bims-ginsta Biomed News
on Genome instability
Issue of 2026–03–15
fifty papers selected by
Jinrong Hu, National University of Singapore



  1. Dev Cell. 2026 Mar 12. pii: S1534-5807(26)00078-X. [Epub ahead of print]
      Subcellular compartmentalization allows cells to spatially control molecular functions. We show that in mouse and human epidermal cells, translational machinery is enriched at the cell cortex, where a large subset of mRNAs is also localized, defining a previously unrecognized axis of mRNA organization. The desmosomal protein desmoplakin is required for the cortical recruitment of both ribosomes and mRNAs via distinct mechanisms. Surprisingly, many cortex-localized transcripts are not actively translated but instead are translationally repressed. This spatially restricted regulation involves the RNA-induced silencing complex (RISC), which is also enriched at the cortex in a desmoplakin-dependent manner. Under homeostatic conditions, cortical RISC associates with mRNAs encoding cell adhesion and cytoskeletal proteins. Following wounding, these RISC-associated transcripts become translationally activated. Together, our findings reveal a dynamic, desmosome-dependent cortical compartmentalization of translation that responds to epithelial barrier disruption.
    Keywords:  RISC; compartmentalization; desmoplakin; desmosome; mRNA localization; ribosome; translation; translatome
    DOI:  https://doi.org/10.1016/j.devcel.2026.02.013
  2. Curr Biol. 2026 Mar 09. pii: S0960-9822(26)00128-4. [Epub ahead of print]36(5): R210-R228
      Aneuploidy, an imbalance in the number of chromosomes, is highly detrimental at both the cellular and the organismal levels and is the major cause of miscarriages in humans. Despite its deleterious effects, recent data have revealed a high prevalence of aneuploidy in early human embryos. On one hand, organismal aneuploidy is strikingly common due to the high frequency of aneuploid gametes, particularly aged oocytes. On the other hand, mosaic aneuploidy has been recently shown to be also widespread in early embryos, due to a high rate of chromosome segregation errors during the first post-zygotic divisions. Of note, aneuploid mosaic embryos can result in healthy individuals. Here, we review the compatibility of aneuploidy with correct embryo development and also address the presence of aneuploidy in normal somatic tissues, and the implication of aneuploid mosaicism for the processes of aging and tumorigenesis. We place particular emphasis on how different kinds of aneuploidies, either trisomies or monosomies, whole-chromosome or segmental, differentially contribute to the discussed processes. Finally, we highlight how cell competition may serve as a crucial mechanism by which both developing and somatic tissues deal with the emergence of aneuploidy.
    DOI:  https://doi.org/10.1016/j.cub.2026.01.056
  3. Nat Commun. 2026 Mar 10.
      Cardiac chambers emerge from a heart tube that balloons and bends to create expanded ventricular and atrial structures, each containing a convex outer curvature (OC) and a recessed inner curvature (IC). The cellular and molecular mechanisms underlying the formation of these characteristic curvatures remain poorly understood. Here, we demonstrate in zebrafish that the initially similar populations of OC and IC ventricular cardiomyocytes diverge in the organization of their actomyosin cytoskeleton and subsequently acquire distinct OC and IC cell shapes. Altering actomyosin dynamics hinders cell shape changes in the OC, and mosaic analyses indicate that actomyosin regulates cardiomyocyte shape in a cell-autonomous manner. Additionally, both biomechanical cues and the transcription factor Tbx5a influence the basal enrichment of actomyosin and squamous cell morphologies in the OC. Together, our findings demonstrate that intrinsic and extrinsic factors intersect to control actomyosin organization in OC cardiomyocytes, which in turn promotes the cell shape changes that accompany curvature morphogenesis.
    DOI:  https://doi.org/10.1038/s41467-026-70384-5
  4. Cell Metab. 2026 Mar 11. pii: S1550-4131(26)00053-7. [Epub ahead of print]
      Aging is associated with oxidative stress, but specific druggable pathways remain elusive. Here, we define a conserved iron-lipid axis driving primate aging, termed "ferro-aging." Multi-tissue profiling in humans and non-human primates reveals age-progressive iron accumulation, fueling chronic lipid peroxidation orchestrated by acyl-coenzyme A (CoA) synthetase long-chain family member 4 (ACSL4). Distinct from acute ferroptosis, this ACSL4-mediated process promotes cellular senescence and systemic functional decline. The therapeutic inhibition of hepatic ACSL4 via gene editing alleviates aging phenotypes in mice. Through functional screening and target engagement studies, we identify vitamin C (VC) as a direct inhibitor of ACSL4. Long-term VC administration in aged monkeys for over 40 months potently reduces ferro-aging signatures across tissues, attenuates multi-organ pathology, and improves neurological and metabolic functions. Multi-omic aging clocks indicate the VC-mediated reversal of biological age. Our work establishes ferro-aging as a core, targetable mechanism of primate aging and positions VC as a translatable geroprotective strategy through ACSL4 inhibition.
    Keywords:  ACSL4; NRF2; aging; ferro-aging; iron; primate; senescence; vitamin C
    DOI:  https://doi.org/10.1016/j.cmet.2026.02.010
  5. Cell Rep. 2026 Mar 06. pii: S2211-1247(26)00104-X. [Epub ahead of print]45(3): 117026
      Endogenous (self) double-stranded RNAs (dsRNAs) in human cells can activate innate immune responses. ADAR1, an A-to-I editing enzyme of dsRNAs, suppresses aberrant immune activation by self-dsRNAs. However, how ADAR1 influences the cellular dsRNA landscape remains unclear. We show that human ADAR1 downregulates self-dsRNA abundance through editing-dependent and editing-independent mechanisms. We further conducted quantitative dsRNA sequencing on wild-type and ADAR1-deficient cells. dsRNAs are enriched in protein-coding mRNAs-especially those with repetitive elements and elongated 3' UTRs-and mitochondrial RNAs. ADAR1-regulated dsRNA transcripts consist of nuclear-encoded mRNAs and, unexpectedly, mitochondria-encoded RNAs rarely edited by ADAR1. Accordingly, dsRNAs accumulate to high levels within the mitochondria of ADAR1-deficient cells. Mass spectrometry and biochemical assays can detect ADAR1p150 in mitochondrial fractions. Notably, ADAR1 loss sensitizes cells to inflammation under mitochondrial stress (e.g., herniation and X-ray irradiation). Hence, we show that dsRNAs regulated by ADAR1 go beyond A-to-I edited transcripts and that ADAR1 can control mitochondrial dsRNAs.
    Keywords:  A-to-I editing; ADAR1; AGS; Aicardi-Goutieres syndrome; CP: immunology; CP: molecular biology; IFN; PKR; double-stranded RNA; dsRNA; dsRNA-seq; innate immunity; mitochondria; mitochondrial stress; protein kinase R; type 1 interferon
    DOI:  https://doi.org/10.1016/j.celrep.2026.117026
  6. Circulation. 2026 Mar 09.
       BACKGROUND: Cardiomyocytes, as highly specialized and differentiated somatic cells, possess a limited capacity for renewal. Neonatal rodents possess the ability to regenerate cardiomyocytes after injury; however, this regenerative capacity declines rapidly with cardiomyocyte maturation, suggesting an inhibitory network between cellular maturation and cardiomyocyte proliferation. Maturing cardiomyocytes undergo a metabolic shift from predominantly glycolysis in the neonatal state to increased fatty acid oxidation in the mature state, which poses a barrier to cardiomyocyte proliferation and cardiac regenerative repair. YAP, a transcriptional cofactor regulated by the Hippo signaling pathway, promotes cardiac regenerative repair. We investigated the role of YAP in mediating metabolic remodeling to overcome the cardiomyocyte proliferation barrier and enable cardiac regenerative repair after heart injury.
    METHODS: We explored how YAP induces metabolic remodeling through single-nucleus RNA sequencing and metabolomic analyses in mice. Using lipidomic analysis, we demonstrated how YAP remodels the balance of fatty acid catabolism and anabolism. We further used a maternal fat overloading model to stimulate fatty acid oxidation, which activates a maturation program in neonatal cardiomyocytes and counteracts YAP-mediated metabolic dematuration. Using chromatin accessibility (assay for transposase-accessible chromatin with high-throughput sequencing), DNA footprinting, and transcriptional profiling (RNA sequencing), we discovered the key transcription factors that YAP interrupts to reprogram the cardiomyocyte metabolic state.
    RESULTS: Our results demonstrate that YAP directs metabolic remodeling of mature cardiomyocytes toward a neonatal-like metabolic state and illustrate the role of fatty acid metabolism in proliferating cardiomyocytes. We found that YAP reduces cardiomyocyte fatty acid utilization, driving fatty acid anabolism and phospholipid biosynthesis. Genome-wide analyses revealed that YAP inhibits the cardiac maturation transcription factor MEF2A (myocyte-specific enhancer factor 2A), resulting in decreased gene expression of cardiomyocyte maturity pathways. Given the role of MEF2A in regulating contractility, energy production, and mitochondrial homeostasis, we found that perturbing MEF2A transcriptional activity can serve as a strategy to interrupt the cardiomyocyte maturation program and restore the regenerative capacity of the heart.
    CONCLUSIONS: Our research endeavors to provide a comprehensive understanding of the balance of cardiomyocyte metabolic maturation and proliferation to overcome barriers to heart regeneration, offering novel insights into the potential for therapeutic intervention in heart failure.
    Keywords:  fatty acids; heart failure; myocardial infarction; myocytes, cardiac; phospholipids
    DOI:  https://doi.org/10.1161/CIRCULATIONAHA.125.074956
  7. Sci Adv. 2026 Mar 13. 12(11): eadr1776
      Commonly expressed at developmental transitions, microRNAs operate as fine-tuners of gene expression to facilitate cell fate acquisition and lineage segregation. Nevertheless, how they might regulate the earliest developmental transitions in early mammalian embryogenesis remains obscure. Here, in a strictly in vivo approach based on genetically engineered mouse models and single-cell RNA sequencing, we identify microRNA-203 (miR-203) as a critical regulator of timely progression in preimplantation mouse embryos. Genetically engineered mouse models including a generated embryonic reporter (early embryo reporter) transgenic mouse carrying murine endogenous retrovirus-L (MERVL)-Tomato and SRY-box 2 (Sox2)-green fluorescent protein transgenes show that loss of miR-203 slows down early preimplantation development leading to the accumulation of embryos with high expression of totipotency-associated markers, including MERVL endogenous retroviral elements. A combination of single-cell transcriptional studies and epigenetic analyses identified histone acetylases including the central coactivator and histone acetyltransferase EP300 as critical miR-203 targets in the control of cell specification in early embryos. These data suggest that miR-203 carves the epigenetic rewiring required for early developmental transitions, allowing a timely and correctly paced development, at least partially by fine-tuning EP300 levels.
    DOI:  https://doi.org/10.1126/sciadv.adr1776
  8. bioRxiv. 2026 Feb 27. pii: 2026.02.26.708215. [Epub ahead of print]
      The histone chaperone FACT is essential for chromatin organization and stem cell identity, yet the sequence of events through which FACT maintains chromatin integrity remains unclear. We generate a high-resolution temporal map of events leading to chromatin destabilization and cell identity loss in murine embryonic stem cells following dTAG-mediated depletion of FACT. Loss of FACT initiates a rapid cascade, with nucleosome phasing disruption and reduced H3K4me3 beginning within 10 minutes in a transcription-dependent manner. This architectural destabilization enables pluripotency transcription factors to ectopically occupy gene bodies. FACT loss results in RNA Polymerase II accumulation within 30 minutes and altered H3K36me3 deposition preceding a global transcriptional collapse at 2 hours of FACT depletion. FACT restoration fails to rescue these defects, demonstrating they are largely irreversible. Our findings define a temporal hierarchy in which FACT loss drives progressive deterioration of chromatin architecture, leading to transcriptional collapse in stem cells.
    DOI:  https://doi.org/10.64898/2026.02.26.708215
  9. J Cell Biol. 2026 May 04. pii: e202509180. [Epub ahead of print]225(5):
      Lysosomes are subject to perturbations that can cause damage to their limiting membrane. Osmotic shifts, pore-forming toxins, and the growth of luminal polymers or pathogens all stand to increase lysosomal membrane tension and/or disrupt the bilayer. In some contexts, this leads to lysosomal rupture and cell death. Here, we describe a mechanism that enables lysosomes to sense and respond to acute increases in tension of their limiting membrane. We report that the lysosome-resident nonselective cation channel, TMEM63A, can drive the directional flux of monovalent cations, major osmoticants, out of the lumen when gated by mechanical tension on the organelle. This results in the ability for lysosomes to relieve hydrostatic pressure and, proportionally, membrane tension, affording lysosomes the time to acquire additional lipids. Lysosomes without this mechanism-either because TMEM63A is deleted or in the case when cells express disease-causing variants of TMEM63A-are an order of magnitude more sensitive to lysis upon increases to their membrane tension when compared with their WT counterparts. These findings suggest that lysosomes are capable of regulating hydrostatic pressure and volume in response to high tension.
    DOI:  https://doi.org/10.1083/jcb.202509180
  10. Nat Cell Biol. 2026 Mar 13.
      Recycling of cellular components through autophagy maintains homeostasis in changing nutrient environments. Although its core mechanisms are extensively studied, understanding of its systems-wide dynamic regulation remains limited, particularly regarding how autophagy is inactivated once nutrients are restored. Here we mapped the genetic network that controls activation and inactivation of autophagy during nitrogen changes by combining time-resolved high-content imaging, deep learning and latent feature analysis. This dataset, termed AutoDRY, categorizes 5,919 mutants based on nutrient response kinetics and their contributions to autophagosome formation and clearance. Integrating these profiles with functional and genetic network data uncovered hierarchical and multilayered control of autophagy and revealed multiple new regulatory pathways. Notably, we identified the retrograde pathway as a pivotal time-varying modulator that tunes the expression of core autophagy genes and plays a central role in autophagy inactivation. Together, this study establishes a systems-level resource to guide future investigations of autophagy.
    DOI:  https://doi.org/10.1038/s41556-025-01837-0
  11. Cell Stem Cell. 2026 Mar 05. pii: S1934-5909(26)00072-X. [Epub ahead of print]33(3): 454-469.e9
      The adrenal cortex produces essential steroid hormones through a concentric zonal architecture, established by the centripetal transdifferentiation of subcapsular progenitors within a capsule-derived niche. To capture this complexity, we establish a human pluripotent stem cell-derived adrenal organoid system that faithfully recapitulates this process. RSPO3/WNT signaling from the capsule specifies definitive zone (DZ) progenitors from the adrenal primordium, which then differentiate into a cortisol-producing transitional zone and an androgen-producing fetal zone under the influence of RSPO3 and ACTH. Loss of NR0B1 impairs DZ specification and triggers direct adrenal primordium-to-fetal zone conversion, mirroring the mechanism of X-linked adrenal hypoplasia congenita. When DZ cells are encapsulated with capsule cells separately derived from pluripotent stem cells, they reconstitute zonation in vivo, forming ACTH-responsive tissue that produces both cortisol and androgens. This organoid platform offers a powerful tool to dissect human adrenal development and establishes a foundation for regenerative therapies targeting adrenal diseases.
    Keywords:  adrenocortical organoids; androgen; definitive zone; fetal zone; functional zonation; glucocorticoids; human adrenal development; pluripotent stem cells; steroidogenesis; transitional zone
    DOI:  https://doi.org/10.1016/j.stem.2026.02.002
  12. Elife. 2026 Mar 11. pii: RP109358. [Epub ahead of print]14
      Mouse female primordial germ cells (PGCs) undergo five synchronous, incomplete mitotic divisions and send each resulting germline cyst into meiosis to fragment and produce 4-6 oocytes and 24-26 supportive nurse cells. However, no system of polarity has been found to specify mammalian oocytes, link them appropriately to nurse cells and enable them to acquire high-quality organelles and cytoplasm. We report that mouse cysts develop an asymmetric Golgi, endoplasmic reticulum (ER), and microtubule-associated 'fusome,' similar to the oocyte-determining fusome in Drosophila cysts. The mouse fusome distributes asymmetrically among cyst cells and enriches in future oocytes with Pard3 and Golgi-endosomal UPR (unfolded protein response) proteins. Spindle remnants rich in stable acetylated microtubules, like those building the Drosophila and Xenopus fusomes, transiently link early mouse cyst cells for part of each cell cycle. A non-random gap in these microtubules predicts that initial cysts fragment into similar six-cell derivatives, providing a potential mechanism for producing uniform oocytes. Together with previous studies, these results argue that a polarized fusome underlies the development of female gametes from the PGC to follicular oocyte stages in diverse animals including mammals.
    Keywords:  apical-basal polarity; cell cycle; developmental biology; fusome; germline cyst; mouse; oocyte development
    DOI:  https://doi.org/10.7554/eLife.109358
  13. Nat Commun. 2026 Mar 11.
      Oocyte development requires tight regulation of transcription and RNA metabolism, which is coordinated by RNA-binding proteins, whose roles in mammalian oogenesis remain incompletely understood. Here, we identify the DEAD-box RNA helicase DDX5 as a key regulator of RNA homeostasis in oocytes. Oocyte-specific deletion of DDX5 leads to female sterility, which is characterized by defective chromatin remodeling, meiotic arrest, increased aneuploidy, and fertilization failure. Mechanistically, DDX5 maintains RNA homeostasis through three interconnected processes: (1) promoting transcription via interaction with RNA polymerase II in nonsurrounded nucleolus-stage germinal vesicle oocytes; (2) clearing retrotransposon RNAs to safeguard transcriptome integrity; and (3) supporting maternal mRNA storage by coordinating nuclear export, mitochondrial organization, and mitochondria-associated ribonucleoprotein domain assembly. Our study establishes DDX5 as a master regulator that integrates transcriptional and post-transcriptional programs to ensure oocyte competence and fertility.
    DOI:  https://doi.org/10.1038/s41467-026-70237-1
  14. bioRxiv. 2026 Feb 28. pii: 2026.02.26.708335. [Epub ahead of print]
      Aging is accompanied by conserved hallmarks including genomic instability, epigenetic alterations, loss of proteostasis, and mitochondrial dysfunction, but how these processes emerge and become mechanistically linked remains unclear. Here we leverage a proteome-wide, single-cell, subcellular atlas of protein expression, localization, and aggregation across yeast replicative aging to map hallmark-linked remodeling in its spatial context. We identify hundreds of previously unappreciated molecular changes that underlie major hallmarks of aging and show that hallmark phenotypes frequently manifest as compartment-specific erosion of spatial confinement, relocalization, and aggregation. 91.6% human orthologs of these hallmark-linked yeast proteins also change during human aging. Integrating these spatial phenotypes reveals many molecular connections linking different hallmarks. Temporal analysis suggests that disorganization of nucleolar ribosome biogenesis, proteostasis decline, and mitochondrial dysfunction precede other hallmarks. Together, our findings substantially deepen the molecular underpinnings of aging hallmarks and provide a framework for linking them into a hierarchical sequence of cellular failures.
    DOI:  https://doi.org/10.64898/2026.02.26.708335
  15. Cell. 2026 Mar 11. pii: S0092-8674(26)00222-9. [Epub ahead of print]
      Aging is a major risk factor for neurodegenerative diseases, yet the underlying epigenetic mechanisms remain unclear. Here, we generated a comprehensive single-nucleus cell atlas of brain aging across multiple brain regions, comprising 132,551 single-cell methylomes and 72,666 joint chromatin conformation-methylome nuclei. Integration with companion transcriptomic and chromatin accessibility data yielded a cross-modality taxonomy of 36 major cell types. We observed that transposable element (TE) methylation alone distinguished age groups, showing cell-type-specific genome-wide demethylation. Chromatin conformation analysis demonstrated age-related increases in topologically associated domain (TAD) boundary strength with enhanced accessibility at CCCTC-binding factor (CTCF) binding sites. Spatial transcriptomics across 895,296 cells revealed regional heterogeneity during aging within identical cell types. Finally, we developed deep-learning models that reliably predict age-related gene expression changes using multi-modal epigenetic features, providing mechanistic insights into gene regulation. Age-related comparisons use a 2-month baseline reflecting the late-adolescent/early-young adult stage. This dataset advances our understanding of brain aging and offers potential translational applications.
    Keywords:  3D genome; DNA methylation; brain aging; deep learning; multi-omic; neurons and glias; single-cell; spatial transcriptome; topologically associating domains; transposable elements
    DOI:  https://doi.org/10.1016/j.cell.2026.02.015
  16. Nat Commun. 2026 Mar 12.
      Mosaic variegated aneuploidy (MVA), a rare human congenital disorder that causes microcephaly, is characterized by extensive abnormalities in chromosome number and results from mutations in genes involved in accurate mitotic chromosome segregation. To characterize the cellular mechanisms underlying this disease, here we generated a Drosophila model of microcephaly caused by the depletion of a single spindle assembly checkpoint (SAC) gene in the neural stem cell (NSC) compartment. We present evidence that loss of stemness - compromised identity and proliferative capacity of NSCs- plays an important role in MVA and results in a reduced number of neurons and glial cells. We show that loss of stemness arises from the accumulation over time of an unbalanced number of gains and losses of more than one chromosome, rather than a direct consequence of chromosomal instability-induced DNA damage or the production of simple aneuploidies. We unravel a contribution of proteostasis failure and mitochondrial dysfunction to the negative impact of complex aneuploidies on stemness, a highly energy demanding cellular state. We identify overexpression of Radical Oxygen Species scavengers, mitochondria chaperones and apoptosis inhibition as genetic interventions capable of dampening the deleterious effects of aneuploidy on brain size.
    DOI:  https://doi.org/10.1038/s41467-026-70521-0
  17. Nat Cell Biol. 2026 Mar 13.
      Membrane protection against oxidative insults is achieved by the concerted action of glutathione peroxidase 4 (GPX4) and endogenous lipophilic antioxidants such as ubiquinone and vitamin E. More recently, ferroptosis suppressor protein 1 (FSP1) was identified as a critical ferroptosis inhibitor, acting via the regeneration of membrane-embedded antioxidants. Yet, regulators of FSP1 are largely uncharacterized, and their identification is essential for understanding the mechanisms buffering phospholipid peroxidation and ferroptosis. Here we report a focused CRISPR-Cas9 screen to uncover factors influencing FSP1 function, identifying riboflavin (vitamin B2) as a modulator of ferroptosis sensitivity. We demonstrate that riboflavin supports FSP1 stability and the recycling of lipid-soluble antioxidants, thereby mitigating phospholipid peroxidation. Furthermore, we show that the riboflavin antimetabolite roseoflavin markedly impairs FSP1 function and sensitizes cancer cells to ferroptosis. Our findings provide a rational strategy to modulate the FSP1-antioxidant recycling pathway and underscore the therapeutic potential of targeting riboflavin metabolism, with implications for understanding the interaction of nutrients, as well as their contributions to a cell's antioxidant capacity.
    DOI:  https://doi.org/10.1038/s41556-025-01856-x
  18. Nat Commun. 2026 Mar 09.
      Stimulating endogenous cardiomyocyte proliferation holds great therapeutic promise for cardiac repair, but how chromatin remodeling governs this process remains poorly understood. RNA-binding motif 22 (RBM22) participates in the regulation of various biological contexts, whereas its role in cardiac regeneration and repair is largely unknown. Here, we identify RBM22 as a pivotal regulator of cardiomyocyte proliferation. Cardiomyocyte-specific deletion of Rbm22 impairs neonatal heart regeneration and exacerbates post-infarction ventricular remodeling in adult mice. Mechanistically, RBM22 selectively binds to the proximal promoters of key cell cycle genes (Cdk4, Ccna2, and Ccne1), where it cooperates with chromatin remodeler SMARCA4 to enhance transcriptional accessibility. Furthermore, RBM22 is essential for the gene-specific recruitment of RNA Polymerase II to these gene loci to drive transcription. AAV9-mediated delivery of Rbm22 promotes cardiomyocyte proliferation in vivo following cardiac damage and increases the proliferation of human induced pluripotent stem cell-derived cardiomyocytes. Our findings establish RBM22 as a transcriptional and epigenetic regulator that overcomes cell-cycle barriers in cardiomyocytes, highlighting its therapeutic potential for cardiac injury.
    DOI:  https://doi.org/10.1038/s41467-026-70235-3
  19. Science. 2026 Mar 12. 391(6790): eadt3439
      Gene expression patterns underlie development, but their systematic detection in whole embryos has remained elusive. We introduce a whole-embryo imaging platform using multiplexed error-robust fluorescent in situ hybridization (weMERFISH). We quantified the expression of 495 genes in zebrafish embryos at subcellular resolution and generated an online atlas detailing the expression of 25,872 genes and accessibility of 294,954 chromatin regions during embryogenesis. Expression patterns often corresponded to composites of tissue-specific accessible elements, and expression changes aligned with cellular maturation and morphogenesis. Integration with live imaging revealed how similar expression patterns can emerge through different dynamics and showed that sharp boundaries develop through changes in gene expression rather than through cell sorting. These results establish multiplexed whole-embryo spatial transcriptomics and reveal the regulation and dynamics of embryonic gene expression patterns.
    DOI:  https://doi.org/10.1126/science.adt3439
  20. Nat Chem Biol. 2026 Mar 11.
      Intensity and duration of biological signals encode a few pathways to direct diverse cellular behaviors, yet quantifying these features in single cells remains difficult. To address this challenge, we developed INSCRIBE, which uses a CRISPR base editor to mutate genomic targets at rates proportional to signaling activity. Edits are recovered at the endpoint through a new ratiometric readout strategy from images of two fluorescence channels. We engineered human cells to record WNT and BMP activity. Following defined exogenous stimulations, INSCRIBE accurately recovered signal intensity in dose-response experiments and exposure duration in time-course experiments. Applying INSCRIBE revealed a persistent memory in the BMP pathway, where progeny of high-responding cells remained more sensitive to subsequent BMP stimulation for up to 3 weeks. Together, our results establish a scalable platform for genetic recording and in situ readout of signaling activity in single cells, advancing quantitative analysis of cell-cell communication during development and disease.
    DOI:  https://doi.org/10.1038/s41589-026-02168-3
  21. Protein Cell. 2026 Mar 09. pii: pwag010. [Epub ahead of print]
      Chromosome substitution strains (CSS) are critical tools for dissecting complex traits, although iterative breeding steps and intraspecific compatibility requirements limit conventional approaches. Here, we developed a Targeted chromosome Elimination And Microcell-mediated chromosome transfer platform (TEAM) for chromosome replacement combing CRISPR/Cas9-mediated chromosome elimination with microcell-mediated chromosome transfer (MMCT). Using this approach, we substituted the endogenous mouse Y chromosome (chrY) with either the mouse or human Y chromosome. Intraspecies substitutions yielded karyotypically stable embryonic stem cells that supported development into adult males. By contrast, in interspecies CSS, human chrY displayed severe instability and progressive DNA damage. Despite partial transcription of human chrY genes, recipient animals exhibited systemic inflammation, high rates of neonatal death, and poor growth. Reduced CENP-A levels were observed at human chrY centromeres, leading to segregation errors, micronuclei formation, and widespread chromosome rearrangements. This technology enables programmable construction of chromosome substitution models for investigating chromosomal function, genome evolution, and synthetic karyotype design in mammals.
    Keywords:  CRISPR/Cas9; MMCT; chromosome elimination; chromosome substitution strains
    DOI:  https://doi.org/10.1093/procel/pwag010
  22. Curr Biol. 2026 Mar 10. pii: S0960-9822(26)00163-6. [Epub ahead of print]
      All animal embryos begin as totipotent zygotes that cleave and produce cells with restricted fate potentials. However, the timing of when totipotency is lost and the processes through which embryonic cells acquire fates vary across species. Embryos with invariant cleavage programs, e.g., of nematodes and spiralians, tend to show early restriction of blastomere potency and limited robustness to perturbation, particularly after asymmetric cleavages have occurred. By contrast, embryos with variant cleavage programs, e.g., of vertebrates, tend to specify fates later in development and correspondingly show higher plasticity at early stages. Here, we report unexpected post-zygotic totipotency and subsequent high plasticity of blastomeres in the acoel Hofstenia miamia, whose embryos undergo an invariant cleavage program called "duet cleavage." Blastomere isolation assays revealed that, at the 4-cell stage, single macromeres, which are products of asymmetric, fate-specifying cleavage, were totipotent and formed whole organisms upon isolation. Photoconversion-based lineage tracing showed that pharyngeal and neuronal tissues, which are not produced by macromeres during normal development, are recovered via blastomere transfating. Remarkably, using embryo reconstitution assays, we found that all 8-cell stage blastomeres could be reprogrammed, demonstrating high plasticity in H. miamia embryos. The embryo manipulation assays we developed have high reproducibility and throughput, making the H. miamia embryo an ideal system to investigate the causes for extended totipotency and plasticity.
    Keywords:  acoel; classical embryology; cleavage; embryogenesis; evolution; plasticity; pluripotency; reprogramming; totipotency
    DOI:  https://doi.org/10.1016/j.cub.2026.02.014
  23. EMBO J. 2026 Mar 12.
      Naive human pluripotent stem cells (hPSCs) represent a pre-implantation epiblast state able to efficiently differentiate into embryonic and extraembryonic pre-implantation lineages and to self-organise in vitro into blastocyst-like structures called blastoids. Naive hPSC maintenance routinely relies on co-culture with mouse embryonic fibroblast (MEFs) as feeder cells, a method prone to variability and analytical confounders. Here, we describe a feeder-free culture system based on serum coating that supports long-term maintenance of naive hPSCs. Across five laboratories, 30 serum batches were evaluated for the expansion of eight naive hPSCs lines for up to 25 passages. Mass spectrometry analysis identified fibronectin and collagens as extracellular matrix proteins consistently present in serum coating. Cells cultured on serum coating displayed growth kinetics, clonogenic capacity, mutation rates, and global gene expression profiles comparable to MEF-based cultures. Importantly, serum-cultured naive hPSCs efficiently underwent germ layer specification, retained trophectoderm competence, and generated blastoids with efficiency similar to MEF-based cultures. Collectively, serum coating provides a scalable, cost-effective, and robust alternative to feeder-based systems, preserving genomic stability and developmental potential while eliminating MEF-associated disadvantages and variability. This platform facilitates large-scale applications of naive hPSCs and enables more reproducible mechanistic studies.
    Keywords:  Blastoids; Extracellular Matrix; Extraembryonic Lineages; Feeder-free; Human Naive Pluripotent Stem Cells
    DOI:  https://doi.org/10.1038/s44318-026-00714-2
  24. Nat Aging. 2026 Mar 10.
      Cellular morphology is tightly linked to function, but how subcellular transcript localization contributes remains unclear. Using microglia, the brain's resident macrophages, as a model, we combined multiplexed error-robust fluorescence in situ hybridization with immunohistochemistry to map how morphology and subcellular mRNA localization interact with function in young and aged mouse brains. We show that mRNA spatial organization varies across microglial states and defines distinct localization patterns within their processes, revealing morphological heterogeneity within transcriptomically defined populations. Notably, we found a subpopulation of disease-associated-like microglia with a ramified morphology (that is, displaying numerous processes), challenging the conventional assumption between morphology and microglial states. Finally, we found that aging may reshape mRNA distributions and their co-localization networks, shifting microglial programs from intracellular signaling and regulation of phagocytosis toward migration and catabolic regulation. Our findings highlight the role of subcellular transcript organization in shaping microglial morphology and function, offering new avenues for studying and modulating microglial states in health, disease and aging.
    DOI:  https://doi.org/10.1038/s43587-026-01089-z
  25. Cell Rep. 2026 Mar 10. pii: S2211-1247(26)00131-2. [Epub ahead of print]45(3): 117053
      Heritable genetic changes continually arise in cancer, especially in solid tumors where cells are sometimes compressed. Rare heritable losses of chromosomes in live cells are quantified here with chromosome reporters (ChReporters), which reveal losses only after imposing a threshold level of confinement. Compression to ∼60% of interphase height ruptures few nuclei compared to deeper compression but perturbs mitotic spindles and prolongs pro/metaphase. Chromosome mis-segregation into micronuclei is discovered only after release from modest confinement, but arrest and death predominate. All such effects are phenocopied by nocodazole washout, which generates a "memory" of prolonged mitosis. The effects also differ from the rapid induction of micronuclei by a spindle-assembly checkpoint inhibitor and by a clinical CDK4/6 inhibitor of cell-cycle entry. Single-cell RNA sequencing confirms chromosome loss days after confinement and reveals dysregulation of chromosome-segregation pathways. Chromosome losses as mitotic memories of confinement ultimately address knowledge gaps in mechanobiology and cancer evolution.
    Keywords:  CP: cell biology; CP: molecular biology; aneuploidy; cancer; compression; evolution; genetics; mechanobiology
    DOI:  https://doi.org/10.1016/j.celrep.2026.117053
  26. Nat Cell Biol. 2026 Mar 13.
      Stimulation of the innate immune system by foreign RNA elicits a potent interferon response and can trigger cell death. The mechanisms by which cells balance a robust response with cell-intrinsic lethality are still being uncovered. Here, using genome-wide CRISPR-Cas9 genetic screens with triphosphorylated RNA stimulation, we discover that promyelocytic leukaemia (PML) nuclear body-localized speckled protein 110 (SP110) is a potent inhibitor of type 1 interferon-driven cell death. Death suppression by SP110 counteracts a toxic activity of SP100, a major constituent of PML bodies. Loss of SP110 leads to mitotic retention of SP100 and PML bodies, which associate with and perturb segregating chromosomes, leading to micronucleus formation, DNA damage and genotoxic cell death. A combination of cryo-electron microscopy, AlphaFold modelling and cellular biochemistry reveals that SP110 dissolves toxic SP100 oligomers via necessary and sufficient direct interactions between their caspase activation and recruitment domains. These data reveal the critical roles of SP100 and SP110 in governing the disassembly of PML bodies during mitosis, as well as the repercussions if this process is misregulated.
    DOI:  https://doi.org/10.1038/s41556-026-01916-w
  27. bioRxiv. 2026 Feb 25. pii: 2026.02.25.708035. [Epub ahead of print]
      Understanding how cells regulate plasma membrane architecture inside intact living organs in a live animal has been limited by the inability to directly measure molecular dynamics in vivo. Here we introduce intravital single-molecule microscopy (iSiMM), an imaging approach that enables tracking of individual, endogenously expressed cytoskeletal components at the plasma membrane in live mice. Applying iSiMM to murine acinar secretory cells, we identify discrete basolateral membrane domains built on deeply folded membrane infolds that function as a pre-existing membrane reservoir. Single-molecule measurements reveal continuous, regulated molecular turnover within these domains. Physiological stimulation accelerates cytoskeletal exchange promoting rapid membrane unfolding and cell expansion. Together, these findings establish iSiMM as a general strategy for probing molecular kinetics underlying dynamic cellular behaviors in intact organs.
    One-sentence summary: Intravital single-molecule microscopy enables direct measurement of molecular kinetics underlying dynamic cellular behaviors in intact living organs.
    DOI:  https://doi.org/10.64898/2026.02.25.708035
  28. Nat Commun. 2026 Mar 09.
      The kidney proximal tubule is a highly specialized epithelium that transports metabolites and maintains body homeostasis. Cells lining this nephron segment are densely packed with lysosomes, but little is known about the dynamic activity of these organelles in situ. Here, using targeted sensors and live cell and intravital imaging we track acidified lysosomes along the mouse proximal tubule and uncover marked axial heterogeneity in their distribution, characteristics and organellar interactions. In the early part, cathepsin-rich lysosomes frequently contact with apical endosomes to receive and catabolize filtered plasma proteins. Conversely, in the later region, lipase-containing lysosomes traverse cells to mobilize and degrade mitochondria-associated lipid droplets and facilitate their extrusion into the tubular lumen. Acutely de-acidifying lysosomes dramatically alters their movement, causing major changes in tubular protein and lipid processing. Thus, lysosomes in proximal tubules are highly dynamic and adapted to perform distinct metabolic tasks within different specialized segments.
    DOI:  https://doi.org/10.1038/s41467-026-70306-5
  29. Nucleic Acids Res. 2026 Feb 24. pii: gkag199. [Epub ahead of print]54(5):
      The BLM helicase is a critical genome maintenance protein involved in diverse cellular processes including DNA replication, repair, transcription, and chromosome segregation. During mitosis, it cooperates with the PICH helicase and topoisomerases to resolve ultrafine DNA bridges (UFBs)-nonchromatinized DNA structures that link sister chromatids-through a mechanism that is not yet fully understood. Here, we tagged endogenous BLM and PICH with fluorescent proteins and BLM with an auxin-inducible degron to generate a cell model system that enables temporal tracking of UFB dynamics in the presence or absence of BLM. Time-resolved lattice light sheet microscopy established the dynamic localization patterns of BLM and PICH throughout the cell cycle. While BLM cycles between PML bodies and DNA repair foci in interphase, these structures disappear at the mitotic entry, and BLM then re-associates with chromatin during anaphase to UFBs as well as to CENP-B-positive mitotic foci. Acute BLM depletion during mitosis increased the fraction of unresolved UFBs, micronuclei containing acentric fragments, binucleation, and resulted in subtle genomic abnormalities detected by single-cell whole genome sequencing. These findings highlight a mitosis-specific role for BLM in UFB resolution and underscore its function in preserving genomic stability.
    DOI:  https://doi.org/10.1093/nar/gkag199
  30. Neuron. 2026 Mar 12. pii: S0896-6273(26)00052-8. [Epub ahead of print]
      Endocytosis actively remodels the neuronal surface proteome to drive diverse cellular processes, yet its global extent and effects on neural circuit development have defied comprehensive interrogation. Here, we introduce endocytome profiling: a systematic, cell-type-specific approach for mapping cell-surface protein (CSP) dynamics in situ. Quantitative proteomic analysis of developing Drosophila olfactory receptor neuron (ORN) axons generated an endocytic atlas comprising over 1,000 proteins and revealed the extent to which the cell-surface proteome is remodeled to meet developmental demands. Targeted interrogation of a junctional CSP showed that its endosome-to-surface ratio is precisely balanced to enable developmental axon pruning while preserving mature axon integrity. Multi-omic integration uncovered widespread transcellular signaling and identified a growth factor secreted by neighboring neurons to direct ORN axon targeting via endocytic regulation of its receptor. Endocytome profiling provides unprecedented access to cell-surface proteome dynamics and offers a platform to dissect proteome-scale remodeling across diverse cell types and contexts.
    Keywords:  Drosophila; axon targeting; cell-surface protein; endosome; olfactory receptor neuron; proteomics; proximity labeling; remodeling
    DOI:  https://doi.org/10.1016/j.neuron.2026.01.027
  31. J Mol Cell Biol. 2026 Mar 09. pii: mjag001. [Epub ahead of print]
      The human testis, a crucial organ in male reproduction, is mainly responsible for spermatogenesis and androgen production. As men age, testicular function declines, yet the underlying molecular mechanisms are still not well understood. To elucidate the mechanisms of human testicular aging, we performed an integrated analysis of single-nucleus transcriptomes and chromatin accessibility (snRNA-seq and snATAC-seq) on pathologically confirmed non-tumor testicular tissues from young and aged individuals. Our integrated multi-omic analysis reveals significant age-induced alterations in the testis transcriptome, particularly affecting genes linked to spermatogenesis. Significant age-related changes were also observed in Sertoli and Leydig cells, with Sertoli cells exhibiting increased sensitivity to environmental influences as age. Furthermore, the expression of Wntless (WLS), a Wnt transporter, was substantially upregulated in Sertoli cells of aged testes, which was correlated with cellular senescence and the disruption of tight junctions. Overexpression of WLS in Sertoli cells significantly accelerated senescence in vitro, implying a potential role for WLS in testicular aging. Our study provides a detailed multi-omic map of the transcriptomic and chromatin accessibility changes in the human testis during aging, offering insights into the cellular and molecular mechanisms behind these changes, and identifying potential therapeutic targets for interventions against age-related declines in male reproductive health.
    Keywords:  WLS; aging; single-nucleus ATAC sequencing; single-nucleus transcriptomic sequencing; testes
    DOI:  https://doi.org/10.1093/jmcb/mjag001
  32. Nature. 2026 Mar 11.
      Lung cancer predominantly affects older individuals, yet how physiological ageing influences tumour evolution remains poorly understood1. Here we show that ageing reprograms the evolutionary trajectory of KRAS-driven lung adenocarcinoma, limiting primary tumour growth while promoting metastatic dissemination through epigenetic activation of the integrated stress response (ISR). The ISR effector ATF4 drives epithelial and metabolic plasticity, conferring metastatic competence. Mechanistically, aged tumour cells show increased sensitivity to the PERK-eIF2α arm of the unfolded protein response, sustaining persistent ATF4 signalling. Targeting ISR-ATF4 genetically or pharmacologically abolishes these adaptations and limits dissemination, whereas ATF4 overexpression alone is sufficient to induce metastasis. The ageing-ATF4 axis imposes a dependency on glutamine metabolism, revealing a therapeutically actionable vulnerability. Clinical analyses confirm that ATF4 is enriched in aged tumours and correlates with poor survival and advanced-stage disease. Collectively, these results define epigenetic ISR-ATF4 activation as a causal driver of lineage plasticity and metastasis in aged tumours, revealing a therapeutic opportunity in older patients with lung adenocarcinoma, the most common yet understudied subset of lung cancer.
    DOI:  https://doi.org/10.1038/s41586-026-10216-0
  33. Nat Commun. 2026 Mar 09.
      Potassium is vital for life, yet how potassium homeostasis is maintained at the tissue or organismal level under dietary scarcity remains poorly understood. Stress-activated signaling pathway p38 MAPK is implicated in immune response and aging, but its specific role in low potassium response is unclear. Here we show that a specific p38 MAPK-ATF-7 pathway orchestrates cross-tissue potassium homeostasis in Caenorhabditis elegans. It drives transcriptional upregulation of a crucial P-type ATPase pump CATP-3 specifically in the hypodermis, a process that integrates cell-autonomous mechanisms with non-autonomous ASI neuronal signals, thereby enhancing organismal survival during potassium deficiency. Notably, this regulation is distinct from canonical osmotic stress responses, revealing a specialized and conserved survival strategy. Analogous p38-mediated control of P-type ATPases occurs in yeast and mammalian cells, suggesting broad relevance. Our findings redefine potassium regulation as a cross-tissue process linked to lifespan, stress signaling, and innate immunity with potential implications for aging and age-related diseases.
    DOI:  https://doi.org/10.1038/s41467-026-70641-7
  34. Sci Adv. 2026 Mar 13. 12(11): eadz3266
      Sepsis-induced cardiac dysfunction arises from complex intercellular communication networks that extend beyond direct cardiomyocyte damage, yet the nanoscale mechanisms governing these interactions remain poorly understood. Here, we identify tunneling nanotubes (TNTs) as dynamic biological nanostructures facilitating intercellular mitochondrial transfer, revealing their critical role in septic cardiac remodeling. Using a murine cecal ligation and puncture (CLP) model and single-cell RNA sequencing, we demonstrate that sepsis reprograms cardiac endothelial cells, fibroblasts, and macrophages, generating metabolically impaired subpopulations with dysfunctional mitochondrial respiration. We uncover a Drp1-driven cytoskeletal remodeling process that orchestrates TNT biogenesis, wherein Drp1 interacts with Filamin and Kinesin to regulate TNT formation and extension, enabling long-range organelle trafficking. Cardiac-specific Drp1 knockout disrupts TNT-mediated mitochondrial exchange, halting metabolic deterioration and reversing cellular reprogramming. These findings establish Drp1-mediated TNT networks as nanoscale conduits of organelle communication, offering insights into biological nanotube engineering, cellular-scale nanotechnology, and potential therapeutic interventions for mitochondrial dysfunction in sepsis.
    DOI:  https://doi.org/10.1126/sciadv.adz3266
  35. Cell Chem Biol. 2026 Mar 11. pii: S2451-9456(26)00063-2. [Epub ahead of print]
      The four major isoforms encoded by RAS proto-oncogenes are differentially associated with cancer, but there are few isoform-specific binding reagents becasue the sequence differences are confined to their disordered C termini. To overcome this limitation, we use deep learning-based methods to design Ras isoform-specific binders (RIBs) for all major Ras isoforms de novo by targeting the Ras C terminus. The RIBs bind to their target Ras isoforms both in vitro and in cells with remarkable specificity, disrupting their membrane localization and inhibiting Ras activity. The RIBs enable dissection of the distinct roles of Ras isoforms during RasG12C inhibitor resistance, demonstrating their utility in understanding Ras biology and disease and suggesting potential therapeutic applications.
    Keywords:  RAS; cancer; intrinsically disordered regions; protein design; protein engineering
    DOI:  https://doi.org/10.1016/j.chembiol.2026.02.008
  36. Proc Natl Acad Sci U S A. 2026 Mar 17. 123(11): e2524427123
      To reach targets outside the bloodstream, immune cells can extravasate and migrate through connective tissue. During tissue infiltration, immune cells migrate in an amoeboid fashion, characterized by weak matrix adhesions and low traction forces, that allows them to achieve high migration speeds of up to 10 µm/min. How immune cells reconcile amoeboid migration with the need to overcome steric hindrance in dense matrices is currently not understood. Here we show that NK92 (natural killer) cells can switch from their default amoeboid migration mode to a contractile, mesenchymal-like migration mode when moving through fibrous human amniotic membrane (HAM) tissue. We subsequently study immune cell migration in reconstituted 3D collagen networks with known mechanical properties and pore sizes and apply time-lapse confocal reflection microscopy to obtain simultaneous measurements of migration speed, directional persistence, and cell contractility. We find that NK92 cells exert substantial acto-myosin driven, integrin-mediated contractile forces of up to 100 nN on the extracellular matrix during short contractile phases. This burst-like contractile behavior is also found in primary B, T, NK cells, neutrophils, and monocytes, and is tightly related to the fraction of cells that become stuck in narrow pores of the surrounding matrix. Our results demonstrate that steric hindrance guides the rapid regulation of integrin-mediated adhesion to the ECM in a large number of immune cell subtypes.
    Keywords:  cell migration; collagen matrices; immune cells; mechanosensitivity; traction forces
    DOI:  https://doi.org/10.1073/pnas.2524427123
  37. Nat Commun. 2026 Mar 12.
      N-terminal acetylation is an abundant and predominantly co-translational modification in eukaryotes that profoundly affects folding, compartmentalization fidelity and turnover of target proteins. Unlike other N-acetyltransferases, human NatD is composed solely of the catalytic subunit NAA40 and exclusively modifies histone proteins H2A and H4. However, the molecular details of co-translational NAA40 activity have remained elusive. Here, we show biochemically and by cryo-EM how NAA40 activity is coordinated at the ribosomal peptide tunnel exit involving the NAC complex. We demonstrate that the NAA40-NAC interaction is required for efficient ribosome binding and histone acetylation. Furthermore, we provide insights on the potential coordination of methionine removal and subsequent NAA40-mediated acetylation by formation of a multienzyme complex on the ribosome involving METAP1. Therefore, our results illustrate the details of N-terminal histone acetylation by NAA40 and highlight the role of NAC as a general coordinator of nascent protein modification.
    DOI:  https://doi.org/10.1038/s41467-026-70279-5
  38. Cell. 2026 Mar 09. pii: S0092-8674(26)00174-1. [Epub ahead of print]
      We present a whole-cell spatial and kinetic model for the ∼100 min cell cycle of the genetically minimal bacterium JCVI-syn3A. We simulate the complete cell cycle in 4D (space and time), including all genetic information processes, metabolic networks, growth, and cell division. By integrating hybrid computational methods, we model the dynamics of morphological transformations. Growth is driven by insertion of lipids and membrane proteins and constrained by fluorescence imaging data. Chromosome replication and segregation are controlled by the essential structural maintenance of chromosome proteins, analogous to condensin (SMC) and topoisomerase proteins in Brownian dynamics simulations, with replication rates responding to deoxyribonucleotide triphosphate (dNTP) pools from metabolism. The model captures the origin-to-terminus ratio measured in our DNA sequencing and recovers other experimental measurements, such as doubling time, mRNA half-lives, protein distributions, and ribosome counts. Because of stochasticity, each replicate cell is unique. We predict not only the average behavior of partitioning to daughter cells but also the heterogeneity among them.
    Keywords:  DNA sequencing; Lattice Microbes; cell cycle; fluorescence imaging; minimal cell; whole-cell modeling
    DOI:  https://doi.org/10.1016/j.cell.2026.02.009
  39. Acta Biomater. 2026 Mar 10. pii: S1742-7061(26)00155-8. [Epub ahead of print]
      Cell alignment is a fundamental process in tissue morphogenesis. While density-dependent collective cell alignment has been widely observed, its underlying mechanisms remain poorly understood. Here, using C2C12 myoblasts, we demonstrate that static uniaxial mechanical stretch induces collective cell alignment in a density-dependent manner: densely populated cultures align robustly, whereas sparse populations do not. We reveal a biphasic alignment process, comprising an initial passive phase and a subsequent active phase. The passive phase, driven by substrate deformation, transiently biases cell orientation along the stretch axis regardless of density. In the active phase, initial alignment progressively dissipates in low-density cultures, but is sustained and reinforced in high-density cultures. Supported by coarse-grained agent-based simulations, we propose that self-generated cellular forces facilitate kinetic transitions between orientations, enabling cells to explore orientational states, whereas cell-cell interactions provide a thermodynamic bias that stabilizes the locally aligned state. In dense cultures, strong intercellular interactions promote this stabilization, enabling persistent alignment. In contrast, sparse cultures lack sufficient cell-cell interaction, leading to alignment dissipation. Within this C2C12 system, our findings highlight the cooperative roles of cellular forces and intercellular interactions in orchestrating multicellular ordering, offering new insights into mechanobiology of tissue morphogenesis. STATEMENT OF SIGNIFICANCE: Cell alignment is essential to build functional tissues, yet how multicellular groups achieve and maintain this order remains unclear. We show that a brief uniaxial stretch can "write" long-lived orientation into myoblast sheets through two phases: a passive phase where cells deform with the substrate, and an active, density-dependent phase in which cell-cell adhesion stabilizes order against stochastic forces. By separating passive deformation from adhesion-mediated reinforcement and ruling out substrate artifacts, we provide a thermodynamic perspective on how mechanics and adhesion cooperate to pattern living tissues. This work links biomechanics, material science, and thermodynamics, and offers a scalable design rule to program persistent anisotropy without patterned scaffolds or continuous loading, advancing strategies for tissue engineering applications.
    Keywords:  Cell alignment; Collective behavior; Mechanical stretch; Self-organization; Thermodynamic stabilization
    DOI:  https://doi.org/10.1016/j.actbio.2026.03.015
  40. Nat Metab. 2026 Mar 12.
      Adipose tissue homeostasis depends on an intact vascular network that ensures adequate nutrient delivery and immune regulation. In obesity, vascular dysfunction, particularly within endothelial cells (ECs), contributes to inflammation and metabolic disease progression, yet the cellular organization of the human adipose vasculature remains poorly defined. Here we show, using single-cell RNA sequencing of nearly 70,000 vascular cells from human subcutaneous adipose tissue of 65 individuals, that the adipose vasculature is highly heterogeneous and consists of seven canonical EC subtypes. In addition, we identify a distinct population of ECs that display mixed endothelial, mesenchymal, adipocytic and immune transcriptional features. Computational analyses and whole-mount imaging support their presence and suggest that they emerge through endothelial-to-mesenchymal transition. Comparative analyses further reveal inflammatory and fibrotic vascular signatures in obesity and type 2 diabetes. Together, this atlas delineates the cellular complexity of the human adipose vasculature and highlights its contribution to metabolic disease.
    DOI:  https://doi.org/10.1038/s42255-026-01475-2
  41. J Biol Chem. 2026 Mar 06. pii: S0021-9258(26)00218-8. [Epub ahead of print] 111348
      TDP-43 and FUS are RNA-binding proteins involved in the regulation of diverse RNA processing events and have been strongly implicated in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). We have previously demonstrated the role of symmetrical dimethylation (me2s) of a conserved arginine residue (R1810 in human POLR2A) in the C-terminal domain (CTD) of RNA polymerase II (RNAPII), which facilitates the recruitment of the Tudor domain-containing protein SMN to resolve R-loops at transcriptional termination sites. Here, we demonstrate that TDP-43 and FUS contribute to transcription termination through the R1810me2s-SMN pathway. Our data show that TDP-43-and to a lesser extent, FUS-are recruited to chromatin via this pathway, and that disruption of their recruitment leads to defective RNAPII termination. This impairment results in the accumulation of R-loops and elevated DNA damage at gene terminators. Using transcriptome-wide analyses, we further show that TDP-43 RNA-binding sites are highly correlated with regions of R-loop formation. Importantly, we find that the RNA-binding activity of TDP-43 is essential for its role in resolving R-loops and promoting efficient transcription termination. These findings establish a mechanistic link between TDP-43/FUS, R-loop resolution, and transcription termination, providing new insights into how their dysfunction may drive genome instability and contribute to the pathogenesis of ALS and FTD.
    Keywords:  ALS; FUS; R-loops; SMN; TDP-43; neurodegenerative diseases; transcription termination
    DOI:  https://doi.org/10.1016/j.jbc.2026.111348
  42. Nat Commun. 2026 Mar 13.
      Protein synthesis plays a central role in cancer development and progression. eukaryotic initiation factor 5 A (eIF5A), a translation factor activated by hypusination, is implicated in tumorigenesis, however, its mode of action is still unclear. We find that hypusinated eIF5A (eIF5Ahyp) promotes metastasis and tumor growth in prostate cancer (PCa) by supporting mitochondrial metabolism and translation. eIF5Ahyp controls the subcellular localization of Mitochondrial Ribonuclease P Protein 3 (MRPP3) mRNA encoding a protein essential for mitochondrial tRNA (mt-tRNA) maturation. We show that eIF5Ahyp regulates the nuclear export of MRPP3 mRNA, its expression, thereby promoting mt-tRNA maturation. Our findings establish that MRPP3 enhances mitochondrial metabolism and supports PCa metastasis. Importantly, its expression restores mitochondrial translation and tumor growth inhibited by the downregulation of eIF5Ahyp. Together, we uncover a critical role for eIF5Ahyp in mitochondrial protein synthesis and highlight its broader implications in coordinating the expression of nuclear and mitochondrial genomes, linking hypusination to cancer progression.
    DOI:  https://doi.org/10.1038/s41467-026-70566-1
  43. Cell Mol Life Sci. 2026 Mar 10.
      Trophoblast and amniotic lineages, representing key extra-embryonic tissues, can be differentiated from human pluripotent stem cells (hPSCs) under chemically defined conditions. However, the regulatory mechanisms coordinating the fate decision between these lineages during PSC differentiation remain incompletely understood. Leveraging CRISPR/Cas9-mediated loss-of-function screening in lineage-reporter PSCs, we identified the transcription factor HAND1 as a critical determinant controlling the bifurcation of trophoblast and amniotic lineages. Genetic ablation of HAND1 effectively abrogated the amniotic differentiation capacity of PSCs while concomitantly enhancing their trophoblast differentiation potential. Conversely, ectopic HAND1 overexpression impaired trophoblast differentiation. Notably, forced HAND1 expression in human trophoblast stem cells (TSCs) induced transcriptional reprogramming toward an amniotic fate, indicating its lineage-instructive capability. Mechanistic analyses demonstrated that HAND1 interacts with the TCFs and Wnt signaling effectors β-catenin to form a transcriptional complex that antagonistically modulates the balance between trophoblast- and amnion-associated gene regulatory networks. Collectively, our findings establish HAND1 as a master regulator orchestrating the amniotic versus trophoblast lineage choice during human PSC differentiation, thereby illuminating fundamental regulatory mechanism underlying extra-embryonic lineage specification.
    Keywords:  CRISPR screening; Lineage specification; Reporter cell lines; Transcriptional complex; Trophoblast development
    DOI:  https://doi.org/10.1007/s00018-026-06120-5
  44. Trends Endocrinol Metab. 2026 Mar 10. pii: S1043-2760(26)00037-8. [Epub ahead of print]
      Cellular senescence is a complex cell fate characterized by stable cell cycle arrest and other heterogeneous changes. Senescent cells play a causal role in aging, although the underlying mechanisms remain under active investigation. In this opinion article, we propose that senescent cells can act as key mediators of interorgan communication of aging. Recent work defines multifaceted mechanisms, including the production of senescence-associated secretory phenotype factors that act to propagate senescence signals to nearby and distant cells, as well as age-related alterations in immune function that drive chronic inflammation, known as 'inflammaging'. Further investigation of these mechanisms could yield improved strategies to target senescent cells and mitigate their effects on systemic aging via interorgan communication of aging.
    Keywords:  cellular senescence; immunosenescence; inflammaging; inflammation; interorgan aging
    DOI:  https://doi.org/10.1016/j.tem.2026.02.002
  45. J Cell Biol. 2026 May 04. pii: e202508066. [Epub ahead of print]225(5):
      How the nucleolus recovers from acute proteostatic stress, particularly in multinucleate syncytia, remains poorly understood. In the highly polarized hyphae of the model filamentous fungus Magnaporthe oryzae, we uncover a novel stress-induced spatial quality control pathway that promotes the inheritance of rejuvenated nucleolar material during nuclear division. This pathway discriminates between newly formed and damaged nucleolar compartments, selectively partitioning and sequestering the latter. Our findings reveal a previously unrecognized mechanism for chaperone-mediated segregation of a membraneless nuclear organelle, extending principles of protein quality control to the unique demands of highly polarized syncytia.
    DOI:  https://doi.org/10.1083/jcb.202508066
  46. Nat Commun. 2026 Mar 09.
      Macrophage-mediated phagocytosis of tumor cells elicits potent antitumor immunity. Nonetheless, sole-blockade of the anti-phagocytosis molecule CD47 has yielded insufficient therapeutic outcomes. Here, we report that glioblastoma (GBM) cells expressed abundant levels of phagocytosis checkpoint CD24. We further show that dual blockade of CD24 and CD47 synergistically enhances the pro-phagocytic activity of macrophages, thereby improving tumor antigen cross-presentation and activating the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway. This innate immune activation facilitates T cell infiltration into tumors and sensitizes tumors to anti-PD1 therapy, improving survival outcomes in murine GBM models, including immunosuppressive tumors reflecting human GBM-like features. Thus, our results indicate that dual-phagocytosis checkpoint blockade offers a promising therapeutic avenue to potentiate cancer immunotherapy.
    DOI:  https://doi.org/10.1038/s41467-026-70221-9
  47. Nat Commun. 2026 Mar 12. pii: 1994. [Epub ahead of print]17(1):
      Splicing factors control exon inclusion in messenger RNAs, shaping transcriptome and proteome diversity. Their catalytic activity is regulated by multiple layers, making single-omic measurements on their own fall short in identifying which splicing factors underlie a phenotype. Here, we posit that splicing factor activity, defined as a splicing factor's ability to modulate exon inclusion, can be estimated from changes in exon inclusion signatures. To test this hypothesis, we benchmark methods for constructing splicing factor→exon networks and estimating splicing factor activity. We find that combining RNA-seq perturbation-based networks with VIPER (Virtual Inference of Protein Activity by Enriched Regulon analysis) accurately captures splicing factor activity as modulated by multiple regulatory layers. This approach integrates splicing factor regulation into a single score derived solely from exon inclusion signatures, allowing functional interpretation of heterogeneous conditions. As a proof of concept, we identify recurrent cancer splicing programs, revealing associations with oncogenic- and tumor suppressor-like splicing factors missed by conventional methods. These programs correlate with patient survival and key cancer hallmarks: initiation, proliferation, and immune evasion. Altogether, we show splicing factor activity can be accurately estimated from exon inclusion changes, enabling comprehensive analyses of splicing regulation with minimal data requirements.
    DOI:  https://doi.org/10.1038/s41467-026-69642-3
  48. Proc Natl Acad Sci U S A. 2026 Mar 17. 123(11): e2514355123
      Aggregation and deposition of TAR DNA-binding protein 43 (TDP-43) is a salient pathological signature of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration-TDP (FTLD-TDP). TDP-43 proteostasis and aggregation are controlled by several posttranslational modifications, including ubiquitination. While multiple E3 ubiquitin ligases are known to facilitate TDP-43 clearance, little is known about the role of deubiquitinases (DUBs) in controlling TDP-43 proteostasis. Through an unbiased discovery screen of DUBs, here we identify and demonstrate using in vitro and in vivo models, as well as human brain tissue, that ubiquitin-specific peptidase-19 (USP19) acts as a TDP-43-directed DUB that removes K48- and K63-linked ubiquitin conjugates from TDP-43 and preferentially promotes cytoplasmic aggregation of TDP-43 C-terminal fragments (TDP-CTFs) through its catalytic activity. Specifically, the endoplasmic reticulum (ER)-anchored USP19 isoform (USP19-ER) exhibits superior activity in deubiquitinating TDP-CTFs, enhancing its phase separation and aggregation, compared to its cytosolic isoform (USP19-Cyto). Furthermore, as TDP-CTFs are generated at the ER, USP19 acts to couple the aggregation of TDP-CTFs to ER stress (ATF6, ATF4, IRE1, & CHOP). In humans, USP19 protein levels increase in FTLD-TDP brains, which extensively colocalize with cytoplasmic phospho-TDP-43 (pTDP-43) pathology. Importantly, we demonstrate in vivo that genetic reduction of usp19 mitigates pTDP-43 pathology, astrogliosis, and ER stress while reversing long-term potentiation (LTP) and motor deficits in a mouse model of TDP-43 pathogenesis (TAR4 mice). These findings establish a critical role of USP19 at the nexus of TDP-43 proteostasis and ER stress, implicating its pathogenic role in FTLD-TDP and ALS.
    Keywords:  ALS; ER stress; FTD; TDP-43; USP19
    DOI:  https://doi.org/10.1073/pnas.2514355123
  49. Aging Cell. 2026 Mar;25(3): e70444
      Aging is a major risk factor for heart failure, yet the molecular mechanisms linking cardiac aging to the inflammatory pathophysiology of heart failure remain elusive. Mitochondrial dysfunction and defective organelle quality control are emerging hallmarks of the aging heart, but their biochemical underpinnings are poorly defined. Using comprehensive glycomics, we found that cardiac mitochondria from physiologically aged mice (≥ 20 months) are the major intracellular reservoirs of advanced glycation end products (AGEs), derived primarily from the chemical attack of some α-oxoaldehydes on proteins. This was associated with mild mitochondrial dysfunction and structural remodeling. Lysosomes in aged hearts were enlarged, more abundant, less acidic, and frequently loaded with lipofuscin. Notably, ~7% of cardiomyocytes showed proinflammatory senescence traits. In vitro, glycative stress in H9c2 myoblasts reproduced mitochondrial AGE buildup, dysfunction, and activation of the mitochondria-lysosome axis. However, AGE-modified mitochondria impaired lysosomal acidification and proteolysis, hindering mitophagic clearance and contributing to lipofuscin accumulation. This sequence of events ultimately led to proinflammatory senescence in a subset of cells. These findings identify mitochondrial AGE accumulation as a novel mechanism of sublethal nonsolved aging-associated stress that eventually triggers geroconversion in cardiomyocytes. This mechanism could facilitate the transition of the aging heart towards a failing phenotype.
    Keywords:  AGEs; aging; cardiomyocytes; lipofuscin; methylglyoxal; mitochondria; senescence
    DOI:  https://doi.org/10.1111/acel.70444
  50. Nat Chem Biol. 2026 Mar 13.
      Reactive oxygen species (ROS) dynamics exhibits rhythmic oscillations in cancer cells but how this rhythm influences tumorigenesis and therapeutic responses remains unclear. Here we found coexistence of ROS rhythmicity and rhythm loss in tumor samples. Under low-ROS conditions, indoleamine 2,3-dioxygenase 1 (IDO1), an immune-checkpoint molecule, binds to KEAP1 for proteasomal degradation in the nucleus. In contrast, elevated ROS levels drive IDO1 translocation into the cytosol, where it binds mitochondria-released heme to form an active holoenzyme. This holoenzyme catalyzes tryptophan to kynurenine that allosterically activates glucose-6-phosphate dehydrogenase, enhancing NADPH production and promoting ROS clearance. However, in hypoxic tumor microenvironments, ROS rhythmicity is lost. Compensating for this, hypoxic tumor cells mobilize the sulfenylated aryl hydrocarbon receptor (AhR)-mediated glycogenolysis pathway to manage disordered ROS accumulation, maintaining elevated ROS levels that favor tumor growth. Dual inhibition of IDO1 and AhR significantly prolongs survival of NSG mice, highlighting enforced disruption of ROS rhythm as a common therapeutic strategy.
    DOI:  https://doi.org/10.1038/s41589-026-02161-w