bioRxiv Preprints

{
  "doi": "10.64898/2026.07.24.740503",
  "url": "https://www.biorxiv.org/content/10.64898/2026.07.24.740503v1",
  "title": "Metagenomic Discovery of Neutral Lipid Metabolism Pathways in the Arctic Ocean Microbiomes Suggests a Potential New Role in Survival and Oceanic Carbon Cycling",
  "source": "biorxiv",
  "authors": "Grevesse, T.; Walsh, D. A.; McLatchie, S.; Onana, V. E.",
  "version": "1",
  "abstract": "The Arctic Ocean microbiomes experience extreme seasonal fluctuations in light, nutrient availability, and organic carbon supply. In this environment, neutral lipid storage may provide a key survival strategy. Here, we investigated the diversity, distribution, and ecological role of neutral lipid metabolism in Arctic microbiomes using metagenome-resolved analyses and global ocean comparisons. Arctic photic-zone microbiomes were strongly enriched in triacylglycerol (TAG) biosynthesis genes relative to other oceans, primarily due to picoeukaryotic phytoplankton, including the ecologically dominant Micromonas and Bathycoccus. In contrast, prokaryotic communities exhibited diverse TAG-degrading taxa and fatty acid transport systems, supporting a previously unrecognized lipotrophic bacterial guild exploiting phytoplankton-derived lipids as carbon and energy sources. Genome-resolved analyses further revealed distinct bacterial lipid-storage strategies: TAG-producing taxa preferentially encoded fatty acid uptake and carbohydrate utilization pathways, whereas polyhydroxyalkanoate-producing taxa were associated with aromatic compound degradation, linking terrestrial organic matter to lipid ",
  "category": "microbiology",
  "published_at": "2026-07-27T00:00:00.000Z",
  "corresponding_author": "Thomas Grevesse",
  "journal_published_doi": null,
  "corresponding_institution": "New York University Abu Dhabi"
}

{
  "doi": "10.64898/2026.04.07.716930",
  "url": "https://www.biorxiv.org/content/10.64898/2026.04.07.716930v2",
  "title": "Ramping-up hippocampal ripples and their neocortical coupling support human visual short-term memory",
  "source": "biorxiv",
  "authors": "Liu, J.; He, X.; Yang, C.; Axmacher, N.; Xue, G.; Zhang, S.; Cai, Y.",
  "version": "2",
  "abstract": "Emerging evidence suggests that the hippocampus contributes to visual short-term memory (VSTM). However, the neural mechanisms through which hippocampal activity supports the maintenance of VSTM representations remain largely unknown. Here, using intracranial EEG recordings from human participants performing a delayed match-to-sample task for naturalistic objects, we investigated the role of hippocampal ripple activity--brief high-frequency oscillations associated with memory replay--in VSTM maintenance and hippocampal-neocortical communication. We found that hippocampal ripple rates progressively ramped up during the maintenance period and supported successful VSTM. More critically, hippocampal ripples were temporally coupled with the ripples in the lateral temporal lobe (LTL), and these coupled ripples were associated with memory reactivation in the LTL. These findings provide direct evidence that hippocampal-neocortical interaction via coupled ripples supports VSTM, extending the role of hippocampal ripples from long-term consolidation to short-term mnemonic processes and offering new insights into the dynamic coding mechanisms of working memory. Impact StatementHippocampal ripp",
  "category": "neuroscience",
  "published_at": "2026-07-27T00:00:00.000Z",
  "corresponding_author": "Ying Cai",
  "journal_published_doi": null,
  "corresponding_institution": "Zhejiang University"
}

{
  "doi": "10.64898/2026.07.24.740442",
  "url": "https://www.biorxiv.org/content/10.64898/2026.07.24.740442v1",
  "title": "Gp130 Orchestrates a Bidirectional Neuron-Microglia Circuit for neuroprotection",
  "source": "biorxiv",
  "authors": "Willis, E. F.; Stuart, S. J. S.; Dierich, M.; Grice, L.; Ettich, J.; Kim, S. J.; Yang, Z.; Xu, Y.; Hooper, C. L.; Bianciotto, C.; Lao, H. W.; Pham, D.; Nguyen, Q.; Febbraio, M.; Corrigan, F.; Teasdale, R.; Scheller, J.; Rose-John, S.; Ruitenberg, M. J.; Vukovic, J.",
  "version": "1",
  "abstract": "Acquired central nervous system (CNS) injury is one of the most common neurological conditions globally, yet effective treatment options are lacking. As the main tissue-resident macrophages of the CNS, microglia have emerged as key functional regulators of CNS repair. However, means to induce neuroprotective microglia and harness their intrinsic repair capabilities have remained elusive. Here we identify gp130 as a key receptor molecule for facilitating bidirectional microglia-neuron communication that improves outcomes from CNS injury. We show that activation of gp130 in CNS-resident microglia triggers the secretion of leukemia inhibitory factor (LIF), a neurotrophic cytokine. LIF induces neuronal IL-6 secretion that then acts back onto the microglial gp130 receptor, thus creating a neuroprotective loop. We demonstrate the broad therapeutic potential of acute gp130 activation across multiple models, including traumatic brain injury, stroke, and spinal cord injury, and that this pathway can be leveraged therapeutically with designer cytokines.",
  "category": "neuroscience",
  "published_at": "2026-07-27T00:00:00.000Z",
  "corresponding_author": "Jana Vukovic",
  "journal_published_doi": null,
  "corresponding_institution": "Faculty of Health, Medicine and Biomedical Sciences, The University of Queensland, Brisbane, Australia"
}

{
  "doi": "10.64898/2026.07.21.739817",
  "url": "https://www.biorxiv.org/content/10.64898/2026.07.21.739817v2",
  "title": "TRIM28 preserves ovarian identity by stabilising lineage-specific transcription factor hubs",
  "source": "biorxiv",
  "authors": "Sitkiewicz, L.; Chaleil, F.; Granes, G.; Rossitto, M.; Dejardin, S.; Cammas, F.; Lefrancois-Martinez, A.-M.; Stevant, I.; Poulat, F.",
  "version": "2",
  "abstract": "Maintenance of ovarian cell identity is required throughout life to prevent the activation of the testicular programme, but the epigenetic mechanisms underlying this process remain poorly understood. Although TRIM28 is required to prevent granulosa-to-Sertoli transdifferentiation, it can act both as a regulator of H3K9me3-dependent heterochromatin and as a transcriptional co-regulator through its E3 SUMOligase activity. Here, we combined CUT&RUN, ATAC-seq and RNA-seq to define the respective contributions of these activities to maintain ovarian cell identity. Strikingly, only a small fraction of TRIM28-bound regions was associated with H3K9me3. Although Trim28 deletion induced focal H3K9me3 loss, it had limited transcriptional consequences and primarily affected repetitive elements rather than regions controlling testis-determining genes. In contrast, Trim28 loss led to reductions in chromatin accessibility and H3K27ac at regions enriched for ovarian transcription factor (TF) motifs FOXL2, NR5A2, ESR2 and RUNX1. Moreover, TRIM28 was frequently co-localised with these factors on chromatin, and the accessibility these co-bound regions were reduced by Trim28 deletion. Finally, SUMOyla",
  "category": "genomics",
  "published_at": "2026-07-27T00:00:00.000Z",
  "corresponding_author": "Isabelle Stevant",
  "journal_published_doi": null,
  "corresponding_institution": "Institute of Human Genetics, CNRS UMR9002 University of Montpellier, 34396, Montpellier, France"
}

{
  "doi": "10.64898/2026.07.24.740626",
  "url": "https://www.biorxiv.org/content/10.64898/2026.07.24.740626v1",
  "title": "Multisensory integration while learning to read: A longitudinal functional and structural MRI study",
  "source": "biorxiv",
  "authors": "Finnemann, J.; Jeong, G.-r.; Horowitz-Kraus, T.; Skeide, M. A.",
  "version": "1",
  "abstract": "Literacy development involves the recognition and integration of auditory and visual signals and as such offers a unique opportunity to track the development of an eventually efficient multisensory processing network. To shed light on this topic we conducted a 12-month longitudinal 3 Tesla functional and structural MRI study in children beginning to receive formal literacy instruction. Twenty-three six-year-old German-speaking participants completed four fMRI sessions during which they were presented with letters, speech sounds, or their audiovisual combinations in congruent and incongruent formats. Longitudinal changes in BOLD response amplitude were assessed using linear mixed-effects models. Over the course of learning to read, we observed significant changes in modulations of BOLD activity for the congruent - incongruent contrast within a left-lateralised network encompassing the central opercular cortex, anterior supramarginal gyrus, inferior frontal gyrus (pars triangularis) and frontal pole. These effects were primarily driven by a gradual increase of response amplitude across sessions, consistent with the refinement of audiovisual integration mechanisms. Together, these fin",
  "category": "neuroscience",
  "published_at": "2026-07-27T00:00:00.000Z",
  "corresponding_author": "Johanna Finnemann",
  "journal_published_doi": null,
  "corresponding_institution": "Max Planck Institute for Human Cognitive and Brain Sciences"
}

{
  "doi": "10.64898/2026.07.24.740570",
  "url": "https://www.biorxiv.org/content/10.64898/2026.07.24.740570v1",
  "title": "Individualized surface parcellation enhances characterization of resting-state brain dynamics and their alterations in schizophrenia",
  "source": "biorxiv",
  "authors": "Watters, H. N.; Furstova, P.; Tintera, J.; Spaniel, F.; Hlinka, J. N.",
  "version": "1",
  "abstract": "Resting-state functional MRI (rs-fMRI) studies in schizophrenia commonly rely on normalization to volumetric templates and fixed atlas parcellations derived from neurotypical populations. While these approaches enable group-level comparisons, they may obscure individual variation in cortical organization and intrinsic brain dynamics. In this study, we compared four preprocessing and parcellation strategies across two independent schizophrenia cohorts (MRI site 1, n=159; MRI site 2, n=255) to evaluate how analytic choices affect static functional connectivity and dynamic quasi-periodic pattern (QPP) measures, including default mode-dorsal attention network opposition, QPP component rank, explained variance, event rate, and associations with PANSS symptom severity. Across datasets, individualized surface-based parcellation (IndiPar) consistently detected more pronounced QPP dynamics, stronger default mode / dorsal attention network opposition, and greater explained variance of QPPs relative to atlas-based pipelines. IndiPar also produced larger and more reproducible patient-control differences in functional connectivity and QPP event-rate measures, suggesting improved sensitivity thr",
  "category": "neuroscience",
  "published_at": "2026-07-27T00:00:00.000Z",
  "corresponding_author": "Harrison Neil Watters",
  "journal_published_doi": null,
  "corresponding_institution": "Weber State University"
}

{
  "doi": "10.64898/2026.07.22.739677",
  "url": "https://www.biorxiv.org/content/10.64898/2026.07.22.739677v1",
  "title": "H5N1 influenza binding and cell entry via human class II MHC, and blocking by cross-reactive antibodies",
  "source": "biorxiv",
  "authors": "Pursell, T.; Mikelov, A.; Wirz, O. F.; Ort, J. T.; Li, S. H.; Atkinson, R. K.; Zhong, J.; Santos, J. J. S.; Joshi, S. A.; Afghani, J.; Han, X.; Haraguchi, E.; Hoh, R. A.; Lee, J.-Y.; Lam, B.; Stanford, A.; DeLaitsch, A. T.; Schuetz, J.; Röltgen, K.; Van Slyck, S.; Smith, D.; Ha, B.; Niemann, C. U.; Hensley, S. E.; Boyd, S. D.",
  "version": "1",
  "abstract": "Highly pathogenic avian influenza H5N1 clade 2.3.4.4b viruses are currently responsible for a multi-species outbreak affecting wild birds, poultry, numerous mammalian species, and humans. Influenza A viruses typically initiate infection through binding to sialic acid, although select bat and human influenza viruses can also exploit class II major histocompatibility complex (MHC-II) molecules for cell entry. Here we show that emerging H5N1 clade 2.3.4.4b viruses, but not historical H5 lineages, bind human MHC-II HLA-DR and mediate sialic acid-independent cell entry. Hemagglutinin binding to primary human immune cells varies with MHC-II expression and is further shaped by HLA-DR allelic variation, identifying host genetic determinants that may influence susceptibility to infection. Mammalian-adaptive substitutions within the hemagglutinin sialic acid receptor-binding domain reduce MHC-II binding, suggesting this interaction is remodeled during clade 2.3.4.4b H5 adaptation to a human host. Lastly, cross-reactive monoclonal antibodies isolated from clade 2.3.4.4b H5-naive humans can block the hemagglutinin-MHC-II interaction. These findings identify a previously unrecognized receptor p",
  "category": "immunology",
  "published_at": "2026-07-26T00:00:00.000Z",
  "corresponding_author": "Scott D Boyd",
  "journal_published_doi": null,
  "corresponding_institution": "Stanford University"
}

{
  "doi": "10.1101/2025.03.07.642033",
  "url": "https://www.biorxiv.org/content/10.1101/2025.03.07.642033v2",
  "title": "Role of mast cells in endomicrobial sepsis revisited: Mast cell-deficient mice show normal immunological protection",
  "source": "biorxiv",
  "authors": "Feyerabend, T. B.; Schochter, F.; Tasdogan, A.; Bechberger, M.; Rodewald, H.-R.",
  "version": "2",
  "abstract": "Kit-mutant mice are highly susceptible to polymicrobial sepsis elicited by cecal ligation and puncture (CLP). This vulnerability has been attributed to the mast cell deficiency of Kit mutants, suggesting key roles of mast cells in antibacterial defense. We show that mice lacking mast cells but wild-type for Kit are as resistant to sepsis as mast cell-proficient mice, excluding mast cells as protective factor. Induction of sepsis by direct injection of intestinal microbiota instead of surgical gut perforation revealed comparable protective responses of Kit-deficient and Kit wild-type mice, indicating intact antibacterial immunity in the absence of Kit. Notably, cecal contents of Kit-mutant mice contained 1000-fold greater Escherichia coli colony-forming units compared to wild-type mice. Consistently, 16S rRNA gene sequencing revealed a broad compositional shift characterized by enrichment of Enterobacteriaceae and other taxa associated with inflammatory intestinal states, in keeping with intestinal dysmotility in Kit-mutant mice. Thus, upon intestinal puncture, overrepresentation of pathogenic bacteria led to a more severe infection of Kit mutants compared to wild-type controls. Hen",
  "category": "immunology",
  "published_at": "2026-07-26T00:00:00.000Z",
  "corresponding_author": "Hans-Reimer Rodewald",
  "journal_published_doi": null,
  "corresponding_institution": "German Cancer Research Center (DKFZ)"
}

{
  "doi": "10.64898/2026.07.24.740563",
  "url": "https://www.biorxiv.org/content/10.64898/2026.07.24.740563v1",
  "title": "Sialyl-Tn-positive tumour-derived extracellular vesicles impair dendritic cell function via horizontal transfer of glycans",
  "source": "biorxiv",
  "authors": "Silva, Z. C.; Andre, N. D.; Sharma, S.; Vieira, M. S.; de Oliveira, B. R.; Videira, P. A.",
  "version": "1",
  "abstract": "The sialyl-Tn (STn) glycan antigen is aberrantly expressed in a subset of triple-negative breast cancer (TNBC) and is associated with poor prognosis and immunosuppressive microenvironment. Tumour-derived extracellular vesicles (TDEVs) are emerging regulators of immune escape, however the role of glycan-mediated mechanisms remains elusive. Aberrant glycosylation is a hallmark of cancer that extends to TDEVs, yet how tumour-associated glycans within EV cargo modulate cell function remains poorly understood. Here, we used engineered MDA-MB-231 TNBC cells to overexpress the glycosyltransferase ST6GalNAc-I, generating STn-positive cells whose EVs were enriched in STn (STn+ EV). The STn+ EVs impaired the maturation of monocyte-derived dendritic cells (DCs), reduced antigen presentation, and diminished CD4 and CD8 T cell priming, alongside the expansion of regulatory T cells. DCs co-cultured with STn EVs display STn at their cell surface. Notably, STn+ EVs transferred both STn antigen and the ST6GalNAc-I to recipient DCs. Enzymatic removal of terminal sialic acids from STn EVs reversed the immunosuppressive effects, confirming the STn-dependent nature of DC dysfunction. These findings add",
  "category": "immunology",
  "published_at": "2026-07-26T00:00:00.000Z",
  "corresponding_author": "Zelia C Silva",
  "journal_published_doi": null,
  "corresponding_institution": "UCIBIO"
}

{
  "doi": "10.64898/2026.07.24.740376",
  "url": "https://www.biorxiv.org/content/10.64898/2026.07.24.740376v1",
  "title": "IL-13 Induces a Tuft Cell-Intrinsic CD45 Checkpoint to Limit Intestinal Type 2 Immunity",
  "source": "biorxiv",
  "authors": "Sochen, C.; Lebon, S.; Habshush-Menachem, A.; Sarusi-Portuguez, A.; Holiar, V.; Rudenko, V.; Toval, B.; Liu, J.; Levin, Y.; Vaaknin, E.; Rosenthal, N.; Tiferet, N.; Orr, I.; Ben-Dor, S.; Haffner-Krausz, R.; Grencis, R.; Munitz, A.; Karo-Atar, D.; Shulman, Z.; Biton, M.",
  "version": "1",
  "abstract": "Tuft cells initiate intestinal type 2 immunity, yet the mechanisms that restrain excessive tuft cell activation remain poorly understood. Here, we identify the receptor tyrosine phosphatase CD45 (Ptprc), previously considered a hematopoietic marker, as a regulator of intestinal tuft cell function. CD45 expression is restricted to a subset of tuft cells and is induced by helminth infection and IL-13. Epithelial-specific deletion of Ptprc activated a tuft cell inflammatory program, promoted an epithelial inflammatory state, and increased eosinophil accumulation at homeostasis. During Heligmosomoides polygyrus bakeri infection, CD45 deficiency enhanced ILC2 and Th2 responses and reduced parasite burden, demonstrating that epithelial CD45 limits type 2 immunity in vivo. Accordingly, in intestinal organoids, CD45 was dispensable for IL-13-driven tuft cell differentiation but restrained IL-13-responsive transcriptional programs. Mechanistically, CD45-deficient tuft cells exhibited altered protein abundance of STAT5 and IL17RB, implicated in tuft cell immune regulation. Together, these findings identify CD45 as a tuft cell-intrinsic regulatory checkpoint that restrains intestinal type 2 i",
  "category": "immunology",
  "published_at": "2026-07-26T00:00:00.000Z",
  "corresponding_author": "Moshe Biton",
  "journal_published_doi": null,
  "corresponding_institution": "Department of Immunology and Regenerative Biology, Weizmann Institute of Science, Rehovot, Israel"
}