Palmitoylation-dependent neurodevelopmental deficits in a mouse model of 22q11 microdeletion
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Individuals with 22q11.2 microdeletions have cognitive deficits and a high risk of developing schizophrenia. Here we provide evidence that primary hippocampal neurons from a mouse model of 22q11.2 deletion (Df(16)A(+/-) mice) have decreased density of dendritic spines and glutamatergic synapses, as well as impaired dendritic growth. These deficits were prevented by introduction of the enzymatically active ZDHHC8 palmitoyltransferase encoded by a gene in the 22q11.2 locus, and they were also observed in primary cultures from Zdhhc8-deficient mice. Many of these deficits were also present in the hippocampi of adult Df(16)A(+/-) and Zdhhc8-deficient mice. Finally, we provide evidence that PSD95 is one of the substrates of ZDHHC8. Our analysis reveals that 22q11.2 microdeletion results in deficits in neuronal development and suggests that impaired neuronal protein palmitoylation contributes to many of these deficits.
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Primary hippocampal neurons from Df(16)A+/− mice show reduced spine density and sizes.
“Primary hippocampal neurons from mice engineered to carry the 1.3-Mb orthologous chromosomal region (Df(16)A+/−) showed reduced spine density and sizes51.”
From Dendritic spine pathology in neuropsychiatric disorders (2011) · cites this paper as [51]
Loss of either ZDHHC8 or DGCR8 is sufficient to impair spine and dendrite morphology.
“Loss of either of two genes in this region (ZDHHC8 and DGCR8) was sufficient to impair spine and dendrite morphology50,51.”
From Dendritic spine pathology in neuropsychiatric disorders (2011) · cites this paper as [51]
ZDHHC8 palmitoylates PSD-95; its loss reduces spine density and simplifies dendrites, and replacement rescues spine and dendrite deficiency in Df(16)A+/− neurons.
“ZDHHC8 is a palmitoyl transferase that palmitoylates the postsynaptic density scaffolding molecule PSD-95; ZDHHC8 loss results in reduced spine density and simpler dendrites and its replacement into Df(16)A+/− neurons rescued spine and dendrite deficiency51.”
From Dendritic spine pathology in neuropsychiatric disorders (2011) · cites this paper as [51]
The Df(16)A+/− mouse model of 22q11.2 microdeletion syndrome has reduced hippocampal spine density and spine size.
“Mice modeling the 22q11.2 microdeletion syndrome (Df(16)A+/−) show reduced hippocampal spine density and sizes51.”
From Dendritic spine pathology in neuropsychiatric disorders (2011) · cites this paper as [51]
ZDHHC8-deficient mice have simplified dendritic trees and lower spine density.
“Mice deficient in individual genes in this region (ZDHHC8 and DGCR8) show simplified dendritic trees and reduced spine density51 or smaller spines50, respectively.”
From Dendritic spine pathology in neuropsychiatric disorders (2011) · cites this paper as [51]
In vitro cultures of hippocampal neurons from Df(16)A+/− mice show fewer mushroom spines, decreased spine head diameter and length, fewer glutamatergic synapses, and decreased presynaptic vesicle density.
“Other studies show fewer mushroom spines, decreased spine head diameter and length, fewer glutamatergic synapses and decreased presynaptic vesicle density using in vitro cultures of hippocampal neurons from Df(16)A+/− mice [249].”
From Autism spectrum disorder: neuropathology and animal models (2017) · cites this paper as [249]
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“ZDHHC8 is a palmitoyl transferase which palmitoylates PSD-95; its loss results in reduced spine density and simpler dendrites, and its replacement into Df(16)A+/− neurons rescued spine and dendrite deficiency [107].”
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- Authors
- Mukai, J., Dhilla, A., Drew, L. J., Stark, K. L., Cao, L., MacDermott, A. B., Karayiorgou, M., & Gogos, J. A.
- Affiliations
- Columbia University (US)
- Corresponding author
- Karayiorgou, Maria
- Gogos, Joseph A
- Venue
- Nature Neuroscience
- Published
- 2008-10-05
- Volume
- 11
- Issue
- 11
- Pages
- 1302-1310
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC2756760
- OpenAlex
- W2095119525
- Cited by
- 260
- References
- 51
- Citations by year
- 2026: 7 · 2025: 14 · 2024: 8 · 2023: 14 · 2022: 6 · 2021: 12 · 2020: 7 · 2019: 12 · 2018: 13 · 2017: 14 · 2016: 11 · 2015: 25 · 2014: 11 · 2013: 27 · 2012: 17
- FWCI
- 11.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Mental Health (MH07723, R01MH067068, R01MH077235, MH 67068)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- 22q11.2 microdeletion, chromosome 22q11.2, palmitoylation, dendritic spines, glutamatergic synapses, hippocampal neurons, PSD-95, neurodevelopmental deficits, schizophrenia, dendritic growth
- MeSH terms
- Disks Large Homolog 4 Protein, Acyltransferases, Animals, Brain Diseases, Cells, Cultured, Chromosome Aberrations, Chromosome Deletion, Chromosomes, Human, Pair 22, Dendrites, Diagnostic Imaging, Disease Models, Animal, Embryo, Mammalian, Hippocampus, Humans, Membrane Potentials, Membrane Proteins, Mice, Transgenic, Neurons, Synapses, Transfection, Glutamic Acid, Intracellular Signaling Peptides and Proteins, Dendritic Spines, Green Fluorescent Proteins, Mice, Guanylate Kinases
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