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Cited by 3Neuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology ResearchNeurogenesis and neuroplasticity mechanisms

Control of microglial dynamics by the Arp2/3 complex and the autism- and schizophrenia-associated protein CYFIP1

Open access
Scott-Solache, James, Pei, Jiaxin, Drew, James, López-Doménech, Guillermo, Jolivet, Renaud B., Nieto-Rostro, Manuela, Davenport, Elizabeth C., Arancibia-Cárcamo, I. Lorena +2 more·2026·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.2532488123PMC PMC12993954
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Abstract

Microglia use a highly complex and dynamic network of branched processes to sense and respond to their surroundings. Despite emerging evidence that microglial motility plays important roles in brain development, neurodegeneration, and neuropsychiatric disease, little is known about the intracellular machinery orchestrating microglial process dynamics. Here, we identify roles for regulators of the actin cytoskeleton in controlling microglial behavior. We show that the actin branching Arp2/3 complex is critical for maintaining microglial morphology and is required for surveillance but not chemotactic motility. Neuropsychiatric disease-associated CYFIP1, a core component of the WAVE regulatory complex linking upstream signaling pathways to activation of the Arp2/3 complex, is highly expressed in microglia but has an unknown function. We report that conditional deletion of Cyfip1 in mouse microglia reduces their morphological complexity and surveillance of the brain parenchyma, with no effect on chemotaxis. Deletion of Cyfip1 also increased microglial CD68 positive lysosome volume and engulfment of presynapses. Thus, actin remodeling by CYFIP1 and the Arp2/3 complex controls microglial dynamics and shifts microglia away from a homeostatic state with potential implications for neuropsychiatric disease.

AI snapshot

Written from the paper’s full text.

TL;DR

The Arp2/3 complex and CYFIP1 are required for maintaining ramified microglial morphology and surveillance motility, while chemotaxis remains intact. Microglial Cyfip1 deletion also increases lysosomal CD68 and presynaptic Bassoon content, suggesting altered phagocytic/lysosomal processing relevant to neuropsychiatric disease.

Key findings

  • Arp2/3 inhibition with CK666 reduced the surveillance index from 200.8 ± 28.85 to 79.66 ± 20.96 pixels per 30 s (P = 0.001), a >50% reduction, but did not significantly affect chemotaxis convergence or single-process speed (DMSO: 3.83 ± 0.34 μm/min; CK666: 3.56 ± 0.18 μm/min; P = 0.097).
  • CK666-treated microglia had fewer branch points (DMSO: 12.96 ± 2.748; CK666: 6.95 ± 3.25; P = 0.018), more blebbing (DMSO: 10.50 ± 4.61%; CK666: 60.04 ± 6.24%; P < 0.0001), and occupied a smaller area (DMSO: 765.40 ± 80.53 μm²; CK666: 554.40 ± 25.75 μm²; P = 0.009), while total process length was unchanged.
  • Microglia-specific Cyfip1 conditional knockout reduced CYFIP1 by approximately 50%, reduced surveillance index by 33% (control: 642.40 ± 75.95; cKO: 452.20 ± 50.13 pixels per 30 s; P = 0.023), left chemotaxis normal, and reduced filopodia per cell by 46% (P < 0.01).
  • Cyfip1-cKO microglia showed increased CD68 lysosomal burden (control: 4.25 ± 0.58%; cKO: 7.49 ± 0.29%; P < 0.001), increased lysosome number relative to cell size (control: 0.025 ± 0.003; cKO: 0.042 ± 0.004; P < 0.001), more Bassoon puncta within lysosomes (control: 0.19 ± 0.15; cKO: 1.32 ± 0.35 puncta/cell; P < 0.001), and increased pS6 intensity (P < 0.05).

Methods

  • Two-photon live imaging of acute hippocampal slices from Iba1GFP mice measured spontaneous surveillance and chemotaxis toward a laser-induced lesion; slices were treated with CK666 (200 μM), cytochalasin D (10 μM), or vinblastine (10 μM).
  • A microglia-specific inducible Cyfip1 cKO was generated by crossing Cyfip1F/F mice with Cx3cr1-CreERT2 and Iba1GFP lines; tamoxifen (4 mg oral) was given at P28 and P30, and experiments were performed at P44. Fixed brain sections were immunostained and 3D-reconstructed for morphology, lysosomes, Bassoon, and pS6.
  • In vitro models included Cyfip1 siRNA knockdown in BV2 microglial cells and Cyfip1 conditional knockout MEFs; readouts included Western blot, phalloidin/DNAse1 staining, F/G-actin ratio, and cell morphology. Statistical analysis used linear mixed-effects models with animal or slice as variance components, plus t tests or ANOVA with Bonferroni correction for cell-culture experiments.

Limitations

  • Stated: it is unclear whether increased synaptic material in lysosomes reflects increased phagocytic uptake or reduced degradation, and it is unclear how CYFIP1 loss increases mTORC1 activity in microglia, which is opposite to prior neuronal findings.
  • Stated/evident: the cKO model is microglia-specific but tamoxifen-induced and achieved only approximately 50% reduction of CYFIP1 in enriched microglial lysates, not complete deletion; BV2 and MEF in vitro models may not fully capture in situ microglial biology.
  • Evident: Arp2/3 dependence was tested pharmacologically with CK666, which may have off-target effects, and some live-imaging chemotaxis experiments used small animal numbers (e.g., N = 2 animals, 6 lesions for CK666 chemotaxis), limiting statistical power.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1073/pnas.2532488123

Cites

89 of 89 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

5 of 6 cited sources checked · 2 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    At postnatal day 44, microglia are in a stable homeostatic state.

    “Experiments were carried out, 2 wk after the second administration, at P44. This is an age at which microglia are in a stable homeostatic state (78, 82, 83).”
    Quote in the paperSubstantial claim3 of 3 sources checked
    • cites [78] D. P. Schafer, Microglia sculpt postnatal neural circuits in an activity and complement-dependent manner. Neuron 74, 691– 705 (2012). 22632727 PMC3528177 source

      The Results section (‘Microglia-mediated engulfment of RGC inputs is developmentally regulated’; page unavailable) contrasts activated early-postnatal microglia with those at P30 and describes resting microglia in the healthy adult brain. It does not assess P44 or establish that microglia are in a stable homeostatic state at that age. (LLM, conf=0.79)

      Experimental — accuracy not yet measured
    • cites [82] K. I. Mosher, T. Wyss-Coray, Microglial dysfunction in brain aging and Alzheimer’s disease. Biochem. Pharmacol. 88, 594– 604 (2014). 24445162 PMC3972294 source

      Section 2 describes microglia in the healthy adult brain as helping maintain tissue homeostasis. It does not establish that microglia are in a stable homeostatic state specifically at postnatal day 44; section 4.1 discusses adulthood without identifying that age. (LLM, conf=0.82)

      Experimental — accuracy not yet measured
    • cites [83] R. C. Paolicelli, Synaptic pruning by microglia is necessary for normal brain development. Science 333, 1456– 1458 (2011). 21778362 source

      The Additional information reports microglial-density differences through P28, while the main text discusses synaptic plasticity at P40; neither assesses whether microglia are in a stable homeostatic state at P44. Searches for P44, homeostatic state, and nearby ages found no passage establishing that claim. (LLM, conf=0.74)

      Experimental — accuracy not yet measured
  • Findingown data

    CK666 treatment reduced the microglial surveillance index by more than 50% compared to DMSO.

    “Analysis of surveillance revealed a >50% reduction in pixels surveyed by Arp2/3 complex-inhibited cells compared to vehicle (DMSO) treatment, for which surveillance remained approximately constant over the imaging period (Fig. 1 C–E, P < 0.005).”
    Quote in the paperSubstantial claim
  • Findingown data

    Cyfip1-cKO microglia had significantly more Bassoon puncta within their lysosomes in the prefrontal cortex.

    “Quantification reveals increase in number of Bassoon puncta within lysosomes in cKO cells of the prefrontal cortex (P < 0.001; control: 0.19 ± 0.15 puncta/cell, cKO: 1.32 ± 0.35; P = 0.018; n = 5 animals, 55 to 56 cells).”
    Quote in the paperSubstantial claim
  • Findingown data

    Cyfip1-cKO microglia showed a 33% reduction in surveillance index compared to controls.

    “Quantifying surveillance of cKO microglia compared to control showed a 33% reduction in surveillance index (Fig. 3 K–M, P < 0.05).”
    Quote in the paperSubstantial claim
  • Findingown data

    Loss of CYFIP1 had no effect on the chemotactic responses of microglia to laser-induced lesion.

    “Interestingly, loss of CYFIP1 had no effect on the chemotactic responses to laser-induced lesion (Fig. 3 N–P), as was observed with Arp2/3 complex inhibition.”
    Quote in the paperSubstantial claim
  • Classified as probably not a substantial claim. 14
  • May combine two claims. 13
  • The quote only partly states this claim. 1

  • Classified as probably not a substantial claim.

    Study design and conductcitation

    Analysis of CD68 positive lysosomes and intralysosomal Bassoon within individual microglia was performed based on a published protocol by Schafer et al.

    “Analysis of CD68 positive lysosomes as well as intralysosomal Bassooon within individual microglia were performed based on a published protocol by Schafer et al. (57).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites Schafer et al. [57] D. P. Schafer, E. K. Lehrman, C. T. Heller, B. Stevens, An engulfment assay: A protocol to assess interactions between CNS phagocytes and neurons. J. Vis. Exp. 88, 51482 (2014). PMC4188069 24962472 source

  • Classified as probably not a substantial claim.

    Study design and conductcitation

    For all experiments involving animals, linear mixed-effects models (LMEMs) were used to account for the nonindependence of cells nested within animals while testing for treatment or genotype effects.

    “For all experiments involving animals, linear mixed-effects models (LMEMs) were used to account for the nonindependence of cells nested within animals while testing for treatment or genotype effects (88).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [88] Z. Yu, Beyond t test and ANOVA: Applications of mixed-effects models for more rigorous statistical analysis in neuroscience research. Neuron 110, 21– 35 (2022). 34784504 PMC8763600 source

  • May combine two claims.

    Findingown data

    Cyfip1-cKO microglia had reduced morphological complexity, including decreased Sholl intersections, reduced total process length, reduced branch points, and a 46% decrease in filopodia per cell.

    “Sholl analysis revealed a decrease in the complexity of microglial processes that appeared consistent across the whole arbor (Fig. 4B, P < 0.05).”
    • Also stated in: § Results · plain
      “Supporting this, total process length and number of branch points were both significantly reduced in the Cyfip1-cKO (Fig. 4 C and D, P < 0.01 and P < 0.001 respectively, SI Appendix, Fig. S3 D and E).”
    • Also stated in: § Results · plain
      “Interestingly, the number of filopodia per cell was decreased by 46% in cKO microglia (Fig. 4F, P < 0.01, SI Appendix, Fig. S3F).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    CK666-treated microglia showed a reduction in the number of branch points and approximately 60% showed membrane blebbing, a sixfold increase over control.

    “3D morphological reconstructions showed a reduction in the number of branch points in CK666-treated microglia compared to DMSO-treated (Fig. 2C, P < 0.05).”
    • Also stated in: § Results · plain
      “When quantified, approximately 60% of CK666-treated cells showed such blebbing, a sixfold increase over control (Fig. 2F, P < 0.001).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Cyfip1-cKO microglia had increased CD68 burden and an increased number of discrete lysosomes relative to cell size.

    “Quantification reveals increase in CD68 burden in cKO cells of the somatosensory cortex as a percentage of total cell volume (P < 0.001; control: 4.25 ± 0.58 %, cKO: 7.49 ± 0.29 %; N = 5 animals, 54 to 56 cells).”
    • Also stated in: § Results · plain
      “and increased number of discrete lysosomes within microglia relative to cell size (P < 0.001; control: 0.025 ± 0.003, cKO: 0.042 ± 0.004; N = 5 animals, 54 to 56 cells).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Cyfip1-KD BV2 cells were larger, lost their characteristic circular morphology in favor of a bipolar morphology, and had an increased F-actin to G-actin ratio.

    “Cyfip1-KD BV2 cells were larger (Fig. 3 D and E, P < 0.0001), had lost their characteristic circular morphology in favor of a bipolar morphology (Fig. 3F, P < 0.0001), and had an increased F-actin to G-actin ratio (Fig. 3G, P < 0.0001).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Findingnone given

    After 8 to 10 passages at low density, the MEF cultures presented a homogeneous cell population and started to grow steadily.

    “After 8 to 10 passages at low density, the cultures presented a homogeneous cell population and started to grow steadily.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Knockdown of Cyfip1 in BV2 microglial cells using two different siRNAs resulted in a ~40% loss of WAVE2 expression without affecting ABI3.

    “Knockdown (KD) of Cyfip1 in the BV2 microglial cell line using two different siRNAs resulted in a ~40% loss of WAVE2 expression (Fig. 3 B and C, siRNA #1 P < 0.01, siRNA #2 P < 0.05), WAVE2 being the subunit that contains the VCA domain that is required to activate Arp2/3 complex activity (47), without affecting protein expression of the AD risk gene, ABI3.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [47] L. M. Machesky, Scar, a WASp-related protein, activates nucleation of actin filaments by the Arp2/3 complex. Proc. Natl. Acad. Sci. U.S.A. 96, 3739– 3744 (1999). 10097107 PMC22364 source

  • May combine two claims.

    Findingown data

    Cortical Cyfip1-cKO microglia had increased pS6 intensity compared to controls, and this effect was also observed in Cyfip1-KO MEFs.

    “Staining of fixed sections for phosphorylated ribosomal protein S6 (pS6), a readout of mTORC1 activity, found cortical Cyfip1-cKO microglia had an increased pS6 intensity compared to controls (SI Appendix, Fig. S4A, P < 0.05).”
    • Also stated in: § Results · plain
      “This effect was also observed in Cyfip1-KO MEFs (SI Appendix, Fig. S2 C and E, P < 0.0001).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    CK666 treatment did not affect the overall convergence of microglial processes toward a laser-induced lesion or the speed of individual processes.

    “The overall convergence of processes toward the lesion site was unchanged (Fig. 1G and SI Appendix, Fig. S1I), with no difference in the speed of individual processes observed (Fig. 1H).”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Study design and conductnone given

    Microglial morphology in Cyfip1-cKO animals was assessed using perfusion-fixed brains from litter matched pairs.

    “Microglial morphology in Cyfip1-cKO animals was assessed using perfusion-fixed brains from litter matched pairs.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    Microglial ramification is dependent on both sustained activity of the Arp2/3 complex and expression of CYFIP1, and targeting either leads to a specific defect in surveillance while chemotaxis remains robust.

    “Here, we report that microglial ramification is dependent on both sustained activity of the Arp2/3 complex, and expression of the neuropsychiatric disease-associated Arp2/3 complex regulator CYFIP1.”
    • Also stated in: § Discussion · plain
      “Targeting either of these components of the actin branching machinery led to a specific defect in surveillance of the brain parenchyma, whereas chemotaxis remained robust.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Cell culture experiments (BV2 microglia and MEFs) were analyzed using classical parametric statistics (t tests or ANOVA) with Bonferroni post hoc corrections for multiple testing when appropriate.

    “Cell culture experiments (BV2 microglia and MEFs) were analyzed using classical parametric statistics (t tests or ANOVA) with Bonferroni post hoc corrections for multiple testing when appropriate.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Study design and conductown data

    Enriched microglial protein lysates from cKO brains showed a significant decrease in CYFIP1 expression of approximately 50% over control, showing that Cre induction leads to specific loss of microglial CYFIP1 in vivo.

    “Recombination of the Cyfip1 cassette was confirmed by PCR of brain tissue from control or Cyfip1-cKO animals (SI Appendix, Fig. S3B) and enriched microglial protein lysates from cKO brains showed a significant decrease in CYFIP1 expression of approximately 50% over control (Fig. 3 I and J, P < 0.05), showing that Cre induction in this model leads to specific loss of microglial CYFIP1 in vivo.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Transformed cell lines were genotyped to confirm genetic background.

    “Transformed cell lines were then genotyped to confirm genetic background.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    For mouse primary antibodies, slices were first incubated overnight at 4 °C with mouse Fab fragment (1:50 with blocking solution).

    “For mouse primary antibodies, slices were first incubated overnight at 4 °C with mouse Fab fragment (1:50 with blocking solution).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). The quote only partly states this claim.

    Study design and conductnone given

    All experiments were carried out after at least eight passages from the immortalization process.

    “All experiments were carried out after at least eight passages from the immortalization process.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    For timelapse recordings, regions containing well-labelled, unactivated microglia between 50 to 150 μm from the slice surface were used.

    “regions containing well-labelled, unactivated microglia between 50 to 150 μm from the slice surface were used for timelapse recordings”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationown data

    Arp2/3 complex activity is required for the normal ramified morphology of microglia and effective surveillance, but is dispensable for chemotaxis.

    “These data suggest that Arp2/3 complex activity is required for the normal ramified morphology of microglia, and effective surveillance, but is dispensable for chemotaxis.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    In IBA1GFP(−/−) mice, microglia were costained with P2Y12R and IBA1 primary antibody both detected with Alexa Fluor 488-conjugated secondary antibodies, enabling a comprehensive visualization of microglia morphology.

    “In IBA1GFP(−/−) mice, microglia were costained with P2Y12R and IBA1 primary antibody both detected with Alexa Fluor 488-conjugated secondary antibodies, enabling a comprehensive visualization of microglia morphology.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Study design and conductreasoning

    To assess the impact of Cyfip1-cKO on microglial morphology independent of methodology, data were normalized by z-scoring all cells within each method.

    “To assess the impact of Cyfip1-cKO on microglial morphology independent of methodology, data were normalized by z-scoring all cells within each method.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Immunohistochemistry of Cyfip1-cKO animals was carried out on perfusion-fixed brains from litter matched pairs.

    “Immunohistochemistry of Cyfip1-cKO animals was carried out on perfusion-fixed brains from litter matched pairs.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Study design and conductreasoning

    The z-scoring procedure ensured comparability of morphology measurements across labeling methods while preserving biological variability between genotypes.

    “This procedure ensured comparability of morphology measurements across labeling methods, while preserving biological variability between genotypes.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductnone given

    Semiautomated 3D reconstructions were produced using the APP2 tracing plugin in Vaa3D software and manually checked with any clear abnormalities corrected.

    “Semiautomated 3D reconstructions were produced using the “APP2” tracing plugin in Vaa3D software (http://home.penglab.com/proj/vaa3d), and manually checked with any clear abnormalities corrected.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    Two Cyfip1 siRNAs (s73706 and s73707) were used in all experiments based on silencing power.

    “We obtained three predesigned Silencer™ Select siRNAs to target Cyfip1 of which two were used in all experiments based on silencing power (siRNA IDs: s73706 and s73707) and one negative control (catalog numbers: 4390771 and 4390846 from Thermofisher).”
    Quote in the paperNot a substantial claim
25 of 25

  • The paper relies on this without support.

    The cytoskeletal mechanisms that generate and maintain ramified microglial structure remain unclear.

    “yet the cytoskeletal mechanisms that generate and maintain ramified microglial structure remain unclear”

  • The paper relies on this without support.

    Specific functions for the actin remodeling machinery in microglia remain largely unknown.

    “specific functions for the actin remodeling machinery in microglia remain largely unknown”

  • The paper relies on this without support.

    Microglial interactions within the brain during both health and disease are critically dependent on their shape and motility.

    “Microglial interactions within the brain during both health and disease are critically dependent on their shape and motility.”

  • The paper relies on this without support.

    Iba1GFP mice avoid the loss of function inherent in using even heterozygote CX3CR1-GFP knock-in mice.

    “All surveillance imaging was done using Iba1GFP mice (which avoid the loss of function inherent in using even heterozygote CX3CR1-GFP knock-in mice).”
4 of 4

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Fig. 4 title reverses the reported direction of synaptic cargo

    Minor

    The figure title says synapse engulfment is decreased, but the paper reports more presynaptic Bassoon within cKO microglial lysosomes and describes this as increased synaptic phagocytosis.

  • Two incompatible P-values are given for Fig. 4L

    Minor

    The same Bassoon-puncta comparison is labeled both P < 0.001 and P = 0.018 in the Fig. 4L caption.

  • Bassoon analysis is assigned to two cortical regions

    Minor

    The Fig. 4 caption and methods place the Bassoon measurements in the somatosensory cortex, but the Fig. 4L quantification says they are from the prefrontal cortex.

  • WAVE2 siRNA significance levels are reversed

    Minor

    The results assign P < 0.01 to siRNA #1 and P < 0.05 to siRNA #2, whereas the Fig. 3 caption assigns those thresholds in the opposite order for WAVE2.

4 of 4

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Authors
Scott-Solache, J., Pei, J., Drew, J., López-Doménech, G., Jolivet, R. B., Nieto-Rostro, M., Davenport, E. C., Arancibia-Cárcamo, I. L., Attwell, D., & Kittler, J. T.
Affiliations
  • University College London (GB)
  • Department of Neuroscience, Physiology and Pharmacology, University College London
  • Maastricht University (NL)
Corresponding author
  • Scott-Solache, James
  • Pei, Jiaxin
  • Drew, James
  • Kittler, Josef T.
ORCID
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2026-03-12
Volume
123
Issue
11
Pages
e2532488123-e2532488123
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.2532488123
PMC
PMC12993954
OpenAlex
W7135096907
Cited by
2
References
86
Citations by year
2026: 2
FWCI
4.87
Type
journal article
Language
en
Open access
Licence
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Research Publications (Maastricht University) (publishedVersion, cc-by)
  • PubMed Central (submittedVersion, cc-by)
Funders
  • Wellcome Trust (22519/Z/21/Z, 223202/Z/21/Z, 099222)
  • Wellcome (219366)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
microglia, Arp2/3 complex, CYFIP1, WAVE regulatory complex, actin cytoskeleton, microglial morphology, microglial surveillance, chemotaxis, neuropsychiatric disorders, autism spectrum disorder, schizophrenia, conditional gene deletion
MeSH terms
CD68 Molecule, Animals, Brain, Chemotaxis, Humans, Lysosomes, Phagocytosis, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Microglia, Mice, Knockout, Adaptor Proteins, Signal Transducing, Actin-Related Protein 2-3 Complex, Mice

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