Genome-Wide Activity-Dependent MeCP2 Phosphorylation Regulates Nervous System Development and Function
Open accessAbstract
Autism spectrum disorders such as Rett syndrome (RTT) have been hypothesized to arise from defects in experience-dependent synapse maturation. RTT is caused by mutations in MECP2, a nuclear protein that becomes phosphorylated at S421 in response to neuronal activation. We show here that disruption of MeCP2 S421 phosphorylation in vivo results in defects in synapse development and behavior, implicating activity-dependent regulation of MeCP2 in brain development and RTT. We investigated the mechanism by which S421 phosphorylation regulates MeCP2 function and show by chromatin immunoprecipitation-sequencing that this modification occurs on MeCP2 bound across the genome. The phosphorylation of MeCP2 S421 appears not to regulate the expression of specific genes; rather, MeCP2 functions as a histone-like factor whose phosphorylation may facilitate a genome-wide response of chromatin to neuronal activity during nervous system development. We propose that RTT results in part from a loss of this experience-dependent chromatin remodeling.
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The AMPA receptor-dependent synaptic potentiation induced by ketamine causes an excitation shift that increases MeCP2 Ser421 phosphorylation, leading to transcriptional changes that support long-term synaptic adaptations essential for sustained antidepressant effects.
“The AMPA receptor-dependent synaptic potentiation induced by ketamine causes an excitation shift that increases MeCP2 Ser421 phosphorylation, leading to transcriptional changes that support long-term synaptic adaptations essential for sustained antidepressant effects [79].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [79]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredMECP2 may have a histone-like role in regulating chromatin structure and gene expression.
“These findings suggest that MECP2 may have a histone-like role in regulating chromatin structure and gene expression79,80.”
From Activity-dependent neuronal signalling and autism spectrum disorder (2013) · cites this paper as [80]
Activity-dependent phosphorylation of MECP2 may mediate a genome-wide chromatin response to neuronal activity.
“raising the possibility that activity-dependent phosphorylation of MECP2 mediates a genome-wide chromatin response to neuronal activity80.”
From Activity-dependent neuronal signalling and autism spectrum disorder (2013) · cites this paper as [80]
Ser421Ala knock-in mice had deficits in their response to new objects or mice.
“Behaviourally, the Ser421Ala knock-in mice had deficits in their response to new objects or mice80.”
From Activity-dependent neuronal signalling and autism spectrum disorder (2013) · cites this paper as [80]
Activity-dependent phosphorylation of MECP2 regulates synapse development and function and behavioural responses to environmental stimuli.
“These findings indicate that activity-dependent phosphorylation of MECP2 regulates synapse development and function and behavioural responses to environmental stimuli.”
From Activity-dependent neuronal signalling and autism spectrum disorder (2013) · cites this paper as [80]
Ser421Ala knock-in mice and wild-type mice express equivalent levels of MECP2, but Ser421Ala mice display increased dendritic complexity and increased inhibitory synaptic strength in the cortex.
“The Ser421Ala knock-in mice and wild-type mice express equivalent levels of MECP2, but the Ser421Ala knock-in mice display increased dendritic complexity and increased inhibitory synaptic strength in the cortex80.”
From Activity-dependent neuronal signalling and autism spectrum disorder (2013) · cites this paper as [80]
Extensive analysis of activity-dependent gene transcription in wild-type and MECP2 Ser421Ala knock-in neurons failed to detect any effect of the Ser421Ala mutation.
“extensive analysis of activity-dependent gene transcription in wild-type and MECP2 Ser421Ala knock-in neurons failed to detect any effect of the Ser421Ala mutation.”
From Activity-dependent neuronal signalling and autism spectrum disorder (2013) · cites this paper as [80]
Reference 80 demonstrates that activity-dependent regulation of MECP2 is important for controlling synapse development and behaviour.
“This paper demonstrates the importance of activity-dependent regulation of MECP2 in the control of synapse development and behaviour.”
From Activity-dependent neuronal signalling and autism spectrum disorder (2013) · cites this paper as [80]
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- Authors
- Cohen, S., Gabel, H. W., Hemberg, M., Hutchinson, A. N., Sadacca, L. A., Ebert, D. H., Harmin, D. A., Greenberg, R. S., Verdine, V. K., Zhou, Z., Wetsel, W. C., West, A. E., & Greenberg, M. E.
- Affiliations
- Harvard University (US)
- Boston Children's Hospital (US)
- Duke Medical Center (US)
- Corresponding author
- Greenberg, Michael E.
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2011-10
- Volume
- 72
- Issue
- 1
- Pages
- 72-85
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC3226708
- OpenAlex
- W2019492932
- Cited by
- 298
- References
- 44
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 11 · 2023: 11 · 2022: 10 · 2021: 13 · 2020: 26 · 2019: 12 · 2018: 20 · 2017: 21 · 2016: 28 · 2015: 19 · 2014: 34 · 2013: 39 · 2012: 35
- FWCI
- 21.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 691 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institutes of Health (1R01NS048276, R01 DA022202)
- March of Dimes Foundation (1-FY07-482, T32CA009361)
- Damon Runyon Cancer Research Foundation (1R21NS070250-01A1, DRG-2048-10, K08MH90306, K99 NS058391)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- MeCP2, Rett syndrome, autism spectrum disorder, activity-dependent regulation, synaptic development, chromatin remodeling, neuronal activity, brain development
- MeSH terms
- Animals, Brain, Chromatin, Dendrites, Exploratory Behavior, Mice, Inbred C57BL, Neurons, Phosphorylation, Genome, Gene Expression Regulation, Developmental, Chromatin Immunoprecipitation, Mice, Methyl-CpG-Binding Protein 2, Gene Knock-In Techniques
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