Biology subjects

Carter, J.

Publications and source records attributed to Carter, J..

At least 19 recordsLinked to original sources

bioRxiv2026

Functional profiling of spacecraft cleanroom microbiomes through genome-wide phenotype predictions

Current planetary protection approaches rely heavily on spore-based tests developed for Mars missions and may not adequately assess contamination risks for icy ocean worlds such as Europa. We developed a genome-based framework combining deep shotgun metagenomics and supervised machine learning to predict survival-relevant microbial traits in ESA JUICE launch-site cleanrooms. From 183 genome bins, 25 representative genomes were analyzed for traits including cryotolerance, desiccation tolerance, salt resilience, anaerobic metabolism, autotrophy, and sporulation. Several skin-associated microbes carried multiple relevant traits, and some appeared actively replicating. A broader meta-analysis of 1,868 genomes showed that trait profiles vary strongly within taxa, demonstrating that taxonomy alone is insufficient for risk assessment. This framework complements current planetary protection assays, helps to predict how microbes would survive in a new biotope, and supports functional, risk-informed contamination monitoring for future space missions.

microbiology↗

bioRxiv2025

Dynamic interaction between stress hormones and neutrophils promotes neutrophil extracellular trap formation with behavioral consequences

Recent studies have highlighted the crosstalk between neuroendocrine responses and the immune system but the mechanisms underlying this cooperation are still not well understood. The stress response is associated with peripheral inflammation suggesting that stress hormones including glucocorticoids and catecholamines could modulate the function of innate immune cells like neutrophils. Likewise, inflammatory mediators produced by immune cells are known to contribute to psychiatric diseases like major depressive disorder. Here we investigated the dynamic relationship between stress hormones and neutrophils and their contribution to mood disorders. We found that chronic restraint stress leads to plasma elevation of neutrophil extracellular traps (NETs) and increased NET formation in mice. Interestingly, the stress hormones, cortisol and epinephrine induce NET formation in human neutrophils ex vivo. Activation of neutrophils to form NETs leads to their increased expression of adrenergic and glucocorticoid receptors and neutrophil production of both cortisol and epinephrine indicating an autocrine/paracrine mechanism for the regulation of neutrophil inflammatory response by stress hormones. Strikingly, administration of NET components to mice induces depressive-like behavior. Moreover, activation of the glucocorticoid receptor in human volunteers leads to increase in gene expression of NET proteins. Furthermore, patients with major depressive disorder show gene upregulation of NET proteins. Our data highlights the bi-directional relationship between neuroendocrine processes and neutrophils that contribute to stress-induced increase in inflammation and the role of neutrophil inflammatory responses in propagation of behavioral changes following stress.

immunology↗

bioRxiv2025

Enhanced Zika Virus Suppression by Coupling Ribavirin with Biodegradable Drug Delivery

Advancement and implementation of nanoparticle-based systems for enhanced drug delivery have become essential for the suppression of viral pathogens due to lack of viable treatment options. This study focuses on characterization and application of mPEG-PCL co-polymers for development of pH-responsive, biodegradable micellar nanoparticles (MNPs) for the delivery of the antiviral drug ribavirin against Zika virus. Synthesis of mPEG-PCL diblock copolymers was confirmed through FTIR and 1H NMR, which validated the formation of ester functional groups and accurate structure of copolymers. mPEG-PCL MNPs, loaded with ribavirin, exhibited a mean diameter of approximately 34.29 {+/-} 5.214 nm and a zeta potential of -3.28 {+/-} 0.718 mV, suitable for evading immune detection and facilitating cellular entry. The ribavirin-loaded mPEG-PCL MNPs demonstrated pH-dependent release, with approximately 88% of ribavirin released at pH 5.5, compared to 20% at pH 7.4. This pH-responsive release is crucial for targeted drug delivery within the endosomal pathway. In vitro studies using JEG-3 cells infected with Zika virus showed that ribavirin-loaded mPEG-PCL MNPs achieved an EC50 of 0.22nM, significantly enhancing drug efficacy compared to unencapsulated ribavirin, which required micromolar concentrations to achieve similar effects. The MTT assay results indicated minimal cytotoxicity of the ribavirin-loaded mPEG-PCL MNPs, with approximately 80% cell viability at the highest concentration evaluated. Confocal microscopy and RT-PCR analysis further confirmed the efficient cellular uptake and potent antiviral activity of the ribavirin-loaded MNPs. These findings highlight the potential of mPEG-PCL MNPs as an effective delivery system for broad-spectrum antivirals like ribavirin, enhancing their therapeutic efficacy while minimizing cytotoxicity.

microbiology↗

bioRxiv2025

Biomni: A General-Purpose Biomedical AI Agent

Biomedical research underpins progress in our understanding of human health and disease, drug discovery, and clinical care. However, with the growth of complex lab experiments, large datasets, many analytical tools, and expansive literature, biomedical research is increasingly constrained by repetitive and fragmented workflows that slow discovery and limit innovation, underscoring the need for a fundamentally new way to scale scientific expertise. Here, we introduce Biomni, a general-purpose biomedical AI agent designed to autonomously execute a wide spectrum of research tasks across diverse biomedical subfields. To systematically map the biomedical action space, Biomni first employs an action discovery agent to create the first unified agentic environment - mining essential tools, databases, and protocols from tens of thousands of publications across 25 biomedical domains. Built on this foundation, Biomni features a generalist agentic architecture that integrates large language model (LLM) reasoning with retrieval-augmented planning and code-based execution, enabling it to dynamically compose and carry out complex biomedical workflows - entirely without relying on predefined templates or rigid task flows. Systematic benchmarking demonstrates that Biomni achieves strong generalization across heterogeneous biomedical tasks - including causal gene prioritization, drug repurposing, rare disease diagnosis, micro-biome analysis, and molecular cloning - without any task-specific prompt tuning. Real-world case studies further showcase Biomnis ability to interpret complex, multi-modal biomedical datasets and autonomously generate experimentally testable protocols. Biomni envisions a future where virtual AI biologists operate alongside and augment human scientists to dramatically enhance research productivity, clinical insight, and healthcare. Biomni is ready to use at https://biomni.stanford.edu, and we invite scientists to explore its capabilities, stress-test its limits, and co-create the next era of biomedical discoveries.

bioinformatics↗

bioRxiv2025

Prenatal alcohol exposure promotes nerve injury-induced pathological pain following morphine treatment via NLRP3-mediated peripheral and central proinflammatory immune actions.

Adverse in-utero conditions may exert a lifelong impact on neuroimmune function. Our prior work showed that prenatal alcohol exposure (PAE) increases pathological pain sensitivity (allodynia) following peripheral sciatic nerve injury. While the immune mechanism(s) of PAE-induced immune dysfunction are poorly understood, prior studies implicated the involvement of Toll-like receptor 4 (TLR4) and the nucleotide-binding domain, leucine-rich repeat-containing family, pyrin domain-containing 3 (NLRP3) inflammasomes. Interestingly, emerging data suggest a surprising overlap of spinal glial proinflammatory activation via the TLR4-NLRP3-interleukin (IL)-1{beta} axis due to opioid treatment in nerve-injured non-PAE rodents. Considering this preclinical evidence, we explored whether PAE poses a risk factor in creating proinflammatory immune bias consequent to opioid (morphine) exposure. We hypothesized that under nerve injury conditions, PAE may interact with morphine, promoting peripheral and CNS proinflammatory factors in a NLRP3-dependent manner. Using a minor nerve injury model in adult mice, we demonstrate that PAE prolongs the chronicity of ongoing allodynia in both sexes, with a more pronounced effect observed in male mice. Our study shows that PAE amplifies proinflammatory responses at the injury site and the spinal cord, driving morphine-prolonged allodynia through NLRP3 inflammasome activation. Furthermore, high mobility group box 1 (HMGB1), a well-established pain-promoting TLR4 agonist, is elevated in allodynic PAE mice. NLRP3 inhibitor, MCC950, effectively reverses morphine-induced allodynia and reduces Caspase-1 activity, IL-1{beta}, and related proinflammatory factors. Although few sex-specific effects were observed, our data convincingly support that PAE and morphine interactions ultimately converge on NLRP3-driven mechanisms in both sexes. Together, this study suggests that PAE modulates later-life neuroimmune function and provides critical insights into immune regulators underlying PAE-induced biological vulnerability to pathological pain processing and adverse effects of opioids.

neuroscience↗

bioRxiv2025

Deletion of a KSF Motif Attenuates NSP1 Host Cell Translation Shutoff and Impairs SARS-CoV-2 Virulence

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), triggered a global pandemic with profound social and economic consequences. The viral spike (S) protein has been identified as a key determinant of SARS-CoV-2 pathogenicity. In this study, we demonstrate that the Omicron BA.4 and BA.5 variants, which have closely related S proteins, exhibit different virulence in K18-hACE2 transgenic mice. A comparison of genomic sequences revealed key differences between variants BA.4 and BA.5, including a three amino acid deletion ({Delta}KSF) in the linker region of the non-structural protein 1 (NSP1) in BA.4. Using reverse genetic systems, we engineered a recombinant (r)SARS-CoV-2 BA.5 expressing BA.4 NSP1, which was significantly attenuated in vivo, similar to the natural BA.4 isolate, compared to rBA.5 wild-type (WT). This finding indicates that NSP1 is responsible, at least in part, for the differences in virulence between BA.4 and BA.5. Mechanistically, BA.4 NSP1 showed a reduced ability to inhibit host gene translation compared to BA.5 NSP1. Notably, a rSARS-CoV-2 WA1 original strain containing the same {Delta}KSF in NSP1 was also attenuated in vivo compared to rWA1 WT. Together, these findings highlight the contributions of the NSP1 linker region to inhibiting host gene expression and SARS-CoV-2 pathogenicity, as well as the feasibility of targeting NSP1 for the rational design of live-attenuated vaccines and/or antivirals. IMPORTANCEUnderstanding why some SARS-CoV-2 variants cause more severe disease than others is crucial for proper management or for the rational design of prophylactic and therapeutic treatments. While most studies focus on the spike (S) protein, we found that another viral protein, NSP1, also plays a key role in disease severity among SARS-CoV-2 variants. A small deletion in NSP1, present in the Omicron BA.4 variant, weakens the virus ability to shut down the hosts immune response, making BA.4 less severe than BA.5. When we introduced the same deletion into the original SARS- CoV-2 WA1 strain, the virus also became less harmful. This discovery suggests that NSP1 is an important virulence factor and supports the feasibility of targeting NSP1 for the development of new prophylactic and therapeutic treatments against SARS-CoV-2. By uncovering NSP1s role in pathogenesis, our study provides insights that could help in designing better strategies to combat future variants of SARS-CoV-2.

microbiology↗

bioRxiv2025

Effects of a temperate heatwave on diel rhythms of insect activity: a comparison across habitats

O_LIThe increasing frequency and intensity of heatwave events in temperate climates threatens to alter behavioural rhythms of ectothermic animals, such as insects. However, it is poorly understood how heatwaves affect daily activity patterns of insects, and whether shaded microclimates can moderate these responses. C_LIO_LIWe investigated impacts of a heatwave on the diel profile of insect activity, comparing effects across open, tree-covered and hedged habitats. Using yellow pan traps, insect activity was monitored from 07:00 to 19:00 on ten non-consecutive days, including two during a heatwave. C_LIO_LIInsect counts exhibited a unimodal relationship with temperature. C_LIO_LIDuring heatwave days, open habitat exhibited a significant ([~]81.9%) reduction in counts compared to two non-heatwave field-days, one before and one after the heatwave. Smaller, non-significant reductions were observed in the tree-covered (38.3%) and hedged (17.8%) habitats. C_LIO_LIThe diel activity profile on non-heatwave days approximated to a unimodal relationship, with GLMM-estimated counts peaking around 15:00; by contrast, heatwave days exhibited a bimodal profile, with predicted counts highest in the morning and evening. C_LIO_LISuch heatwave-induced deformations of activity patterns, modelled as interactions between heatwave and time-of-day, were significant across all three habitat types. C_LIO_LIThe findings suggest that temperate heatwaves can markedly decrease insect activity levels, and that whilst shade-providing vegetational features may reduce this effect, diel patterns of activity are affected landscape-wide. As heatwaves become more frequent, preservation of trees and hedges in temperate landscapes is likely crucial to support resilience of insect activity and wider ecosystem functioning. C_LI

ecology↗

bioRxiv2024

Cell-free expression of Nipah virus transmembrane proteins for proteoliposome vaccine design

Membrane proteins expressed on the surface of enveloped viruses are potent antigens in a vaccine, yet are difficult to produce and present due to their instability without a lipid scaffold. Current vaccination strategies that incorporate viral membrane proteins, such as live attenuated viruses, inactivated viruses, or extracellular vesicles, have limitations including lengthy production time, poor immunogenicity, extensive processing steps, and/or poor stability. Cell-free protein synthesis of viral membrane proteins offers a rapid, one-step method to assemble vaccine nanoparticles via cotranslational folding of membrane proteins into nanoscale liposomes. Here, we develop a vaccine candidate for the deadly Nipah virus (NiV), a highly lethal virus listed by the World Health Organization as a priority pathogen, by cell-free expressing two full-length Nipah virus membrane proteins. We demonstrate that both NiV fusion protein (NiV F) and NiV glycoprotein (NiV G) can be expressed and cotranslationally integrated into liposomes and that they fold into their native conformation. We find the removal of a signal peptide sequence and alteration of liposome lipid composition improves viral membrane protein incorporation. Furthermore, a lipid adjuvant, monophosphoryl lipid A (MPLA), can be readily added to liposomes without disrupting protein-vesicle loading or protein folding conformations. Finally, we demonstrate that our generated liposomal formulations lead to enhanced humoral responses in mice compared to empty and single-protein controls. This work establishes a platform to quickly assemble and present membrane antigens as multivalent vaccines that will enable a rapid response to the broad range of emerging pathogenic threats.

synthetic biology↗

bioRxiv2023

How to barcode (almost all) freshwater biodiversity

Freshwater ecosystems are complex, diverse and face a variety of imminent threats that have led to changes in both ecosystem structure and function. It is urgent that we develop and standardize monitoring tools allowing for rapid and comprehensive assessment of freshwater communities to understand their changing dynamics and to inform conservation. Environmental DNA surveys offer a means to inventory and monitor aquatic diversity, yet most studies focus on one or a few taxonomic groups only. In this study, we sought to 1) identify thoroughly validated, cost-efficient primer pair combinations that maximize detection of broad swaths of freshwater diversity, and 2) facilitate future primer pair selection by creating a free online and user-friendly tool. We first evaluated the completeness of public reference sequence databases and the efficiency of 14 primer pairs using an in silico approach, and then performed eDNA surveys using five mock communities (mix of DNA from tissues), water samples from aquarium samples with known taxonomic composition, and finally water samples from freshwater systems in Eastern Canada. We highlight the power of eDNA-based metabarcoding for reconstructing freshwater communities, including prey, parasite, pathogen, invasive, and declining species. Our work reveals the importance of the marker choice on species resolution, as well as the importance of degenerate primers, the length of the target fragment and the filtering parameters on detection success in water eDNA samples. Our new online tool SNIPe revealed that 13 to 14 primer pairs are necessary to recover 100% of the species in water samples (aquarium and natural systems), but four primer pairs are sufficient to recover almost 75% of taxa with little overlap. These results highlight the usefulness of eDNA for freshwater monitoring and should prompt more studies on tools to survey all-inclusive communities.

ecology↗

bioRxiv2022

Transgene by Germplasm Interactions Can Impact Transgene Evaluation

Transgenes have been successfully commercialized for qualitatively inherited insect and herbicide resistance traits that show similar effects across genetic backgrounds. However, for quantitative traits like yield, genetic background may affect the measured transgene value. In this paper, we evaluated whether different genetic backgrounds impact the estimated value of a transgene for grain yield, ear height, and anthesis-silking interval for maize by developing isogenic pairs of lines with and without a transgene and testing them in hybrid combination with non-transgenic lines from a complementary heterotic group across eleven environments in the USA. Over all hybrid combinations, the transgene increased yield by 0.2 Mg ha-1. Across multiple non-transgenic lines of the opposing heterotic group, the transgene effect within a line pair ranged from an increase of 0.8 Mg ha-1 for the NSS4 and SS7 transgenic lines to a reduction of 0.3 Mg ha-1 for the NSS5 transgenic line when compared to their non-transgenic isoline. Transgenic hybrids were often taller than non-transgenic hybrids (P<0.05). Anthesis to silking interval was reduced by 4{square}C growing degree units overall, but no transgene x genotype interaction was detected among line pairs. Our results show the importance of testing transgene efficacy across a large sample of elite hybrid pairs to assess the genes value. By only testing in a specific hybrid background, as may be done for qualitative traits like insect resistance, transgenes could be erroneously advanced or eliminated.

plant biology↗

bioRxiv2022

Methods for Evaluating Effects of Transgenes for Quantitative Traits

Transgenes that improve quantitative traits have traditionally been evaluated in one or a few genetic backgrounds across multiple environments. However, testing across multiple genetic backgrounds can be equally important to accurately quantify the value of a transgene for breeding objectives. Creating near-isogenic lines across a wide germplasm space is costly and time consuming, which renders it impractical during early stages of testing. In this experiment, we evaluate three approaches to sample the genetic space while concurrently testing across environments. We created both transgenic and non-transgenic doubled haploid lines, F2:3 lines, and bulk F3 families to determine if all methods resulted in similar estimation of transgene value and to identify the number of yield trial plots from each method necessary to obtain a stable estimate of the transgene value. With one exception, the three methods consistently estimated a similar effect of the transgene. We suggest that bulked F3 lines topcrossed to a tester inbred is the most effective method to estimate the value of a transgene across both genetic space and environments.

plant biology↗

bioRxiv2021

The tunicate metabolite 2-(3,5-diiodo-4-methoxyphenyl)ethan-1-amine targets ion channels of vertebrate sensory neurons

Marine tunicates produce defensive amino-acid derived metabolites, including 2-(3,5-diiodo-4-methoxyphenyl)ethan-1-amine (DIMTA), but their mechanisms of action are rarely known. Using an assay-guided approach, we found that out of the many different sensory cells in the mouse dorsal root ganglion (DRG), DIMTA selectively affected low-threshold cold thermosensors. Whole-cell electrophysiology experiments using DRG cells, channels expressed in Xenopus oocytes and human cell lines revealed that DIMTA blocks several potassium channels, reducing the magnitude of the afterhyperpolarization and increasing the baseline [Ca2+]i of low-threshold cold thermosensors. When injected into mice, DIMTA increased the threshold of cold sensation by >3 oC. DIMTA may thus serve as a lead in the further design of compounds that inhibit problems in the cold-sensory system, such as cold allodynia and other neuropathic pain conditions.

neuroscience↗

bioRxiv2021

Deciphering Bedaquiline and Clofazimine Resistance in Tuberculosis: An Evolutionary Medicine Approach

Bedaquiline (BDQ) and clofazimine (CFZ) are core drugs for treatment of multidrug resistant tuberculosis (MDR-TB), however, our understanding of the resistance mechanisms for these drugs is sparse which is hampering rapid molecular diagnostics. To address this, we employed a unique approach using experimental evolution, protein modelling, genome sequencing, and minimum inhibitory concentration data combined with genomes from a global strain collection of over 14,151 Mycobacterium tuberculosis complex isolates and an extensive literature review. Overall, 230 genomic variants causing elevated BDQ and/or CFZ MICs could be discerned, with 201 (87.4%) variants affecting the transcriptional repressor (Rv0678) of an efflux system (mmpS5-mmpL5). Structural modelling of Rv0678 suggests four major mechanisms that confer resistance: impairment of DNA binding, reduction in protein stability, disruption of protein dimerization, and alteration in affinity for its fatty acid ligand. These modelling and experimental techniques will improve personalized medicine in an impending drug resistant era.

microbiology↗

bioRxiv2019

Deep sequencing of 3 cancer cell lines on 2 sequencing platforms

To test the performance of a new sequencing platform, develop an updated somatic calling pipeline and establish a reference for future benchmarking experiments, we sequenced 3 common cancer cell lines along with their matched normal cell lines to great sequencing depths (up to 278X coverage) on both Illumina HiSeqX and NovaSeq sequencing instruments. Somatic calling was generally consistent between the two platforms despite minor differences at the read level. We designed and implemented a novel pipeline for the analysis of tumor-normal samples, using multiple variant callers. We show that coupled with a high-confidence filtering strategy, it improves the accuracy of somatic calls. We also demonstrate the utility of the dataset by creating an artificial purity ladder to evaluate the somatic pipeline and benchmark methods for estimating purity and ploidy from tumor-normal pairs. The data and results of the pipeline are made accessible to the cancer genomics community.

genomics↗

bioRxiv2019

Prediction of pyrazinamide resistance in Mycobacterium tuberculosis using structure-based machine learning approaches.

SynopsisO_ST_ABSBackgroundC_ST_ABSPyrazinamide is one of four first-line antibiotics used to treat tuberculosis, however antibiotic susceptibility testing for pyrazinamide is challenging. Resistance to pyrazinamide is primarily driven by genetic variation in pncA, an enzyme that converts pyrazinamide into its active form. MethodsWe curated a dataset of 664 non-redundant, missense amino acid mutations in pncA with associated high-confidence phenotypes from published studies and then trained three different machine learning models to predict pyrazinamide resistance. All models had access to a range of protein structural-, chemical- and sequence-based features. ResultsThe best model, a gradient-boosted decision tree, achieved a sensitivity of 80.2% and a specificity of 76.9% on the hold-out Test dataset. The clinical performance of the models was then estimated by predicting the binary pyrazinamide resistance phenotype of 4,027 samples harboring 367 unique missense mutations in pncA derived from 24,231 clinical isolates. ConclusionsThis work demonstrates how machine learning can enhance the sensitivity/specificity of pyrazinamide resistance prediction in genetics-based clinical microbiology workflows, highlights novel mutations for future biochemical investigation, and is a proof of concept for using this approach in other drugs.

microbiology↗

bioRxiv2018

Cyfip1 haploinsufficiency is associated with white matter changes, myelin thinning, reduction of mature oligodendrocytes and behavioural inflexibility

The biological basis of the increased risk for psychiatric disorders due to the pathogenic 15q11.2 copy number deletion is unknown. Previous work has shown disturbances in white matter tracts in human carriers of the deletion at this locus. Using a novel rat model, we have recapitulated low dosage of the candidate risk gene CYFIP1 present within the 15q11.2 interval to reveal alterations in white matter microstructure. Using diffusion tensor imaging, we first showed extensive white matter changes in Cyfip1 mutants that were most pronounced in the corpus callosum and external capsule. Transmission electron microscopy showed that these changes were associated with thinning of the myelin sheath in the corpus callosum. Myelin thinning was independent of changes in axon number or diameter but was associated with a reduction in the number of mature oligodendrocytes. Finally, we demonstrated functional effects on cognitive phenotypes sensitive to both disruptions in myelin and callosal circuitry.

neuroscience↗

bioRxiv2018

Structure reveals mechanism of CRISPR RNA-guided nuclease recruitment and anti-CRISPR viral mimicry

Bacteria and archaea have evolved sophisticated adaptive immune systems that rely on CRISPR RNA (crRNA)-guided detection and nuclease-mediated elimination of invading nucleic acids. Here we present the cryo-EM structure of the type I-F CRISPR RNA-guided surveillance complex (Csy complex) from Pseudomonas aeruginosa bound to a double-stranded DNA target. Comparison of this structure to previously determined structures of this complex reveals a I180-degree rotation of the C-terminal helical bundle on the \"large\" Cas8f subunit. We show that the dsDNA-induced conformational change in Cas8f exposes a Cas2/3 \"nuclease recruitment helix\" that is structurally homologous to a virally encoded anti-CRISPR protein (AcrIF3). Structural homology between Cas8f and AcrIF3 suggests that AcrIF3 is a mimic of the Cas8f \"nuclease recruitment helix\", implying that cas genes may sometimes serve as genetic fodder for the evolution of anti-CRISPRs.

molecular biology↗

bioRxiv2018

Haploinsufficiency of the schizophrenia risk gene Cyfip1 causes abnormal postnatal hippocampal neurogenesis through a novel microglia dependent mechanism

Genetic risk factors can significantly increase chances of developing psychiatric disorders, but the underlying biological processes through which this risk is effected remain largely unknown. Here we show that haploinsufficiency of Cyfip1, a candidate risk gene present in the pathogenic 15q11.2(BP1-BP2) deletion may impact on psychopathology via abnormalities in cell survival and migration of newborn neurons during postnatal hippocampal neurogenesis. We demonstrate that haploinsufficiency of Cyfip1 leads to increased numbers of adult born hippocampal neurons due to reduced apoptosis, without altering proliferation. We confirm this is due to a cell autonomous failure of microglia to induce apoptosis through the secretion of the appropriate factors. Furthermore, we show an abnormal migration of adult-born neurons due to altered Arp2/3 mediated actin dynamics. Together, our findings throw new light on how the genetic risk candidate Cyfip1 may influence the hippocampus, a brain region with strong evidence for involvement in psychopathology.

neuroscience↗