Biology subjects

Chen, X.

Publications and source records attributed to Chen, X..

At least 199 records · Page 11Linked to original sources

bioRxiv2026

Chronic Paraventricular OX1R Overexpression Induces Oxidative Stress and Hypertension in Rats

BackgroundHyperactivity of the orexin system has been implicated in hypertension, yet the long-term impact of orexin 1 receptor (OX1R) overexpression in the paraventricular nucleus (PVN), a key brain region involved in arterial blood pressure (ABP) regulation, remains unclear. This study examined whether chronic OX1R overexpression in the PVN alters cardiovascular, neuroendocrine, and oxidative functions. MethodsAdult male Sprague-Dawley rats received bilateral PVN injections of AAV2-OX1R or control virus AAV2-GFP. Their ABP and heart rate (HR) were monitored for eight weeks via radiotelemetry. Renal sympathetic nerve activity (RSNA) and ABP responses to PVN orexin A administration were assessed using in vivo recordings. Reactive oxygen species (ROS) were quantified using MitoProbe, and gene expression was analyzed by qPCR. Primary neuronal cultures were used to explore underlying mechanism involved in increased ROS production and neuronal activity. ResultsPVN OX1R overexpression increased mean ABP ([~]10 mmHg), water intake, and ROS levels in both the PVN and peripheral organs. In addition, orexin A evoked exaggerated RSNA (155% vs. 73%) and pressor responses (27 vs. 16 mmHg) in PVN OX1R overexpression rats compared to control rats, these effects were attenuated by the OX1R antagonist SB408124. Plasma vasopressin levels were elevated, and brain sections confirmed increased ROS in OX1R-positive neurons. In vitro experiments further demonstrated that orexin A upregulated ROS-generating enzymes, suppressed antioxidant genes, and enhanced neuronal excitability. ConclusionChronic PVN OX1R overexpression induces oxidative stress, sympathetic overactivity, and increased plasma vasopressin, contributing to hypertension development. Targeting PVN OX1R signaling may provide therapeutic benefit for hypertension.

physiology↗

bioRxiv2026

Protenix-v1: Toward High-Accuracy Open-Source Biomolecular Structure Prediction

We introduce Protenix-v1 (PX-v1), the first fully open-source structure prediction model to attain superior performance to AlphaFold3 while strictly adhering to the same training data cutoff, model size, and inference budget. Beyond standard evaluations, we highlight the effectiveness of inference-time scaling behavior of Protenix-v1, demonstrating that increasing the sampling budget yields consistent improvements in prediction quality--a behavior previously observed in AlphaFold3 and largely absent from prior open-source models. In addition to improved accuracy, Protenix-v1 incorporates key capabilities including protein template integration and RNA MSA support. Furthermore, to better support real-world applications such as drug discovery, we additionally release Protenix-v1-20250630, a variant trained on a larger dataset (cutoff: June 30, 2025), delivering further improved prediction accuracy. Finally, we identify limitations in existing benchmarking practices and provide updated evaluation tools and year-stratified benchmarks to support more reliable and transparent assessment. Collectively, these contributions provide a robust foundation for the Protenix series and the broader field.

bioinformatics↗

bioRxiv2026

Systematic mapping of emergent transcriptional states in interacting single-cell dyads by Cell-Cell-seq

Cell-cell interactions drive rapid and heterogeneous changes in gene expression, yet most transcriptomic methods either dissociate cells, losing pair identity and interaction timing, or infer communication indirectly from ligand-receptor co-expression. Here we present Cell-Cell-seq, a scalable workflow for profiling defined cell pairs ("dyads") with single-cell transcriptomic resolution. Cell-Cell-seq uses cavity-containing hydrogel microparticles (Nanovials) to confine two cells, synchronize contact onset, protect fragile conjugates during handling and sorting, and interface directly with droplet-based RNA sequencing. Using antigen-matched prostate tumor cells and engineered T cells as a model system, Cell-Cell-seq captured thousands of tumor-T cell dyads and revealed broad functional and transcriptional heterogeneity across interactions. Dyads unmasked transient activation programs that were obscured in standard well-plate co-culture, consistent with asynchronous contact in bulk assays. To distinguish interaction-induced programs from the composite nature of dyad transcriptomes, we developed a pseudo-mixing framework that generates in silico pseudo-dyads to construct an empirical null distribution under "no interaction," enabling statistically robust identification of emergent genes and partner-resolved attribution of responses. Dyad-resolved analysis further revealed coordinated cross-cell programs, including coupled chemokine expression consistent with bidirectional paracrine signaling and inverse coupling between tumor immunoregulatory programs and T cell activation. Finally, we introduce ccRepair to correct compositional dilution in mixed transcriptomes, improving interpretability while preserving genuine cross-cell coordination. Together, Cell-Cell-seq provides a generalizable platform for dissecting immune synapse biology and mapping interaction-dependent programs across heterogeneous cell populations, with applications in profiling tumor-immune communication and functionally screening immunotherapies.

bioengineering↗

bioRxiv2026

Hog1/p38 and ZAKα drive Shwachman-Diamond syndrome and provide targets to improve cell growth

Shwachman-Diamond syndrome (SDS) is a ribosomopathy characterized by neutropenia, pancreatic insufficiency, skeletal defects, and predisposition to leukemia. Most cases result from biallelic SBDS mutations that impairing 80S ribosome and polysome assembly. In yeast lacking SDO1 (the SBDS ortholog), growth slows dramatically and the p38 ortholog Hog1 signaling is elevated by multiple types of stress. SBDS-deficient HeLa cells exhibited reduced proliferation and slowed cell cycling. The p38 kinase was constitutively activated in SBDS mutants and SDS patient-derived blood cells. Because ZAK detects ribosome dysfunction, its activation links ribosomal defects to stress kinase pathways in SDS. Suppressing p38 or its upstream activator ZAK restored cell growth and reduced stress signaling. These findings reveal an evolutionarily conserved-independent mechanism via p38 drives SDS pathophysiology and identifies stress kinases as potential therapeutic targets for ribosomal dysfunction.

cell biology↗

bioRxiv2026

Decomposing multi-scale dynamic regulation from single-cell multiomics with scMagnify

Deciphering the highly coupled regulatory circuits that drive cellular dynamics remains a fundamental goal in biology. However, capturing the multi-scale time-lagged dynamics and combinatorial regulatory logic of gene regulation remains computationally challenging. Here we present scMagnify, a deep-learning-based framework that leverages multiomic single-cell assays of chromatin accessibility and gene expression via nonlinear Granger causality to reconstruct and decompose multi-scale gene regulatory networks (GRNs). Benchmarking on both simulated and real datasets demonstrates that scMagnify achieves superior performance. scMagnify employs tensor decomposition to systematically identify combinatorial TF modules and their activation profiles across different time-lags. It enables a hierarchical dissection of the regulatory landscape-- from the activity of individual regulator to the combinatorial logic of regulatory modules and intercellular communications. We applied scMagnify to human hematopoiesis and mouse pancreas development, where it successfully recovered known lineage-driving regulators and provided novel insights into the combinatorial logic that governs cell fate decisions. Furthermore, in the context of kidney injury, scMagnifys intracellular communication module mapped key signaling-to-transcription cascades linking microenvironment cues to pathological epithelial cell changes. In summary, scMagnify provides a powerful and versatile computational framework for dissecting the multi-scale regulatory logic that governs complex biological processes in development and disease.

bioinformatics↗

bioRxiv2026

Molecular basis of BET family protein inhibition by four clinical-stage small-molecule inhibitor drugs

The bromodomain and extra-terminal (BET) family proteins are critical epigenetic readers involved in various diseases, making them attractive therapeutic targets. This study elucidates the molecular basis of inhibition by four clinical-stage BET inhibitors (ZEN-3694, INCB054329, PLX51107, and INCB057643) through detailed structural comparison and analysis. Using X-ray crystallography, we determined their complex structures with the second bromodomain of human BRD2 at 1.4-1.5 [A] resolution. All inhibitors occupy the conserved acetyl-lysine binding pocket via extensive hydrophobic interactions. This hydrophobic network is further coupled with hydrogen-bond contacts for inhibitor-binding stabilization. A common feature is the formation of at least one hydrogen bond with a conserved residue of N429. Notably, INCB057643 exhibits an enhanced polar network, forming additional hydrogen bonds with residues D377 and N429, which may contribute to its improved pharmacological profile. These structures reveal a shared competitive inhibition mechanism by occluding the acetyl-lysine binding site, providing a rational basis for their transcriptional repression and guiding future inhibitor design.

biophysics↗

bioRxiv2026

Characterizing the metabolomes of microglia, astrocytes, and neurons in aging and Alzheimer's brains

Neurons and glia are distinct in their morphology, development, and function, possessing unique transcriptomes and proteomes, but little is known about their metabolomes. The challenge of brain cell metabolic profiling is to obtain a large number of cells for reliable analysis. Here, we purified microglia, astrocytes, and neurons from mouse brains, identifying >70 metabolites through targeted metabolomics and 9,854 metabolite features via untargeted metabolomics. We systematically characterized cell type-enriched metabolites and metabolic pathways, revealing an enrichment of glutathione (GSH) and polyamine metabolism in microglia. This enrichment was validated in vivo and showed significant decreases with aging and in an Alzheimers disease (AD) model. Notably, GSH and polyamine metabolism correlated strongly with chemokine-related gene expression. Disrupting the GSH pathway in microglia resulted in downregulation of chemokine-related genes, aberrant morphogenesis, and {beta}-amyloid deposition. Our results provide a valuable resource (https://metabolismocean.org/braincell) for metabolic studies related to aging, AD, and other neurological diseases.

neuroscience↗

bioRxiv2026

SPCoral: diagonal integration of spatial multi-omics across diverse modalities and technologies

Spatial multi-omics is indispensable for decoding the comprehensive molecular landscape of biological systems. However, the integration of multi-omics remains largely unresolved due to inherent disparities in molecular features, spatial morphology, and resolution. Here we developed SPCoral for diagonal integration of spatial multiomics across adjacent slices. SPCoral extracts spatial covariation patterns via graph attention networks, followed by the use of optimal transport to identify high-confidence anchors in an unsupervised, feature-independent manner. SPCoral utilizes a crossmodality attention network to enable seamless cross-resolution feature integration alongside robust cross-omics prediction. Comprehensive benchmarking demonstrates SPCorals superior performance across different technologies, modalities and varied resolutions. The integrated multi-omics representation further improves spatial domain identification, effectively augments experimental data, enables cross-modal association analysis, and facilitates cell-cell communication. SPCoral exhibits good scalability with data size, reveals biological insights that are not attainable using a single modality. In summary, SPCoral offers a powerful framework for spatial multi-omics integration across various technologies and biological scenarios.

bioinformatics↗

bioRxiv2026

Glucose hypometabolism and hyperphosphorylated Tau synergistically drive neuronal necroptosis

The combination of brain glucose hypometabolism and hyperphosphorylated Tau (p-Tau) pathology is the strongest known clinical predictor of imminent cognitive decline, yet how these factors cooperate to drive dementia remains unknown. Here, we show that glucose hypometabolism synergizes with p-Tau to trigger neuronal loss through necroptosis. Under low-glucose conditions, accumulated p-Tau forms a molecular scaffold that directly recruits the necroptotic kinase RIPK1, while concomitant loss of the necroptosis checkpoint protein A20 removes a critical brake on this death pathway. This dual mechanism thereby precipitates neuronal necroptosis independent of classical TNF/TNFR1 signaling paradigm. Restoring A20 expression with acetyl-L-carnitine as a dietary supplement or preventing the p-Tau - RIPK1 interaction using a RIPK1 derived competitive peptide alleviates neuronal necroptosis and brain atrophy in a Tau transgenic mouse model. Collectively, our findings uncover a previously unrecognized metabolism-driven necroptotic signaling cascade initiated by a p-Tau-RIPK1 hub, providing mechanical insight into how glucose hypometabolism synergizes with p-Tau to drive neurodegeneration.

neuroscience↗

bioRxiv2026

Analysis of the assembly, stabilization and maturation of the multiphasic TAZ biomolecular condensates

Phase separation is an important mechanism ensuring efficient regulation and function in Hippo signaling. Particularly, phase separation of nuclear TAZ has been demonstrated to be essential for its activity. However, the mechanisms of TAZ condensate assembly and maturation are yet undefined. Here we explored these mechanisms using FRAP with two laser beam sizes complemented by microscopy and cell biology approaches. We show that TAZ condensates are multiphasic, with a more stable core and labile periphery. TAZ initially forms small nascent clusters, likely via self-nucleation through the CC domain. These gradually mature into larger condensates through interaction with additional proteins via the WW domain. The condensates are further stabilized/activated by interaction with transcription factors and complexes including TEAD4 and P-TEFb. Of note, the ability of TAZ to form mature condensates is essential for its activities in cellular morphogenesis and tumorigenesis. Our study presents detailed mechanistic analysis of TAZ phase separation, revealing a highly dynamic nature of TAZ condensate maturation and activation. TeaserTAZ condensates grow from nascent clusters into mature condensates by interactions with transcription factors and complexes.

cell biology↗

bioRxiv2026

Ketone body beta-hydroxybutyrate restores neuronal Tau proteostasis via ketolysis-independent mechanism

Metabolic interventions that induce ketosis, including ketogenic diets, caloric restriction, intermittent fasting, and exercise, show promise in the treatment of Alzheimers disease (AD) and related tauopathies. {beta}-hydroxybutyrate ({beta}HB), the primary ketone body produced during ketosis, reproduces key features of these metabolic interventions, but the molecular mechanism underlying its neuroprotective properties is not fully understood. Here, we demonstrate that a {beta}HB precursor diet is sufficient to ameliorate Tau pathophysiology in a tauopathy mouse model. Furthermore, across in vitro, ex vivo, and in vivo models, we find that {beta}HB enhances neuronal Tau proteostasis and reduces Tau aggregation and secretion. Importantly, these effects are independent of {beta}HBs oxidation for ATP production, as its ketolysis-resistant enantiomer reproduces these benefits, indicating that ketolysis is dispensable for these effects. Overall, these data position {beta}HB as a novel therapeutic avenue for AD and tauopathy and elucidate a novel mechanism of action of metabolic interventions in neurodegenerative disease.

neuroscience↗

bioRxiv2026

Single cell profiling reveals GSM-15606 attenuates air pollution-induced inflammation and preserves hippocampal neurogenesis

1.IntroductionAir pollution (AirPoll) is a major environmental risk factor for age-related cognitive decline and dementia, yet we poorly understood the cellular and molecular mechanisms underlying its effects and their potential attenuation. MethodsWe combined single cell RNA sequencing with immunohistochemistry to determine transcriptional responses in microglia, astrocytes, neurons and neural stem cells in the hippocampus of mice following exposure to chronic diesel exhaust particle (DEP). Differential gene expression profiles were compared between filtered-air and DEP exposed animals. The gamma secretase modulator GSM-15606 (BPN) was used to probe selective rescue of inflammatory signatures across distinct cell populations. ResultsDEP exposure triggered robust inflammatory programs in microglia and astrocytes, including upregulation of cytokine signaling components, innate immune receptors, stress-responsive transcription factors, and markers of reactive glial phenotypes. In neural stem cells, DEP induced activation of gliosis-associated pathways, including Il6st, Stat3, and Txnip, consistent with a pro-inflammatory state that may bias lineage decisions. Immunostaining confirmed a significant reduction in immature neurons in the neurogenic niche after AirPoll exposure. GSM-15606 attenuated many DEP-induced transcriptional alterations in microglia and astrocytes, reducing expression of inflammatory mediators and reactive gliosis markers, but did not modulate the inflammatory profile of neural stem cells. ConclusionsAirPoll activates divergent inflammatory pathways across hippocampal cell populations and suppresses neurogenesis. Targeting inflammation with GSM-15606 selectively reverses glial but not neural stem cell responses, highlighting cell-type-specific mechanisms and potential therapeutic pathways to mitigate pollution-related cognitive vulnerability. These results support GSM-15606 as a protective agent against AirPoll-induced hippocampal dysfunction and amyloidogenic stress.

neuroscience↗

bioRxiv2026

Methionine metabolism and the NOP2 methyltransferase are essential for MYC-Driven liver tumorigenesis.

Hepatocellular carcinoma (HCC) represents the third leading cause of cancer-related death worldwide and has been increasing in developed nations.1,2 The MYC oncogene or its paralogs are frequently amplified or overexpressed in subtypes of cancer associated with stem cell-like features and worse clinical outcomes,3,4 including in liver cancer.5 Unfortunately, selective inhibitors that target MYC or its transcriptional program are not yet clinically available for therapy of HCC. Here, we identified methionine metabolism as a selective vulnerability for MYC but not RAS-driven liver cancers. MYC-driven liver cancer cells are methionine dependent, with markedly diminished tumor growth when mice are fed a methionine low diet. While RAS-driven liver cancer was resistant to a low methionine diet. S-adenosylmethionine (SAM), the predominant methyl donor, partially rescues cell proliferation following methionine depletion, suggesting that methylation processes are especially critical in the context of MYC high tumor cells. Heavy isotope methionine tracing in MYC high cells identified increased levels of m5C nucleotides. We found NOP2, an rRNA m5C-methyltransferase, was regulated by both MYC overexpression and methionine abundance linking the two processes. Methionine depletion reduced methylation of multiple 28S rRNA residues as did NOP2 knockdown. Depletion of NOP2 selectively inhibited MYC liver cancer cell proliferation and in vivo tumor growth. Thus, methionine catabolism is critical for MYC-driven liver tumorigenesis and the rRNA methyltransferase NOP2 may serve as a new therapeutic target in liver cancer.

cancer biology↗

bioRxiv2026

Injury-transduced SerpinOLs modulate neuroinflammation and glial activation in the diseased and non-diseased CNS

Oligodendroglial dysfunction is common in CNS diseases and injuries, but the molecular and functional responses of oligodendroglia to CNS pathologies remain poorly defined. Here, we report that oligodendrocytes (OLs) respond to demyelinating diseases by dysregulating serine protease inhibitor clade A member 3N (SERPINA3N). Homeostatic OLs transition to Serpina3n-expressing OLs (SerpinOLs) under other diseased conditions including stroke, endotoxicity, neurodegeneration, neurotrauma, and non-diseased healthy aging conditions. Mechanistically, general neuroinflammation or inflammatory mediators is insufficient for SerpinOL transition. Instead, oligodendrocyte damage/injury, even in the absence of neuroinflammation or glial activation, is sufficient for the transition. Phenotypically, SerpinOLs are characterized by molecular signatures of inflammatory and immune regulation and STAT3 signaling activation. Functionally, SerpinOLs exacerbate neuroinflammation and promote glial activation toward pro-inflammatory and neurodegenerative states. Together, our findings suggest SerpinOLs are a common population of injury-transduced OLs that amplify neuroinflammation and glial activation in the diseased and non-diseased CNS through SERPINA3N secretion. Our findings provide new insights into myelination-independent role of OLs in regulating CNS pathophysiology.

neuroscience↗

bioRxiv2026

Stromal estrogen signaling regulates fallopian tube homeostasis and cancer initiation via inflammatory pathways

Lifetime estrogen exposure is a major risk factor for ovarian cancer, which can originate from fallopian tube epithelial (FTE) cells. Here we report that estrogen receptor (ER) signaling in fallopian tube (FT) stromal cells plays a critical developmental role in maintaining epithelial homeostasis by promoting FTE proliferation and ciliated differentiation. Stromal ER regulates expression of inflammatory cytokines, growth factors, and extracellular matrix components, creating a differentiation-supportive, tumor-suppressive niche that coordinates epithelial regeneration during hormonal cycles. Excessive or prolonged estrogen exposure, however, shifts this niche toward a tumor-promoting state by inducing inflammation and activating stemness-associated pathways, including JAK/STAT, in FTE cells. This effect is exacerbated in genetically altered FTE cells lacking key tumor suppressors, which resist differentiation while remaining responsive to stromal proliferation signals. These findings reveal how stromal ER signaling integrates hormonal cues, inflammation, aging, and genetic susceptibility to influence early events in FT carcinogenesis. In BriefEstrogen receptor signaling in fallopian tube stromal cells maintains epithelial homeostasis by promoting proliferation and ciliated differentiation. Excessive estrogen shifts this niche toward inflammation and stemness, cooperating with genetic susceptibility to drive early fallopian tube carcinogenesis. O_FIG O_LINKSMALLFIG WIDTH=190 HEIGHT=200 SRC="FIGDIR/small/700864v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@113b543org.highwire.dtl.DTLVardef@e1465corg.highwire.dtl.DTLVardef@1d279dcorg.highwire.dtl.DTLVardef@13e782c_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIStromal ER signaling maintains fallopian tube epithelial (FTE) cell homeostasis C_LIO_LIStromal ER promotes proliferation and ciliated differentiation of FTE cells C_LIO_LIExcess estrogen shifts this stromal niche toward tumor promotion via inflammation C_LIO_LIDifferentiation-resistant mutant FTE cells respond to stromal proliferation signals C_LI

cancer biology↗

bioRxiv2026

Conserved assembly architecture of the essential herpesvirus packaging accessory factor

To create a new wave of infectious virions, all herpesviruses require an accessory factor of unknown function to package their viral genomes into nascent capsids. Here, we present cryo-EM structures of the packaging accessory factor from the -herpesvirus herpes simplex virus type 1 (HSV-1, UL32) and the {beta}-herpesvirus human cytomegalovirus (HCMV, UL52). Unlike homologs from the {gamma}-herpesviruses, neither UL32 nor UL52 form stable homopentameric rings. UL52 forms incomplete pentameric rings lacking one or two protomers. UL32 does not form stable higher-order species, but stabilization through chemical crosslinking revealed a novel quaternary structure where three pentameric rings assemble into a "tripentamer." Our results reveal that herpesvirus packaging accessory factors adopt distinct oligomeric states but are constrained to pentameric symmetry. Assembly of protomers into a ring creates a positively charged central channel that we show is critical for infectious virus production in HSV-1. Taken together, our study points to a structurally conserved, essential function of packaging accessory factors across the Herpesviridae. AUTHOR SUMMARYHerpesviruses are a diverse family of pathogens that drive human disease. At the end of their life cycle, all herpesviruses must actively package their genomes into newly formed capsids. Although some aspects of packaging are conserved with tailed bacteriophages, herpesviruses require an additional packaging accessory factor of unknown function. Here, we present two high-resolution structures of the packaging accessory factor from herpes simplex virus and human cytomegalovirus and identify pentameric symmetry as a unifying structural feature. We propose that the packaging accessory factor oligomerizes to concentrate positively charges in a central channel critical for packaging progression.

microbiology↗

bioRxiv2026

Scattering-enabled epi-quantitative phase imaging reveals subcellular detail in organoids and deep mouse brains

Imaging subcellular structures deep within thick, turbid biological tissues remains fundamentally limited by light scattering, which distorts optical wavefronts and degrades contrast, resolution, and sensitivity. These limitations hinder quantitative interrogation of complex biological systems where resolving dynamic microenvironments at subcellular resolution is critical. Here, we introduce scattering-enabled epi-quantitative phase imaging (SEEQPI), a label-free method that leverages tissue scattering and provides subcellular spatial resolution, nanometer-scale spatiotemporal phase sensitivity, and millimeter-scale imaging depth in murine brains. SEEQPI is enabled by common-path phase-shifting confocal epi-interferometry with near-infrared illumination and the scattering-enabled phase reconstruction algorithm. SEEQPI requires low illumination power, minimizing tissue damage while enabling high-speed imaging of biological dynamics. We demonstrate simultaneous, colocalized imaging of subcellular structures with SEEQPI, third-harmonic generation, and three-photon fluorescence microscopy in liver cancer spheroids and in vivo mouse brains. SEEQPI enables quantitative, longitudinal studies of dry mass dynamics in intact, living biological systems.

bioengineering↗

bioRxiv2026

Phosphatidylserine exposure by developing astrocytes initiates microglia-mediated developmental cell death

Developmental cell death is classically attributed to apoptosis, yet in mammalian retina, large numbers of developing astrocytes die non-apoptotically during a defined developmental window. Astrocyte death is important for patterning a cellular template that guides angiogenesis, but the underlying mechanism remains unknown. Here we show that healthy developing astrocytes initiate their own elimination by recruiting microglia via regulated exposure of the membrane lipid phosphatidylserine. Experimentally increasing phosphatidylserine exposure in astrocytes, but not neurons, accelerates their removal by microglia without changing how many astrocytes ultimately survive. This acceleration causes profound vascular defects resembling pathological features of retinopathy of prematurity. Genetic disruption of MFGE8, a phosphatidylserine-binding protein, suppresses microglia-mediated astrocyte killing and prevents vascular pathology despite continued phosphatidylserine exposure. This mechanism extends beyond the retina, because phosphatidylserine also initiates astrocyte death in developing cerebral cortex. Together, these findings identify phosphatidylserine exposure as a developmental signal that times microglia-mediated astrocyte elimination, with essential consequences for neurovascular development.

neuroscience↗