bims-nimamd Biomed News
on Neuroimmunity and neuroinflammation in ageing and metabolic disease
Issue of 2025–05–11
23 papers selected by
Fawaz Alzaïd, Sorbonne Université
  1. The structure of human sweetness.
  2. Leveraging neonatal Fc receptor (FcRn) to enhance antibody transport across the blood brain barrier.
  3. SPP1 + macrophages cause exhaustion of tumor-specific T cells in liver metastases.
  4. Progenitor exhausted T cells contribute to the formation of immunological memory.
  5. Molecular basis of SIFI activity in the integrated stress response.
  6. A high-performance fluorescent sensor spatiotemporally reveals cell-type specific regulation of intracellular adenosine in vivo.
  7. Astrocytic GLUT1 deletion in adult mice enhances glucose metabolism and resilience to stroke.
  8. Teens with anxiety and depression spend more time on social media.
  9. Guess how much of the ocean floor humans have explored.
  10. Coupling the 3D epigenome to the transcriptome in single cells.
  11. An energy blueprint of the human brain.
  12. Somatic hypermutation unlocks antibody specificities beyond the primary repertoire.
  13. How we taste sweetness: long-sought structure of human receptor mapped at last.
  14. A hidden cysteine in Fis1 targeted to prevent excessive mitochondrial fission and dysfunction under oxidative stress.
  15. Regulation of RIG-I activity by phase separation reveals new therapeutic opportunities.
  16. Dysregulated mast cell activation induced by diabetic milieu exacerbates the progression of diabetic peripheral neuropathy in mice.
  17. Widespread brain-body integration during changes of arousal.
  18. Cuts to US science will take a generation to repair - leaders must speak up now.
  19. Reduced Palmitoylation of SQSTM1/p62 in Huntington Disease Is Associated With Impaired Autophagy.
  20. Lymphatic endothelial mTORC1 instructs metabolic and developmental signaling during lymphangiogenesis.
  21. CD45-PET imaging gives a panoramic view of in vivo immune activity.
  22. A hierarchy of intestinal antigens instructs the CD4+ T cell receptor repertoire.
  23. Hdac1 as an early determinant of intermediate-exhausted CD8+ T cell fate in chronic viral infection.
  1. Cell. 2025 May 02. pii: S0092-8674(25)00456-8. [Epub ahead of print]
    The structure of human sweetness.
    Zhang Juen, Zhengyuan Lu, Ruihuan Yu, Andrew N Chang, Brian Wang, Anthony W P Fitzpatrick, Charles S Zuker.
      In humans, the detection and ultimately the perception of sweetness begin in the oral cavity, where taste receptor cells (TRCs) dedicated to sweet-sensing interact with sugars, artificial sweeteners, and other sweet-tasting chemicals. Human sweet TRCs express on their cell surface a sweet receptor that initiates the cascade of signaling events responsible for our strong attraction to sweet stimuli. Here, we describe the cryo-electron microscopy (cryo-EM) structure of the human sweet receptor bound to two of the most widely used artificial sweeteners-sucralose and aspartame. Our results reveal the structural basis for sweet detection, provide insights into how a single receptor mediates all our responses to such a wide range of sweet-tasting compounds, and open up unique possibilities for designing a generation of taste modulators informed by the structure of the human receptor.
    Keywords:  GPCR; cryo-EM; human; sensory biology; structure; sweet receptor; sweeteners; taste
    DOI:  https://doi.org/10.1016/j.cell.2025.04.021
  2. Nat Commun. 2025 May 03. 16(1): 4143
    Leveraging neonatal Fc receptor (FcRn) to enhance antibody transport across the blood brain barrier.
    Julien Lafrance-Vanasse, Shraddha S Sadekar, Yanli Yang, Daniela Bumbaca Yadav, William J Meilandt, Monica K Wetzel-Smith, Hao Cai, Susan R Crowell, Van Nguyen, Vivian Lee, Ben Chih, Mandy Kwong, Pamela Chan, Sara Santagostino, Donna Lee, Shan Chung, Greg A Lazar, James A Ernst, Jasvinder K Atwal.
      The blood-brain barrier (BBB) restricts efficient penetration of systemically delivered therapeutic antibodies into the brain, limiting the development of this class of drugs to treat neurodegenerative diseases. Here we demonstrate that the neonatal Fc receptor (FcRn), which is highly expressed at the BBB, can be used to facilitate IgG transport to the brain. Engineering of the antibody Fc region to promote binding to FcRn at neutral pH enhances antibody transcytosis in a cellular model. In vivo, these modifications improve brain penetration, as well as brain target engagement and activity, of systemically administered antibodies in both mice and non-human primates. This engineering approach can be broadly implemented to enhance central nervous system (CNS) exposure of antibody- and Fc-based drugs, improving the clinical potential of biotherapeutics for the treatment of human brain diseases.
    DOI:  https://doi.org/10.1038/s41467-025-59447-1
  3. Nat Commun. 2025 May 07. 16(1): 4242
    SPP1 + macrophages cause exhaustion of tumor-specific T cells in liver metastases.
    Rajiv Trehan, Patrick Huang, Xiao Bin Zhu, Xin Wang, Marlaine Soliman, Dillon Strepay, Amran Nur, Noemi Kedei, Martin Arhin, Shadin Ghabra, Francisco Rodríguez-Matos, Mohamed-Reda Benmebarek, Chi Ma, Firouzeh Korangy, Tim F Greten.
      Functional tumor-specific CD8+ T cells are essential for effective anti-tumor immune response and immune checkpoint inhibitor therapy. Here we show that, compared to other organ sites, primary, metastatic liver tumors in murine models contain a higher number of tumor-specific CD8+ T cells which are also dysfunctional. High-dimensional, multi-omic analysis of patient samples reveals a higher frequency of exhausted tumor-reactive CD8+ T cells and enriched interactions between these cells and SPP1+ macrophages in profibrotic, alpha-SMA rich regions specifically in the liver. Differential pseudotime trajectory inference analysis reveals that extrahepatic signaling promotes an intermediate cell (IC) population in the liver, characterized by co-expression of VISG4, CSF1R, CD163, TGF-βR, IL-6R, and SPP1. Analysis of premetastatic adenocarcinoma patient samples reveals enrichment of this population may predict liver metastasis. These findings suggest a mechanism by which extrahepatic tumors drive liver metastasis by promoting an IC population that inhibits tumor-reactive CD8+ T cell function.
    DOI:  https://doi.org/10.1038/s41467-025-59529-0
  4. Nat Rev Immunol. 2025 May 06.
    Progenitor exhausted T cells contribute to the formation of immunological memory.
    Annette Wu, Wen Jiang.
      
    DOI:  https://doi.org/10.1038/s41577-025-01182-1
  5. Nature. 2025 May 06.
    Molecular basis of SIFI activity in the integrated stress response.
    Zhi Yang, Diane L Haakonsen, Michael Heider, Samuel R Witus, Alex Zelter, Tobias Beschauner, Michael J MacCoss, Michael Rapé.
      Chronic stress response activation impairs cell survival and causes devastating degenerative di-seases 1-3. Organisms accordingly deploy silencing factors, such as the E3 ubiquitin ligase SIFI, to terminate stress response signaling and ensure cellular homeostasis 4. How a silencing factor can sense stress across cellular scales to elicit timely stress response inactivation is poorly understood. Here, we combine cryo-electron microscopy of endogenous SIFI with AlphaFold modeling and biochemical analyses to report the structural and mechanistic basis of integrated stress response silencing. SIFI detects both stress-indicators and stress response components through flexible domains within an easily accessible scaffold, before building linkage-specific ubiquitin chains at separate, sterically restricted elongation modules. Ubiquitin handover by a ubiquitin-like domain couples versatile substrate modification to linkage-specific ubiquitin polymer formation. Stress response silencing therefore exploits a catalytic mechanism that is geared towards processing many diverse proteins and hence allows a single enzyme to monitor and, if needed, modulate a complex cellular state.
    DOI:  https://doi.org/10.1038/s41586-025-09074-z
  6. Nat Commun. 2025 May 07. 16(1): 4245
    A high-performance fluorescent sensor spatiotemporally reveals cell-type specific regulation of intracellular adenosine in vivo.
    Qingpeng Wei, Zexiao Bai, Lei Wang, Jing Wang, Yipan Wang, Yufei Hu, Shiyi Ding, Zhixiong Ma, Chun Li, Yumo Li, Yizhou Zhuo, Wenzhe Li, Fei Deng, Bingjie Liu, Pengcheng Zhou, Yulong Li, Zhaofa Wu, Jing Wang.
      Adenosine (Ado), a nucleoside bridging intracellular metabolism with intercellular communication, plays an essential role in regulating processes such as sleep and seizure. While the functions of extracellular Ado ("eAdo") are well documented, our knowledge about the distribution and regulatory functions of intracellular Ado ("iAdo") is limited by a lack of methods for detecting iAdo in vivo. Here, we develop HypnoS, a genetically encoded fluorescent sensor for iAdo characterized by its high sensitivity, specificity, spatiotemporal resolution, and rapid response (sub-seconds). HypnoS enables real-time visualization of iAdo dynamics in live cultures, acute brain slices, flies, and freely moving mice. Using HypnoS for dual-color mesoscopic imaging in mice, we show that seizure-induced iAdo waves propagated across the cortex, following calcium signals. Additionally, two-photon imaging reveals that iAdo decays more rapidly in astrocytes than in neurons during seizures. Moreover, by recording iAdo dynamics in the basal forebrain during the sleep-wake cycle, we observe that iAdo signals are present during wakefulness and rapid eye movement (REM) sleep, regulated by equilibrative nucleoside transporters (ENT1/2). Thus, HypnoS is a versatile and powerful tool for investigating the biological functions of iAdo across a range of physiological and pathological states.
    DOI:  https://doi.org/10.1038/s41467-025-59530-7
  7. Nat Commun. 2025 May 06. 16(1): 4190
    Astrocytic GLUT1 deletion in adult mice enhances glucose metabolism and resilience to stroke.
    Laetitia Thieren, Henri S Zanker, Jeanne Droux, Urvashi Dalvi, Matthias T Wyss, Rebecca Waag, Pierre-Luc Germain, Lukas M von Ziegler, Zoe J Looser, Ladina Hösli, Luca Ravotto, E Dale Abel, Johannes Bohacek, Susanne Wegener, L Felipe Barros, Mohamad El Amki, Bruno Weber, Aiman S Saab.
      Brain activity relies on a steady supply of blood glucose. Astrocytes express glucose transporter 1 (GLUT1), considered their primary route for glucose uptake to sustain metabolic and antioxidant support for neurons. While GLUT1 deficiency causes severe developmental impairments, its role in adult astrocytes remains unclear. Here, we show that astrocytes and neurons tolerate the inducible, astrocyte-specific deletion of GLUT1 in adulthood. Sensorimotor and memory functions remain intact in male GLUT1 cKO mice, indicating that GLUT1 loss does not impair behavior. Despite GLUT1 loss, two-photon glucose sensor imaging reveals that astrocytes maintain normal resting glucose levels but exhibit a more than two-fold increase in glucose consumption, indicating enhanced metabolic activity. Notably, male GLUT1 cKO mice display reduced infarct volumes following stroke, suggesting a neuroprotective effect of increased astrocytic glucose metabolism. Our findings reveal metabolic adaptability in astrocytes, ensuring glucose uptake and neuronal support despite the absence of their primary transporter.
    DOI:  https://doi.org/10.1038/s41467-025-59400-2
  8. Nature. 2025 May 05.
    Teens with anxiety and depression spend more time on social media.
    Mariana Lenharo.
      
    Keywords:  Depression; Human behaviour; Media; Psychiatric disorders
    DOI:  https://doi.org/10.1038/d41586-025-01359-7
  9. Nature. 2025 May 08.
    Guess how much of the ocean floor humans have explored.
    Davide Castelvecchi.
      
    Keywords:  Geography; Geophysics; Ocean sciences
    DOI:  https://doi.org/10.1038/d41586-025-01431-2
  10. Nat Methods. 2025 May 08.
    Coupling the 3D epigenome to the transcriptome in single cells.
      
    DOI:  https://doi.org/10.1038/s41592-025-02666-7
  11. Nat Neurosci. 2025 May 08.
    An energy blueprint of the human brain.
    Henrietta Howells.
      
    DOI:  https://doi.org/10.1038/s41593-025-01967-6
  12. Immunity. 2025 May 02. pii: S1074-7613(25)00177-3. [Epub ahead of print]
    Somatic hypermutation unlocks antibody specificities beyond the primary repertoire.
    Teng Zuo, Avneesh Gautam, Shahab Saghaei, Sweta N Khobragade, Rahaman Ahmed, Azadeh Mahdavinia, Mehrdad Zarghami, Gaspar A Pacheco, Kenneth Green, Meghan Travers, Nicholas Garcia, Zahra Allahyari, Vishal Rao, Sachin Kumar, Robert Novak, Joyce K Hwang, Duane R Wesemann.
      B cell somatic hypermutation (SHM) and selection in germinal centers (GCs) enhance antibody affinity for antigen. Here, we investigated whether SHM-based antibody evolution is restricted to specificities established through V(D)J recombination in the primary repertoire. Tracking pre-defined non-specific B cells across multiple immunization models revealed that non-cognate B cells within GCs undergo SHM. Under conditions of limited B cell competition, these B cells generated de novo antigen recognition to multiple epitopes across diverse model antigens. Phylogenetic analyses identified diverse mutational pathways leading to new antigen affinities, and enhanced T cell co-stimulation further promoted new antigen recognition. Our data support a model in which B cell competition-rather than an intrinsic requirement for specific affinity-limits the emergence of new affinities through SHM, highlighting the mammalian adaptive immune system's ability to explore antibody-antigen interactions beyond those encoded by the V(D)J-dependent primary repertoire, demonstrating the flexibility of SHM in not only ripening but also reshaping specificity.
    Keywords:  B cell; BCR diversifications; affinity maturation; antibody; antibody evolution; antibody specificity; competition; de novo antigen recognition; germinal center; somatic hypermutation
    DOI:  https://doi.org/10.1016/j.immuni.2025.04.014
  13. Nature. 2025 May 07.
    How we taste sweetness: long-sought structure of human receptor mapped at last.
    Elie Dolgin.
      
    Keywords:  Biochemistry; Molecular biology; Sensory systems
    DOI:  https://doi.org/10.1038/d41586-025-01408-1
  14. Nat Commun. 2025 May 06. 16(1): 4187
    A hidden cysteine in Fis1 targeted to prevent excessive mitochondrial fission and dysfunction under oxidative stress.
    Suman Pokhrel, Gwangbeom Heo, Irimpan Mathews, Shun Yokoi, Tsutomu Matsui, Ayori Mitsutake, Soichi Wakatsuki, Daria Mochly-Rosen.
      Fis1-mediated mitochondrial localization of Drp1 and excessive mitochondrial fission occur in human pathologies associated with oxidative stress. However, it is not known how Fis1 detects oxidative stress and what structural changes in Fis1 enable mitochondrial recruitment of Drp1. We find that conformational change involving α1 helix in Fis1 exposes its only cysteine, Cys41. In the presence of oxidative stress, the exposed Cys41 in activated Fis1 forms a disulfide bridge and the Fis1 covalent homodimers cause increased mitochondrial fission through increased Drp1 recruitment to mitochondria. Our discovery of a small molecule, SP11, that binds only to activated Fis1 by engaging Cys41, and data from genetically engineered cell lines lacking Cys41 strongly suggest a role of Fis1 homodimerization in Drp1 recruitment to mitochondria and excessive mitochondrial fission. The structure of activated Fis1-SP11 complex further confirms these insights related to Cys41 being the sensor for oxidative stress. Importantly, SP11 preserves mitochondrial integrity and function in cells during oxidative stress and thus may serve as a candidate molecule for the development of treatment for diseases with underlying Fis1-mediated mitochondrial fragmentation and dysfunction.
    DOI:  https://doi.org/10.1038/s41467-025-59434-6
  15. Nat Cell Biol. 2025 May 09.
    Regulation of RIG-I activity by phase separation reveals new therapeutic opportunities.
      
    DOI:  https://doi.org/10.1038/s41556-025-01656-3
  16. Nat Commun. 2025 May 05. 16(1): 4170
    Dysregulated mast cell activation induced by diabetic milieu exacerbates the progression of diabetic peripheral neuropathy in mice.
    Xiangyun Yao, Xin Wang, Rui Zhang, Lingchi Kong, Cunyi Fan, Yun Qian.
      Diabetic peripheral neuropathy (DPN), a common disorder in diabetes, is associated with severe microenvironment imbalance due to immunometabolic stress. However, the underlying mechanistic drivers remain unclear. Here, we generate a single-cell atlas of human peripheral nerves and identify cell-specific transcriptional changes in DPN as well as aberrant amplification of mast cells. Using streptozotocin-induced mouse diabetes models, we further find that glucose uptake mediated by GLUT3 in high-glucose (HG) diabetic milieu upregulates ERK1/2 phosphorylation in mouse mast cells. Sustained HG stimulation also induces aberrant mTOR hyperactivity, resulting in endoplasmic reticulum stress and mitochondrial oxidative stress, thereby impairing mitochondrial functions of mast cells. Dysregulated mast cells then degranulate and release histamine, tryptase and inflammatory factors into neural microenvironment to cause neuropathy in diabetic mice. Lastly, mice with mast cell deficiency are protected from the immune imbalance in nerves and progression of neuropathy. Our findings thus implicate dysregulated activation of mast cells as a potential driver in the progression of DPN.
    DOI:  https://doi.org/10.1038/s41467-025-59562-z
  17. Nat Neurosci. 2025 May 09.
    Widespread brain-body integration during changes of arousal.
      
    DOI:  https://doi.org/10.1038/s41593-025-01946-x
  18. Nature. 2025 May;641(8062): 284
    Cuts to US science will take a generation to repair - leaders must speak up now.
    Michael S Lubell.
      
    Keywords:  Government; Policy; Scientific community; Society
    DOI:  https://doi.org/10.1038/d41586-025-01348-w
  19. FASEB J. 2025 May 15. 39(9): e70549
    Reduced Palmitoylation of SQSTM1/p62 in Huntington Disease Is Associated With Impaired Autophagy.
    F Abrar, M C Davies, Y Alshehabi, A Kumar, A Dang, Y T N Nguyen, J Collins, N S Caron, J S Choudhary, S S Sanders, M O Collins, M R Hayden, D D O Martin.
      Disruption of autophagy has emerged as a common feature in many neurodegenerative diseases. Autophagy is a membrane-dependent pathway that requires many key regulators to quickly localize on and off membranes during induction, promoting membrane fusion. Previously, our bioinformatic approaches have shown that autophagy and Huntington disease (HD) are enriched in palmitoylated proteins. Palmitoylation involves the reversible addition of long-chain fatty acids to promote membrane binding. Herein, we show that inhibition of palmitoylation regulates the abundance of several key regulators of autophagy and leads to a partial block of autophagic flux. We confirm that the autophagy receptor SQSTM1/p62 (sequestosome 1) is palmitoylated and directed to the lysosome. Importantly, we report that SQSTM1 palmitoylation is significantly reduced in HD patient and mouse model brains. This finding reveals a novel mechanism contributing to the generation of empty autophagosomes previously seen in HD models and patient-derived cells.
    DOI:  https://doi.org/10.1096/fj.202401781R
  20. Dev Cell. 2025 May 02. pii: S1534-5807(25)00250-3. [Epub ahead of print]
    Lymphatic endothelial mTORC1 instructs metabolic and developmental signaling during lymphangiogenesis.
    Fei Han, Summer Simeroth, Jie Zhu, Irma Gryniuk, Atul Pranay, Weiqing Chen, Yuan Wang, Yuanyuan Cai, Zhiyuan Shen, Guangyu Wang, Courtney T Griffin, Lijun Xia, Pengchun Yu.
      The lymphatic vasculature comprises lymphatic capillaries and collecting vessels. To support lymphatic development, lymphatic endothelial cells (LECs) utilize nutrients to fuel lymphangiogenic processes. Meanwhile, LECs maintain constant prospero homeobox 1 (PROX1) expression critical for lymphatic specification. However, molecular mechanisms orchestrating nutrient metabolism while sustaining PROX1 levels in LECs remain unclear. Here, we show that loss of RAPTOR, an indispensable mechanistic target of rapamycin complex 1 (mTORC1) component, downregulates PROX1 and impairs lymphatic capillary growth and differentiation of collecting lymphatics in mice. Mechanistically, mTORC1 inhibition in mouse and human LECs causes Myc reduction, which decreases hexokinase 2 (HK2) and glutaminase (GLS), inhibiting glycolysis and glutaminolysis. Myc or HK2/GLS ablation impedes lymphatic capillary and collecting vessel formation. Interestingly, mTORC1 regulation of PROX1 is independent of Myc-HK2/GLS signaling. Moreover, genetic interaction analysis indicates that Myc and PROX1 play crucial roles in mTORC1-regulated lymphatic development. Collectively, our findings identify mTORC1 as a key regulator of metabolic programs and PROX1 expression during lymphangiogenesis.
    Keywords:  Myc; PROX1; glutaminase; glutaminolysis; glycolysis; hexokinase 2; lymphangiogenesis; lymphatic endothelial cell; lymphatic vessel; mTORC1
    DOI:  https://doi.org/10.1016/j.devcel.2025.04.012
  21. Nat Rev Immunol. 2025 May 06.
    CD45-PET imaging gives a panoramic view of in vivo immune activity.
    Sina Djafari Rouhani, Mohammad Rashidian.
      
    DOI:  https://doi.org/10.1038/s41577-025-01183-0
  22. Immunity. 2025 May 02. pii: S1074-7613(25)00174-8. [Epub ahead of print]
    A hierarchy of intestinal antigens instructs the CD4+ T cell receptor repertoire.
    Jaeu Yi, Jisun Jung, David Horton, Patricia Hsieh, Yangqing Peng, Sean J Wang, Rodney Newberry, Aaron C Ericsson, Kwang Soon Kim, Andrew L Kau, Chyi-Song Hsieh.
      Intestinal CD4+ T cells that are specific for self-, diet-, or commensal-derived antigens are critical for host tolerance but must also be tightly regulated to prevent aberrant activation and conditions like inflammatory bowel disease (IBD). However, it is unclear how the antigen source and location dictate the intestinal TCR repertoire. Here, we hierarchically classified self-, diet-, or microbiota-dependent TCRs using TCliβ TCRβ transgenic mice. This demonstrated that microbiota had a greater influence than diet on CD4+ T cell responses throughout the intestine at homeostasis. Complex bi-directional interactions between microbes and diet were also observed. In the context of murine colitis as a model of IBD, we showed that antigen-free diet substantially altered the microbiota and associated T cell responses, which ameliorated intestinal inflammation. Collectively, these findings suggest how deconvoluting the gut immune interactome may facilitate identifying primary microbial and dietary drivers of T cell responses during health and disease.
    Keywords:  CD4(+) T cell responses to self-, diet, and microbial antigens; hierarchical TCR classification; inflammatory bowel disease; intestinal CD4(+) T cell responses; macro- and micro-immunologic CD4(+) T cell response; network analysis of TCR and microbe 16S sequences
    DOI:  https://doi.org/10.1016/j.immuni.2025.04.011
  23. Proc Natl Acad Sci U S A. 2025 May 13. 122(19): e2502256122
    Hdac1 as an early determinant of intermediate-exhausted CD8+ T cell fate in chronic viral infection.
    Wei Hu, Shengen Shawn Hu, Shaoqi Zhu, Weiqun Peng, Vladimir P Badovinac, Chongzhi Zang, Xudong Zhao, Hai-Hui Xue.
      The exhausted CD8+ T (TEX) cells consist of distinct subsets including Tcf1+ stem-like, Tcf1-Cx3cr1+ intermediate (TEX-int) and Tcf1-Cx3cr1- terminally exhausted cells; yet, epigenetic determinants of TEX subset differentiation remain incompletely understood. Using chronic viral infection, we show that histone deacetylase 1 (Hdac1) was specifically required for the formation of antigen-specific TEX-int cells at the effector phase of responses. Single-cell transcriptomics validated that Hdac1 deficiency depleted TEX-int cells and revealed that Hdac1 was critical for positive regulation of TEX-int-characteristic genes, including Cx3cr1, Cxcr6, and Klf2. Furthermore, profiling chromatin accessibility landscape in TEX subsets demonstrated that loss of Hdac1 resulted in a prevalent increase in chromatin open state, as evidently observed at the exhaustion program genes, which were linked to induced expression of exhaustion-inducing Tox transcription factor, PD1 and Lag3 coinhibitory receptors in TEX cells. Hdac1 thus has dual regulatory functions: promoting TEX-int cell fate and preventing excessive activation of the exhaustion program to curtail uncontrolled virus replication.
    Keywords:  T cell exhaustion; epigentic regulation; histone deacetylase; transitory state
    DOI:  https://doi.org/10.1073/pnas.2502256122
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