together, these findings uncover a novel mechanism by which DPR attenuates cardiac inflammation and supports mitochondrial homeostasis, highlighting its therapeutic potential for enhancing cardiovascular health during obesity-mediated inflammaging.
    Keywords:  bioenergetics; fission; fusion; heart; mitochondria; obesity; quality control
    DOI:  https://doi.org/10.1111/acel.70386
  22. Nature. 2026 Jan 21.
      Physiological and pathological processes such as inflammation and cancer emerge from interactions between cells over time1. However, methods to follow cell populations over time within the native context of a human tissue are lacking because a biopsy offers only a single snapshot. Here we present one-shot tissue dynamics reconstruction (OSDR), an approach to estimate a dynamical model of cell populations based on a single tissue sample. OSDR uses spatial proteomics to learn how the composition of cellular neighbourhoods influences division rate, providing a dynamical model of cell population change over time. We apply OSDR to human breast cancer data2-4, and reconstruct two fixed points of fibroblasts and macrophage interactions5,6. These fixed points correspond to hot and cold fibrosis7, in agreement with co-culture experiments that measured these dynamics directly8. We then use OSDR to discover a pulse-generating excitable circuit of T and B cells in the tumour microenvironment, suggesting temporal flares of anticancer immune responses. Finally, we study longitudinal biopsies from a triple-negative breast cancer clinical trial3, in which OSDR predicts the collapse of the tumour cell population in responders but not in non-responders, based on early-treatment biopsies. OSDR can be applied to a wide range of spatial proteomics assays to enable analysis of tissue dynamics based on patient biopsies.
    DOI:  https://doi.org/10.1038/s41586-025-09876-1
  23. Biophys J. 2026 Jan 16. pii: S0006-3495(26)00041-X. [Epub ahead of print]
      Cell junction remodeling is central to epithelial morphogenesis and tissue rheology, and depends on the interplay between adhesion molecules and the actomyosin cortex. E-cadherin constitutes the molecular basis for epithelial cell adhesion, while cortical actomyosin plays a major role in intracellular force generation. However, the precise nanoscale organization and relationship between F-actin and E-cadherin at the cell interface still remain insufficiently understood. Here, we applied super-resolution DNA/peptide-PAINT microscopy to reveal the nanoscopic clustering of E-cadherin and its junctional distribution in relation to cortical F-actin at adherens junctions in the Drosophila embryonic epidermis. We were able to resolve distinct pairs of E-cadherin clusters approximately 45 nm apart on opposite sides of the adherens junctions. Intriguingly, these paired clusters were interspersed with unpaired clusters, lacking corresponding counterparts across the junction. We observed that cluster size, spatial arrangement, and cross-junction matching change during development and depend on N-glycosylation, a post-translational modification affecting E-cadherin. Moreover, the organization of F-actin cortices between neighboring cells were found to be strongly correlated at junctions. Contrary to expectations, this intercellular F-actin correlation was observed independently of E-cadherin. Our study provides new insights into the nanoscale organization of adherens junctions, opening a window into the molecular mechanism of adhesion and mechanics of epithelial cells during morphogenesis.
    DOI:  https://doi.org/10.1016/j.bpj.2026.01.026
  24. Science. 2026 Jan 22. 391(6783): eadu2896
      Oligodendrocytes form myelin sheaths around axons to enable rapid signaling within neural circuits. The generation of new oligodendrocytes through differentiation of oligodendrocyte precursor cells (OPCs) promotes myelin plasticity and repair in the adult brain. Here, we performed genetic interrogation and in vivo analysis of OPCs in the mouse brain to determine their differentiation dynamics. Our results show that OPCs attempt to differentiate throughout the adult central nervous system with spatial and temporal regularity. The differentiation rate was not influenced by myelin demand or oligodendrocyte loss and declined with age and in response to acute inflammation. The results suggest that OPC differentiation is governed primarily by constitutive processes and might be negatively influenced by aging and inflammation.
    DOI:  https://doi.org/10.1126/science.adu2896
  25. Science. 2026 Jan 22. 391(6783): eadv5257
      Zygotic genome activation (ZGA) failure leads to developmental arrest and poses a clinical challenge to women's fertility. We observed that human embryos arresting at the eight-cell ZGA stage exhibited specific down-regulation of endogenous retrovirus MLT2A1. Depleting MLT2A1 resulted in a failure in embryo development and a reduction in ZGA gene expression. Mechanistically, MLT2A1s synthesized chimeric transcripts with downstream coding and noncoding sequences, predominantly with heterologous retro-transposable elements. These diverse fusion sequences expanded the genome-targeting spectrum of MLT2A1 RNAs. Nevertheless, the shared MLT2A1 sequences partnered with heterogeneous nuclear ribonucleoprotein U (HNRNPU) to recruit RNA polymerase II, promoting global transcription of ZGA genes and autoamplification of the MLT2A1 subfamily. Thus, MLT2A1 chimeric RNAs formed an interlocking network that acts synergistically to boost human ZGA and early embryogenesis.
    DOI:  https://doi.org/10.1126/science.adv5257
  26. Nature. 2026 Jan 21.
      Tissue-resident macrophages (RTMs) form during embryogenesis, self-renew locally, and regulate tissue homeostasis by clearing dead cells and debris1-6. During tissue damage, however, bone-marrow-derived monocytes enter tissues and differentiate into RTMs, repairing the tissue and replenishing macrophages in the niche1. The universal cell-intrinsic mechanisms that control the monocyte-to-RTM transition and the maintenance of mature RTMs across tissues remain elusive3. Here we show that deoxyhypusine synthase (DHPS), an enzyme that mediates spermidine-dependent hypusine modification of translation factor eIF5A5,7, is required for RTM differentiation and maintenance. Mice with myeloid cell lack of DHPS (Dhps-ΔM mice) had a global defect in RTMs across tissues, resulting in persistent but ultimately futile monocyte influx. Transcriptional analyses of DHPS-deficient macrophages indicated a block in their ability to differentiate into mature RTMs, whereas proteomics revealed defects in cell adhesion and signalling pathways. Sequencing of ribosome-engaged transcripts identified a subset of mRNAs involved in cell adhesion and signalling that rely on DHPS for efficient translation. Imaging of DHPS-deficient macrophages in tissues showed differences in morphology and tissue interactions, which were correlated with their failed RTM differentiation. DHPS-deficient macrophages were also defective in critical homeostatic RTM functions including efferocytosis and tissue maintenance. Together, our results demonstrate a cell-intrinsic, tissue-agnostic pathway that drives differentiation of monocyte-derived macrophages into RTMs.
    DOI:  https://doi.org/10.1038/s41586-025-09972-2
  27. Nat Commun. 2026 Jan 21.
      Stem cell pluripotency relies on a finely tuned interplay between transcription factors and epigenetic regulators. Here, we identify a direct interaction between NANOG, a master pluripotency transcription factor, and WDR5, a core chromatin regulator essential for maintaining stem cell identity. Mechanistically, WDR5 remodels irregular NANOG aggregates into dynamic, liquid-liquid phase-separated condensates at pluripotency-associated promoters to activate target genes. Structural analyses show that the NANOG homeodomain engages WDR5 through an extended interface distinct from previously characterized short linear motifs. The NANOG R153A mutation disrupts this interaction, leading to impaired condensate formation, reduced chromatin co-occupancy, and diminished levels of active histone marks, ultimately compromising embryonic stem cell pluripotency. Pharmacological inhibition of the WDR5-NANOG interaction suppresses leukemia stem cell expansion in vivo, highlighting its therapeutic potential. Collectively, this study reveals that WDR5-dependent regulation of NANOG condensate dynamics links phase-separated assemblies to transcriptional control of stem cell identity in physiological and pathological contexts.
    DOI:  https://doi.org/10.1038/s41467-026-68623-w