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Davis, E.

Publications and source records attributed to Davis, E..

At least 19 recordsLinked to original sources

A molecular circuit integrates environmental cues to coordinate the exit from developmental dormancy

Diapause is a reversible dormancy state that enables organisms to survive extreme environments. In annual killifishes, embryos use diapause to bridge seasonal drought, but how environmental cues are integrated to trigger exit remains unclear. Here, we combine model-based single-embryo transcriptomics with cross-clade small-molecule screening to define the molecular logic of diapause exit. In the African turquoise killifish (Nothobranchius furzeri), high-resolution profiling uncovered a temporal transcriptional cascade, while transcriptomic-clock analysis revealed reduced transcriptional noise during developmental reactivation. Transcriptome-guided drug-enrichment analysis nominated overlapping compounds across two annual killifish clades, leading to a targeted chemical screen that identified shared activators and inhibitors of diapause exit. Functional assays support a model in which HSP90 integrates temperature-dependent cues with steroid-hormone signaling. Together, these findings reveal shared molecular machinery that couples environmental sensing to developmental timing, aligns diapause exit with favorable conditions, and provides a powerful comparative framework for dissecting vertebrate dormancy control.

developmental biology↗

Phenolic Chemical Defense Contributes to Resistance against Multiple Soybean Cyst Nematode Populations in Wild Soybean

Soybean cyst nematode (Heterodera glycines, SCN) is one of the most damaging pathogens of soybean worldwide. Virulence diversity among SCN populations and reliance on a limited number of resistance sources present major challenges for durable SCN management. Here, we investigated a wild soybean (Glycine soja) genotype (WsR), that is resistant to two SCN populations, race 2 (HG type 1.2.5.7) and race 5 (HG type 2.5.7), and compared its transcriptional and metabolic responses with those of the susceptible genotype (WsS). WsR exhibited a substantially stronger defense-associated transcriptional response to both SCN populations, including preferential induction of genes associated with Ca2+/calmodulin and salicylic acid signaling. Integration of transcriptomic and time-resolved metabolomic analyses revealed convergence on phenolic metabolism, with enhanced accumulation of phenolic acids, flavonoids, and isoflavonoids in resistant WsR. Genes involved in phenolic biosynthesis and modification were also preferentially induced in WsR, linking transcriptional reprogramming with the observed metabolic response. Importantly, two resistance-associated phenolic compounds, 4-hydroxybenzaldehyde and 2,3-dihydroxybenzoic acid, directly increased mortality of SCN second-stage juveniles from both populations in a concentration-dependent manner. By connecting resistance-associated transcriptional responses and metabolic reprogramming with direct activity of specific phenolic compounds against SCN, our study provides functional evidence linking phenolic metabolism to chemical defense against SCN. Together, these findings identify enhanced phenolic chemical defense as a major component of resistance to multiple SCN populations in wild soybean and highlight wild soybean as a valuable source of molecular and biochemical diversity for SCN resistance.

plant biology↗

Infrapatellar Fat Pad Extracellular Vesicles Induce a Pro-Angiogenic VEGFAhigh/BMP4low Switch in Articular Chondrocytes: Implications for Chondrosarcoma

Chondrosarcoma is a hyper-vascularised, chemoresistant cartilage malignancy driven by VEGF-centred angiogenesis, and local adipose depots are increasingly recognised as paracrine drivers of tumour angiogenesis via adipokines and extracellular vesicles (EVs). The infrapatellar fat pad (IFP), an inflammatory adipose depot within the articular joint in direct cartilage contact, is a key local source of adipose-derived EVs, and thus a candidate driver of angiogenesis in chondrosarcoma. The aim of this study was to determine whether the IFP is a productive source of EVs, and whether IFP-derived EVs induce angiogenesis in articular chondrocytes. The IFP released significantly more EVs than subcutaneous fat (n = 8 per depot; p = 0.027). Treating primary human articular chondrocytes with IFP EVs for 24 h upregulated VEGFA (+1.6-fold, p = 0.036) and downregulated BMP4 (-2.4-fold, p = 0.011), engaging the VEGF/eNOS/ERK axis that drives chondrosarcoma angiogenesis. Re-analysis of a previously published phospho-kinase dataset from the same donor EVs, corroborated by a pooled donor-group analysis (n = 3), supported activation of eNOS, ERK1/2, PLC-{gamma}1 and HSP27. These findings identify the IFP as a dominant source of EVs within the articular joint, which can induce a pro-angiogenic, VEGF-axis switch in articular cartilage cells, supporting a signalling model relevant to chondrosarcoma angiogenesis.

cancer biology↗

A high-throughput, 3D microtissue platform for multiparametric analysis of tissue remodeling.

Extracellular matrix (ECM) remodeling and force generation are fundamental drivers of tissue morphogenesis and repair, yet scalable methods to quantitatively interrogate these dynamic mechanical processes remain limited. Here, we present a high-throughput screening platform that integrates engineered three-dimensional (3D) microtissues within a standardized 96-well format. We introduce a robust mold-casting fabrication process and a layer-by-layer surface modification strategy, that ensures long-term tissue stability and prevents detachment (95% tissue formation success; stable in culture for more than 10 days). This system enables simultaneous, longitudinal quantification of tissue closure, tissue contractility, and tissue compaction from a phase-contrast imaging modality. The computational data analysis tools that accompany this framework ensure reproducibility through deterministic computation and accelerate data extraction 80-fold relative to manual annotation. Using pharmacological compounds, we show that tissue closure dynamics, force generation, and compaction represent independent variables of ECM-driven tissue remodeling, challenging assumptions embedded in commonly used contraction-based assays. Furthermore, benchmarking against reported clinical drug responses demonstrates that the 3D platform better aligns with clinical outcomes (Kendall{tau} -b = 0.72, p=0.045, n =8/10) than a conventional two-dimensional scratch wound assay (Kendall{tau} -b = 0.52, p=0.25, n =4/10). Together, this work establishes a scalable assay for functional screening and quantitative assessment of tissue remodeling dynamics in three-dimensional systems.

bioengineering↗

Aberrant chromatin looping by NUP98-HOXA9 is constrained by CTCF and facilitated by cohesin

The acute myeloid leukemia (AML) fusion protein NUP98-HOXA9 (NHA9) drives leukemogenesis by promoting aberrant chromatin loop formation through phase separation, yet the mechanisms underlying these interactions remain unclear. To address this, we dissect the interplay between NHA9 and individual loop extrusion factors using in situ Hi-C, CUT&RUN, RNA-seq, and Auxin-inducible degradation of CTCF or RAD21. CTCF was found to be dispensable for NHA9 loop formation, although CTCF binding constrained a subset of loops that emerged only upon CTCF depletion. In contrast, cohesin played a distance-dependent role where short-range NHA9 loops formed independently of RAD21, while long-range loops were strongly cohesin-dependent. Despite this requirement, RAD21 showed minimal enrichment at NHA9 loop anchors, indicating that NHA9 does not function as a canonical cohesin barrier. Instead, these findings support a non-canonical model in which cohesin transiently facilitates interactions between distal NHA9-bound loci, which are subsequently stabilized through NHA9 phase separation. Together, this work reveals a distinct mechanism of oncogenic chromatin looping in which NUP98-HOXA9 cooperates with canonical loop extrusion machinery to reprogram genome architecture in AML.

Molecular Biology↗

A specific computational role for early-life unpredictability, and not lifelong stressful experience, in decision-making under uncertainty.

It has been shown that early-life adversity (ELA) shapes how individuals learn, remember, and make decisions, yet the precise computations altered by these experiences remain unclear. Here, we combine a structured foraging task with computational modeling to test a recently developed theory for how a particular kind of ELA, early-life unpredictability (ELU), specifically influences choice under uncertainty. Adult participants (N=297) performed a sequential foraging task requiring continuous trade-offs between exploiting depleting resources and exploring alternatives. Subsets also completed assessments of early-life unpredictability (QUIC) and for trauma symptoms arising from lifelong stressors (PCL). We fit participants behavior with a Bayesian learning-and-planning model in which uncertainty modulates the valuation of leaving a current resource patch. Critically, the subjective influence of local uncertainty was allowed to vary freely between participants. Consistent with theoretical proposals, computational model fits and mediation analyses revealed a robust indirect pathway: ELU predicted increased discounting in the face of uncertainty, which in turn predicted greater overharvesting. This pattern was consistent across environmental conditions, indicating that early-life unpredictability primarily influences behavior through a general influence on uncertainty processing. Importantly, although PCL scores were also correlated with uncertainty adaptation, these effects were fully accounted for by shared variance with ELU, offering a clear dissociation between developmental unpredictability and lifelong traumatic experience. Together, our results show that early-life unpredictability causes long-lasting changes in decision-making by amplifying the subjective experience of uncertainty.

neuroscience↗

Anhedonia buffers the effects of early-life unpredictability on threat-reward decision-making.

Anhedonia - the diminished capacity to experience or anticipate pleasure - is among the most common consequences of early-life unpredictability, yet how these co-occurring conditions jointly shape real-world decision-making remains unknown. Here, we use a sequential foraging-under-threat task to probe motivational conflict decisions in 357 individuals varying in early-life unpredictability and anhedonia symptoms. We find that unpredictability and anhedonia exert opposing influences on choice: unpredictability shifts behavior away from the survival-optimal policy in a sex-dependent manner, while anhedonia promotes adherence to it, partly through heightened sensitivity to unexpected threatening outcomes. A mediation analysis reveals that anhedonia partially buffers the deleterious effects of unpredictability on decision quality. These results demonstrate that co-occurring conditions can mask one anothers behavioral signatures and suggest that the heterogeneous expression of transdiagnostic constructs like anhedonia may reflect context-dependent adaptations to distinct underlying etiologies.

neuroscience↗

Hyperglycemia promotes maladaptive Dectin-1 signaling and impairs skin antifungal host defense.

People with chronic hyperglycemia are more susceptible to fungal skin infections, but the mechanisms underlying their worse clinical outcomes remain unclear. Using both in vivo and in vitro models, we explored how hyperglycemia influences skin antifungal defenses and how GLP1 agonists might restore host defense in diabetic conditions. Hyperglycemic mice showed increased susceptibility to Candida albicans skin infections, with larger lesions and higher fungal loads at all time points tested. Histology revealed larger abscesses, more extensive myeloid cell infiltration, and poorer control of fungal invasion, associated with increased chemoattractant production on day 1 post-infection. Despite heightened inflammatory responses, macrophages and keratinocytes exposed to high glucose exhibit markedly impaired fungal ingestion. RNAseq analysis of C. albicans-infected dermal macrophages cultured in high glucose showed enrichment of genes related to antimicrobial effectors and the C-type lectin receptor pathway, including Clec7a (Dectin-1), while suppressing downstream signaling pathways required for effective phagocytosis. Pharmacologic blockade or genetic deletion of Dectin-1 restored fungal uptake under high-glucose conditions and improved host defense in vivo. Mechanistically, Dectin-1 signaling in hyperglycemia promoted increased prostaglandin E2 (PGE2) production via induction of microsomal Prostaglandin E Synthase-1 (mPGES-1), and inhibition of PGE2 synthesis rescued deficient phagocytic function. Finally, treatment with the glucagon-like peptide-1 (GLP-1) receptor agonist liraglutide reduced lesion size, fungal burden, inflammation, and tissue damage in diabetic mice, linking metabolic control to restoration of innate immune function. These findings identify maladaptive innate immune sensing as a key mechanism underlying susceptibility to fungal infection in diabetes and reveal how metabolic stress converts antifungal recognition pathways into drivers of inflammatory dysfunction.

immunology↗

Menaquinone depletion resensitises bedaquiline-resistant tuberculosis

Tuberculosis remains a leading cause of global mortality, and rising bedaquiline resistance threatens the effectiveness of current drug-resistant treatment regimens. Bedaquiline resistance typically arises through mutations in Rv0678 that upregulate drug efflux and confer cross-resistance to multiple drug classes. Here, we identify and optimise a chemical series targeting MenG, a central enzyme in the menaquinone biosynthesis pathway, yielding potent bactericidal inhibitors with in vivo efficacy. Strikingly, MenG inhibition restored bedaquiline susceptibility in efflux-mediated resistant strains, an effect confirmed in vivo where combination therapy achieved a 99.8% reduction in bacterial burden compared with bedaquiline alone. Potentiation also extended to pretomanid and other key agents. Disruption of upstream menaquinone and shikimate pathway enzymes produced similar resensitisation, establishing these pathways as tractable targets for restoring drug susceptibility in Mycobacterium tuberculosis. These findings provide a novel strategy to overcome bedaquiline resistance and strengthen future regimens for efflux-mediated drug-resistant tuberculosis.

microbiology↗

Obesity reprograms adipose extracellular vesicles to induce muscle atrophy via miR-150-5p-mediated transcriptional silencing

BackgroundSarcopenic obesity, where excess body fat coexists with reduced muscle mass and function, is becoming increasingly common in ageing populations and contributes to poor physical and metabolic health. Although adipose tissue-secreted factors are implicated in muscle decline, the specific mechanisms remain unclear. Extracellular vesicles (EVs), which carry regulatory cargo such as microRNAs (miRNAs) between cells, may play a key role in this adipose-muscle communication. MethodsEVs were isolated from adipose-conditioned media (ACM) collected from lean and non-lean human donors using ultracentrifugation. Donors were grouped by BMI (lean: 20.7-24.4; non-lean: 25.3-39.3) and age (younger: 31-56 years; older: 60-84 years). EVs were characterised using nanoparticle tracking analysis (NTA), ExoView, nanoscale flow cytometry (CytoFLEX Nano), and transmission electron microscopy (TEM). Primary human myoblasts were differentiated into myotubes and treated for 24 hours with lean or non-lean EVs (1.3x10 particles/ml) or left untreated. Myotube thickness was measured by immunofluorescence microscopy. Transcriptomic changes were assessed by bulk RNA sequencing. EV miRNA cargo was profiled by small RNA-seq and validated by qPCR. The role of miR-150-5p was tested using antagomir inhibition. ResultsNon-lean EVs significantly reduced myotube thickness compared to both untreated controls (8.7 {+/-} 1.66 {micro}m vs. 12.4 {+/-} 1.72 {micro}m, p < 0.01) and lean EV-treated myotubes (8.7 {+/-} 1.66 {micro}m vs. 13.2 {+/-} 3.84 {micro}m, p < 0.05), indicating a donor BMI-specific effect. This atrophy was restricted to myotubes derived from older donors. MAFbx expression was significantly increased in response to non-lean EVs (p < 0.05). RNA-seq revealed 471 differentially expressed genes (DEGs) in EV-treated vs. untreated cells and 293 DEGs between lean and non-lean EV conditions, with enrichment in inflammatory (TNF, IL1B), oxidative stress, mitochondrial, and chromatin pathways. Small RNA-seq identified 7 differentially expressed miRNAs, including miR-150-5p and miR-193b-5p, both significantly upregulated in non-lean EVs and validated by qPCR. Inhibiting miR-150-5p partially rescued myotube thickness (10.5 {+/-} 1.37 {micro}m vs. 8.7 {+/-} 1.66 {micro}m, p < 0.05) and reduced MAFbx expression. ConclusionsEVs from non-lean adipose tissue drive muscle atrophy and transcriptional changes in an age-dependent manner. These effects are partially mediated by miR-150-5p, highlighting a mechanistic role for EV cargo in adipose-muscle signalling. Targeting EV-derived miRNAs may offer a novel strategy to combat muscle loss in obesity and ageing.

cell biology↗

Context-Dependent miRNA Regulatory Landscapes in Breast Cancer Uncovered by Network Community Structure

MicroRNAs (miRNAs) regulate gene expression through many-to-many interactions that are cooperative, context-dependent, and challenging to interpret from individual miRNA-target pairs alone. Yet, no framework simultaneously captures the cooperative, systems-level, and context-specific dimensions of miRNA regulation across the heterogeneous subtypes of a breast cancer. Here, we integrated paired miRNA and mRNA expression profiles from 1,161 breast cancers from The Cancer Genome Atlas (TCGA) with experimentally validated miRNA-target interactions and protein interaction networks to define cooperative miRNA regulatory modules in breast cancer. Community-resolved analysis of the resulting networks identified 16 functionally coherent miRNA modules associated with core cancer processes. To capture pathway-level network context beyond direct targets, we quantified the proximity of miRNA target sets to pathway proteins within a breast cancer-specific protein interaction network. This framework identified cooperative miRNA modules associated with cell cycle progression, DNA repair, PTEN/TP53-related signaling, and epithelial-mesenchymal transition. Subtype-resolved network analysis further showed that most inferred miRNA functions are strongly context dependent, not being associated in all of basal-like, HER2-enriched, luminal A, and luminal B tumors. In contrast, a limited set of pathway-level associations was conserved across subtypes. Among these, the miR-29 family (miR-29a/b/c-3p) emerged as a consistent regulator of collagen remodeling, extracellular matrix organization, PDGF signaling, and EMT. Notably, this functional conservation persisted despite subtype-specific variation in the underlying target genes. Together, these results define the cooperative miRNA modules that post-transcriptional regulate breast cancer subtypes, identify the miR-29 family as a candidate pan-subtype therapeutic target for EMT-driven metastasis, and establish a generalizable computational framework for resolving miRNA programs across heterogeneous cancers.

cancer biology↗

Comparative genomic analysis of DNA motif frequency across the animal kingdom

Withdrawal StatementThe authors have withdrawn this pre-print manuscript because of some inadvertent errors and inconclusive data discovered upon further review. Therefore, the authors do not wish this work to be cited as reference for research and review articles from other research groups. If you have any questions, please contact the corresponding author.

bioinformatics↗

Unbiased whole genome comparison of Pan paniscus (bonobo) and Homo sapiens (human) through a novel sequence match-based approach

Due to technical and computational limitations, original attempts to compare humans to other non-human primates (NHP) were restricted to specific gene and protein comparisons. With the advances in supercomputing and whole genome sequencing technology, these studies can be revisited to explore entire genomes unbiasedly. A novel alignment-dependent homology algorithm that utilizes a linear search-based approach to find segments of homolog sequences based on a given length of word size, ranging from 32 bp to 1000 bp, was used to perform whole genome comparisons. These sequences were then compared over each chromosome of both the target and control species. Chromosome similarities between Pan paniscus and Homo sapiens varied greatly across various chromosomes. At 32-bp granularity, chromosome 3 showed the highest similarity (91.96%), while chromosome 5 showed the lowest similarity (59.66%). Overall, this indicates that while there are significant similarities in the anatomical structures, physiological structures, and protein similarities, there are significant differences in the genomic code between the two species. Additionally, not all sequences are conserved equally, underscoring the need to study the role that gene duplications, transpositions, and horizontal gene transfer may play in species divergence.

bioinformatics↗

SOX2-VSX2 Co-Occupancy Shapes Retinal Neurogenesis Through Dynamic Chromatin Regulation

Retinal neurogenesis is mediated by the coordinated activities of a complex gene regulatory network (GRN) of transcription factors (TFs) in multipotent retinal progenitor cells (RPCs). How this GRN mechanistically guides neural competence remains poorly understood. In this study, we present integrated transcriptional, genetic, and genomic analyses to uncover the regulatory mechanisms of SOX2, a key factor in establishing neural identity in RPCs. We show that SOX2 is preferentially enriched in the RPC-specific enhancer landscape associated with essential regulators of retinogenesis. Disruption of SOX2 expression impairs retinogenesis, marked by a selective loss of enhancer activity near genes essential for RPC proliferation and lineage specification. We identified the RPC transcription factor VSX2 as a binding partner for SOX2, and together, SOX2 and VSX2 co-target a core, retina-specific chromatin repertoire characterized by enhanced TF binding and robust chromatin accessibility. This cooperative binding establishes a shared SOX2-VSX2 transcriptional code that promotes the expression of critical regulators of neurogenesis while repressing the acquisition of alternative lineage cell fate. Our data illuminate fundamental biological insights on how transcription factors act in concert to drive chromatin-based genetic programs underlying retinal neural identity.

developmental biology↗

βA3/A1-crystallin is an epigenetic regulator of histone deacetylase 3 (HDAC3) in the retinal pigmented epithelial (RPE) cells

Introductory paragraphThe retinal pigmented epithelial (RPE) cells maintain retinal homeostasis, and alterations in their function contribute to non-exudative age-related macular degeneration (AMD)1,2. Here, we explore the intricate relationship between RPE cells, epigenetic modifications, and the development of AMD. Importantly, the study reveals a substantial decrease in histone deacetylase 3 (HDAC3) activity and elevated histone acetylation in the RPE of human AMD donor eyes. To investigate epigenetic mechanisms in AMD development, we used a mouse model with RPE-specific Cryba1 knockout3-5, revealing that the loss of {beta}A3/A1-crystallin selectively reduces HDAC3 activity, resulting in increased histone acetylation. {beta}A3/A1-crystallin activates HDAC3 by facilitating its interaction with the casein kinase II (CK2) and phosphorylating HDAC3, as well as by regulating intracellular InsP6 (phytic acid) levels, required for activating HDAC3. These findings highlight a novel function of {beta}A3/A1-crystallin as an epigenetic regulator of HDAC3 in the RPE cells and provide insights into potential therapeutic strategies in non-exudative AMD.

cell biology↗

Enhancer heterogeneity of lung neuroendocrine tumors reveals sensitivity to FGF signaling inhibition

Well-differentiated low-grade lung neuroendocrine tumors (lung carcinoids or LNETs) are histopathologically classified as typical and atypical LNETs, but each subtype is still heterogeneous at both the molecular level and its clinical manifestation. Here, we report the first genome-wide profiles of primary LNETs cis-regulatory elements by H3K27ac ChIP-seq with matching RNA-seq profiles. Analysis of these regulatory landscapes revealed three regulatory subtypes, independent of the typical / atypical classification. We identified unique differentiation signals that delineate each subtype. The proneuronal subtype emerges under the influence of ASCL1, TCF4, and SOX4 transcription factors, embodying a pronounced proneuronal signature. The luminal subtype is characterized by gain of acetylation at markers of luminal cells and GATA2 activation, and loss of LRP5 and OTP. The HNF+ subtype is characterized by a robust enhancer landscape driven by HNF1A, HNF4A, and FOXA3, with a notable acetylation and expression of FGF signaling genes, especially FGFR3 and FGFR4 genes, pivotal components of the FGF pathway. Our findings not only deepen the understanding of LNETs regulatory and developmental diversity but also spotlight the HNF+ subtypes reliance on FGFR signaling. We demonstrate that targeting this pathway with FGF inhibitors curtails tumor growth both in vitro and in xenograft models, unveiling a potential vulnerability and paving the way for targeted therapies. Overall, our work provides an important resource for studying LNETs to uncover regulatory networks, differentiation signals and therapeutically relevant dependences.

cancer biology↗

The mitochondrial Cu+ transporter PiC2 (SLC25A3) is a target of MTF1 and contributes to the development of skeletal muscle in vitro

The loading of copper (Cu) into cytochrome c oxidase (COX) in mitochondria is essential for energy production in cells. Extensive studies have been performed with mitochondrial cuproenzymes, such as Sco1, Sco2 and Cox17, which contributes to the metallation of the oxidase. However, limited information is available on the upstream mechanism of Cu transport and delivery to mitochondria, especially through Cu-impermeable membranes, in mammalian cells. The mitochondrial phosphate transporter SLC25A3, also known as PiC2, is also able to bind Cu+ and acts as an active copper transporter in eukaryotic cells through these membranes, and ultimately aid in the metallation of COX. We used a well-established differentiation model of primary myoblasts derived from mouse satellite cells, where Cu availability is necessary for growth and maturation, and showed PiC2 is a target of MTF1, its expression is induced during myogenesis and favored by Cu supplementation. PiC2 deletion using CRISPR/Cas9 showed that the transporter is required for proliferation and differentiation of primary myoblasts, as both processes are delayed upon PiC2 knock-out. The effects of PiC2 deletion were ameliorated by the addition of Cu to the growth medium, implying the deleterious effects of PiC2 knockout in myoblasts may be in part due to a failure to deliver sufficient Cu to the mitochondria, which can be compensated by other mitochondrial cuproproteins. Co-localization and co-immunoprecipitation of PiC2 and COX also strongly suggest that PiC2 may act to directly load Cu into COX, which was verified by in vitro Cu+-transfer experiments. The data indicate an important role for PiC2 in both the delivery of Cu to the mitochondria, COX and, subsequently, the differentiation of primary myoblasts.

cell biology↗

Deep proteomic analysis of human microglia and model systems reveal fundamental biological differences of in vitro and ex vivo cells

Using high resolution quantitative mass spectrometry, we have generated the most comprehensive human and mouse microglia proteomic datasets to date, consisting of over 11,000 proteins across all six microglia groups. Microglia from different sources share a core protein signature of over 5600 proteins, yet fundamental differences are observed between species and culture conditions, indicating limitations for human disease modelling in mouse or in in vitro cultures of microglia. Mouse ex vivo microglia show important differences at the proteome level such as differential expression of inflammation and Alzheimers Disease associated proteins. We identify a tenfold difference in the protein content of ex vivo and in vitro cells and significant proteome differences associated with protein synthesis, metabolism, microglia marker expression and environmental sensors. Culturing microglia induces rapidly increased growth, protein content and inflammatory protein expression. These changes can be restored by engrafting in vitro cells into the brain, with xenografted hESC-derived microglia closely resembling microglia from human brain. This data provides an important resource for the field and highlights important considerations needed when using model systems to study human physiology and pathology of microglia.

neuroscience↗