Pat Levitt

Vanderbilt University, Нашвилл, Michigan, United States

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Publications (185)1209.91 Total impact

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    ABSTRACT: Hepatocyte growth factor (HGF) activation of the MET receptor tyrosine kinase influences multiple neurodevelopmental processes. Evidence from human imaging and mouse models shows that, in the forebrain, disruptions in MET signaling alter circuit formation and function. One likely means of modulation is by controlling neuron maturation. Here, we examined the signaling mechanisms through which MET exerts developmental effects in the neocortex. In situ hybridization revealed that hgf is located near MET-expressing neurons, including deep neocortical layers and periventricular zones. Western blot analyses of neocortical crude membranes demonstrated that HGF-induced MET autophosphorylation peaks during synaptogenesis, with a striking reduction in activation between P14 and P17 just prior to pruning. In vitro analysis of postnatal neocortical neurons assessed the roles of intracellular signaling following MET activation. There is rapid, HGF-induced phosphorylation of MET, ERK1/2 and Akt that is accompanied by two major morphological changes increases in total dendritic growth and synapse density. Selective inhibition of each signaling pathway altered only one of the two distinct events. MAPK/ERK pathway inhibition significantly reduced the HGF-induced increase in dendritic length, but had no effect on synapse density. In contrast, inhibition of the PI-3K/Akt pathway reduced HGF-induced increases in synapse density, with no effect on dendritic length. The data reveal a key role for MET activation during the period of neocortical neuron growth and synaptogenesis, with distinct biological outcomes mediated via discrete MET-linked intracellular signaling pathways in the same neurons. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · Developmental Neurobiology
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    ABSTRACT: The neurotransmitter serotonin [5-hydroxytryptamine (5-HT)] modulates many key brain functions including those subserving sensation, emotion, reward, and cognition. Efficient clearance of 5-HT after release is achieved by the antidepressant-sensitive 5-HT transporter (SERT, SLC6A4). To identify novel SERT regulators, we pursued a proteomic analysis of mouse midbrain SERT complexes, evaluating findings in the context of prior studies that established a SERT-linked transcriptome. Remarkably, both efforts converged on a relationship of SERT with the synaptic adhesion protein neuroligin 2 (NLGN2), a post-synaptic partner for presynaptic neurexins, and a protein well-known to organize inhibitory GABAergic synapses. Western blots of midbrain reciprocal immunoprecipitations confirmed SERT/NLGN2 associations, and also extended to other NLGN2 associated proteins [e.g., α-neurexin (NRXN), gephyrin]. Midbrain SERT/NLGN2 interactions were found to be Ca2+-independent, supporting cis vs. trans-synaptic interactions, and were absent in hippocampal preparations, consistent with interactions arising in somatodendritic compartments. Dual color in situ hybridization confirmed co-expression of Tph2 and Nlgn2 mRNA in the dorsal raphe, with immunocytochemical studies confirming SERT:NLGN2 co-localization in raphe cell bodies but not axons. Consistent with correlative mRNA expression studies, loss of NLGN2 expression in Nlgn2 null mice produced significant reductions in midbrain and hippocampal SERT expression and function. Additionally, dorsal raphe 5-HT neurons from Nlgn2 null mice exhibit reduced excitability, a loss of GABAA receptor-mediated IPSCs, and increased 5-HT1A autoreceptor sensitivity. Finally, Nlgn2 null mice display significant changes in behaviors known to be responsive to SERT and/or 5-HT receptor manipulations. We discuss our findings in relation to the possible coordination of intrinsic and extrinsic regulation afforded by somatodendritic SERT:NLGN2 complexes.
    Preview · Article · Jan 2016 · Frontiers in Synaptic Neuroscience
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    ABSTRACT: Deciphering the molecular basis for guiding specific aspects of neocortical development remains a challenge due to the complexity of histogenic events and the vast array of protein interactions that mediate these events. The Eph family of receptor tyrosine kinases is implicated in a number of these neurodevelopmental activities. Eph receptors have been known to be capable of responding to several ephrin ligands within their respective subgroups, often eliciting similar downstream effects. However, several recent studies have reported specificity between receptor-ligand pairs within each subfamily, the functional relevance of which is not defined. Here, we show that a receptor of the EphA subfamily, EphA4, has distinct effects from its close relative EphA7 in the developing brain. Both EphA4 and EphA7 interact similarly with corresponding ligands expressed in the developing neocortex. However, only EphA7 shows strong interaction with ligands in the somatosensory thalamic nuclei; EphA4 affects only cortical neuronal migration with no visible effects on the guidance of CT axons, while EphA7 affects both cortical neuronal migration and CT axon guidance. Our data provide new evidence that Eph receptors in the same subfamily are not simply interchangeable, but functionally specified through selective interactions with distinct ligands in vivo. This article is protected by copyright. All rights reserved.
    No preview · Article · Nov 2015 · The Journal of Comparative Neurology
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    Barbara L Thompson · Pat Levitt
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    ABSTRACT: Background: Our laboratory discovered that the gene encoding the receptor tyrosine kinase, MET, contributes to autism risk. Expression of MET is reduced in human postmortem temporal lobe in autism and Rett Syndrome. Subsequent studies revealed a role for MET in human and mouse functional and structural cortical connectivity. To further understand the contribution of Met to brain development and its impact on behavior, we generated two conditional mouse lines in which Met is deleted from select populations of central nervous system neurons. Mice were then tested to determine the consequences of disrupting Met expression. Methods: Mating of Emx1 (cre) and Met (fx/fx) mice eliminates receptor signaling from all cells arising from the dorsal pallium. Met (fx/fx) and Nestin (cre) crosses result in receptor signaling elimination from all neural cells. Behavioral tests were performed to assess cognitive, emotional, and social impairments that are observed in multiple neurodevelopmental disorders and that are in part subserved by circuits that express Met. Results: Met (fx/fx) /Emx1 (cre) null mice displayed significant hypoactivity in the activity chamber and in the T-maze despite superior performance on the rotarod. Additionally, these animals showed a deficit in spontaneous alternation. Surprisingly, Met (fx/fx; fx/+) /Nestin (cre) null and heterozygous mice exhibited deficits in contextual fear conditioning, and Met (fx/+) /Nestin (cre) heterozygous mice spent less time in the closed arms of the elevated plus maze. Conclusions: These data suggest a complex contribution of Met in the development of circuits mediating social, emotional, and cognitive behavior. The impact of disrupting developmental Met expression is dependent upon circuit-specific deletion patterns and levels of receptor activity.
    Preview · Article · Nov 2015 · Journal of Neurodevelopmental Disorders
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    ABSTRACT: Elevated whole blood serotonin levels are observed in more than 25 % of children with autism spectrum disorder (ASD). Co-occurring gastrointestinal (GI) symptoms are also common in ASD but have not previously been examined in relationship with hyperserotonemia, despite the synthesis of serotonin in the gut. In 82 children and adolescents with ASD, we observed a correlation between a quantitative measure of lower GI symptoms and whole blood serotonin levels. No significant association was seen between functional constipation diagnosis and serotonin levels in the hyperserotonemia range, suggesting that this correlation is not driven by a single subgroup. More specific assessment of gut function, including the microbiome, will be necessary to evaluate the contribution of gut physiology to serotonin levels in ASD.
    No preview · Article · Nov 2015 · Journal of Autism and Developmental Disorders
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    ABSTRACT: Given the underrepresentation of ethnic minorities in health research (Heiat et al. in Arch Int Med 162(15):1-17, 2002; Kelly et al. in J Nat Med Assoc 97:777-783, 2005; United States Department of Health and Human Services. Monitoring adherence to the NIH policy on the inclusion of women and minorities as subjects in clinical research. , 2013), this study evaluated promising strategies to effectively recruit Latinos into genetic research on autism spectrum disorders (ASD). The study included 97 children, aged 5-17 years, with ASD; 82.5 % of the participants were identified as Latino/Hispanic. Traditional and culture-specific recruitment and retention strategies were compared between the Latino and non-Latino groups. Culture-specific, parent-centered approaches were found to be successful in engaging and retaining Latino participants for research involving genetic testing.
    No preview · Article · Sep 2015 · Journal of Autism and Developmental Disorders
  • Ruth I Wood · Allison T Knoll · Pat Levitt
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    ABSTRACT: Social behavior modulates response to alcohol.Because oxytocin (OXT) and vasopressin (AVP) contribute to rewarding social behavior, the present study utilized a genetic strategy to determine whether OXT and AVP receptors (OXTR, AVPR1a) are essential for female mice to demonstrate a conditioned social preference for ethanol.The study compared wild-type (WT) and knock-out (KO) females lacking either Oxtr or Apr1a in a conditioned social preference (CSP) test.KO females and WT females from Het-Het crosses were pair-housed: KO and WT(ko).WT females from Het-WT crosses were pair-housed: WT(wt). Test mice received 2g/kg ethanol or saline ip, and were paired four times each with one stimulus female (CS-) after saline, and with another female (CS+) following ethanol.After pairing, the time spent with CS+ and CS- females was measured.WT(wt) females showed conditioned preference for the CS+ female paired with ethanol, demonstrated by greater interaction time (p<0.05).In both KO lines, ethanol significantly reduced interaction with the CS+ female (p<0.05), and there was no change in interaction for WT(ko) females.Response to odors by habituation-dishabituation was unaffected in both KO lines, and the response to a hypnotic dose of ethanol also was the same as in WT mice.However, anxiety, measured as time on the open arms of the elevated plus maze, was reduced in KO(Oxtr) females compared with WT(wt).The results suggest that Oxtr and Avpr1a are required for conditioned effects of an ethanol-associated social stimulus.The lack of CSP in WT(ko) females suggests that the quality of social interactions during postnatal and postweaning life may modulate development and expression of normal social responses. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Aug 2015 · Physiology & Behavior
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    ABSTRACT: Children with autism spectrum disorder (ASD) may present with multiple medical conditions in addition to ASD symptoms. This study investigated whether there are predictive patterns of medical conditions that co-occur with ASD, which could inform medical evaluation and treatment in ASD, as well as potentially identify etiologically meaningful subgroups. Medical history data were queried in the multiplex family Autism Genetic Resource Exchange (AGRE). Fourteen medical conditions were analyzed. Replication in the Simons Simplex Collection (SSC) was attempted using available medical condition data on gastrointestinal disturbances (GID), sleep problems, allergy and epilepsy. In the AGRE cohort, no discrete clusters emerged among 14 medical conditions. GID and seizures were enriched in unaffected family members, and together with sleep problems, were represented in both AGRE and SSC. Further analysis of these medical conditions identified predictive co-occurring patterns in both samples. For a child with ASD, the presence of GID predicts sleep problems and vice versa, with an approximately 2-fold odds ratio in each direction. These risk patterns were replicated in the SSC sample, and in addition, there was increased risk for seizures and sleep problems to co-occur with GID. In these cohorts, seizure alone was not predictive of the other conditions co-occurring, but behavioral impairments were more severe as the number of co-occurring medical symptoms increased. These findings indicate that interdisciplinary clinical care for children with ASD will benefit from evaluation for specific patterns of medical conditions in the affected child and their family members. Autism Res 2015. © 2015 The Authors Autism Research published by Wiley Periodicals, Inc. on behalf of International Society for Autism Research. © 2015 The Authors Autism Research published by Wiley Periodicals, Inc. on behalf of International Society for Autism Research.
    No preview · Article · May 2015 · Autism Research

  • No preview · Article · Jan 2015 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
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    Shenfeng Qiu · Zhongming Lu · Pat Levitt
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    ABSTRACT: The MET receptor tyrosine kinase (RTK), implicated in risk for autism spectrum disorder (ASD) and in functional and structural circuit integrity in humans, is a temporally and spatially regulated receptor enriched in dorsal pallial-derived structures during mouse forebrain development. Here we report that loss or gain of function of MET in vitro or in vivo leads to changes, opposite in nature, in dendritic complexity, spine morphogenesis, and the timing of glutamatergic synapse maturation onto hippocampus CA1 neurons. Consistent with the morphological and biochemical changes, deletion of Met in mutant mice results in precocious maturation of excitatory synapse, as indicated by a reduction of the proportion of silent synapses, a faster GluN2A subunit switch, and an enhanced acquisition of AMPA receptors at synaptic sites. Thus, MET-mediated signaling appears to serve as a mechanism for controlling the timing of neuronal growth and functional maturation. These studies suggest that mistimed maturation of glutamatergic synapses leads to the aberrant neural circuits that may be associated with ASD risk. Copyright © 2014 the authors 0270-6474/14/3416166-14$15.00/0.
    Preview · Article · Dec 2014 · The Journal of Neuroscience : The Official Journal of the Society for Neuroscience
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    Full-text · Conference Paper · May 2014
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    ABSTRACT: The anatomical and functional architecture of the human brain is mainly determined by prenatal transcriptional processes. We describe an anatomically comprehensive atlas of the mid-gestational human brain, including de novo reference atlases, in situ hybridization, ultra-high resolution magnetic resonance imaging (MRI) and microarray analysis on highly discrete laser-microdissected brain regions. In developing cerebral cortex, transcriptional differences are found between different proliferative and post-mitotic layers, wherein laminar signatures reflect cellular composition and developmental processes. Cytoarchitectural differences between human and mouse have molecular correlates, including species differences in gene expression in subplate, although surprisingly we find minimal differences between the inner and outer subventricular zones even though the outer zone is expanded in humans. Both germinal and post-mitotic cortical layers exhibit fronto-temporal gradients, with particular enrichment in the frontal lobe. Finally, many neurodevelopmental disorder and human-evolution-related genes show patterned expression, potentially underlying unique features of human cortical formation. These data provide a rich, freely-accessible resource for understanding human brain development.
    Full-text · Article · Apr 2014 · Nature
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    ABSTRACT: Purpose: The purpose of this study was to examine relationships between prosodic speech cues and autism spectrum disorder (ASD) severity, hypothesizing a mutually interactive relationship between the speech characteristics of the psychologist and the child. The authors objectively quantified acoustic-prosodic cues of the psychologist and of the child with ASD during spontaneous interaction, establishing a methodology for future large-sample analysis. Method: Speech acoustic-prosodic features were semiautomatically derived from segments of semistructured interviews (Autism Diagnostic Observation Schedule, ADOS; Lord, Rutter, DiLavore, & Risi, 1999; Lord et al., 2012) with 28 children who had previously been diagnosed with ASD. Prosody was quantified in terms of intonation, volume, rate, and voice quality. Research hypotheses were tested via correlation as well as hierarchical and predictive regression between ADOS severity and prosodic cues. Results: Automatically extracted speech features demonstrated prosodic characteristics of dyadic interactions. As rated ASD severity increased, both the psychologist and the child demonstrated effects for turn-end pitch slope, and both spoke with atypical voice quality. The psychologist's acoustic cues predicted the child's symptom severity better than did the child's acoustic cues. Conclusion: The psychologist, acting as evaluator and interlocutor, was shown to adjust his or her behavior in predictable ways based on the child's social-communicative impairments. The results support future study of speech prosody of both interaction partners during spontaneous conversation, while using automatic computational methods that allow for scalable analysis on much larger corpora.
    No preview · Article · Feb 2014 · Journal of Speech Language and Hearing Research
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    Elizabeth A D Hammock · Pat Levitt
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    ABSTRACT: Oxytocin (OXT) has drawn increasing attention as a developmentally relevant neuropeptide given its role in the brain regulation of social behavior. It has been suggested that OXT plays an important role in the infant brain during caregiver attachment in nurturing familial contexts, but there is incomplete experimental evidence. Mouse models of OXT system genes have been particularly informative for the role of the OXT system in social behavior, however, the developing brain areas that could respond to ligand activation of the OXT receptor (OXTR) have yet to be identified in this species. Here we report new data revealing dynamic ligand-binding distribution of OXTR in the developing mouse brain. Using male and female C57BL/6J mice at postnatal days (P) 0, 7, 14, 21, 35, and 60 we quantified OXTR ligand binding in several brain areas which changed across development. Further, we describe OXTR ligand binding in select tissues of the near-term whole embryo at E18.5. Together, these data aid in the interpretation of findings in mouse models of the OXT system and generate new testable hypotheses for developmental roles for OXT in mammalian systems. We discuss our findings in the context of developmental disorders (including autism), attachment biology, and infant physiological regulation. Summary: Quantitative mapping of selective OXTR ligand binding during postnatal development in the mouse reveals an unexpected, transient expression in layers II/III throughout the mouse neocortex. OXTR are also identified in several tissues in the whole late embryo, including the adrenal glands, brown adipose tissue, and the oronasal cavity.
    Full-text · Article · Dec 2013 · Frontiers in Behavioral Neuroscience
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    ABSTRACT: Based on clinical experience, we hypothesized that rigid-compulsive behaviors are associated with severe constipation and co-occurring diarrhea or underwear staining in children with autism spectrum disorder. Using data from the Autism Treatment Network, we evaluated the association between these gastrointestinal symptoms and measures of rigid compulsive behavior in children ages 2-17. Following statistical correction, four of five primary measures were significantly associated with constipation and diarrhea or underwear staining, including parental report of repetitive behavior, parental report of compulsive behavior, clinician diagnosis of obsessive-compulsive disorder, and report of rituals observed on the autism diagnostic observation schedule. This association could point to a causal connection between these symptoms or to a common biological pathway that impacts both gut and brain.
    Full-text · Article · Nov 2013 · Journal of Autism and Developmental Disorders
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    ABSTRACT: MET, a replicated autism risk gene, encodes a pleiotropic receptor tyrosine kinase implicated in multiple cellular processes during development and following injury. Previous studies suggest that Met modulates excitatory synapse development in the neocortex and hippocampus, although the underlying mechanism is unknown. The peak of Met expression corresponds to the period of process outgrowth and synaptogenesis, with robust expression in hippocampal and neocortical neuropil. Resolving whether neuropil expression represents presynaptic, postsynaptic or glial localization provides insight into potential mechanisms of Met action. The subcellular distribution of Met was characterized using complementary ultrastructural, in situ proximity ligation assay (PLA) and biochemical approaches. At postnatal day (P) 7, immuno-electron microscopy revealed near-equivalent proportions of Met-immunoreactive pre- (axons and terminals) and post- (dendritic shafts and spines) synaptic profiles in the stratum radiatum in the hippocampal CA1 region. Staining was typically in elements in which the corresponding pre- or postsynaptic apposition was unlabeled. By P21, Met-immunoreactive presynaptic profiles predominated and approximately 20% of Met-expressing profiles were glial. A different distribution of Met-immunoreactive profiles was observed in layer V of somatosensory cortex: Met-labeled spines were rare and a smaller proportion of glial profiles expressed Met. Strikingly, Met-immunoreactive presynaptic profiles predominated over postsynaptic profiles as early as P7. PLA analysis of neurons in vitro and biochemical analysis of tissue subsynaptic fractions confirmed the localization of Met in specific synaptic subcompartments. The study demonstrates that Met is enriched at synapses during development and its activation may modulate synapse formation and stability through both pre- and post-synaptic mechanisms. J. Comp. Neurol. , 2013. © 2013 Wiley Periodicals, Inc.
    No preview · Article · Oct 2013 · The Journal of Comparative Neurology
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    ABSTRACT: Attachment to an abusive caregiver has wide phylogenetic representation, suggesting that animal models are useful in understanding the neural basis underlying this phenomenon and subsequent behavioral outcomes. We previously developed a rat model, in which we use classical conditioning to parallel learning processes evoked during secure attachment (odor-stroke, with stroke mimicking tactile stimulation from the caregiver) or attachment despite adversity (odor-shock, with shock mimicking maltreatment). Here we extend this model to mice. We conditioned infant mice (postnatal day (PN) 7-9 or 13-14) with presentations of peppermint odor and either stroking or shock. We used (14) C 2-deoxyglucose (2-DG) to assess olfactory bulb and amygdala metabolic changes following learning. PN7-9 mice learned to prefer an odor following either odor-stroke or shock conditioning, whereas odor-shock conditioning at PN13-14 resulted in aversion/fear learning. 2-DG data indicated enhanced bulbar activity in PN7-9 preference learning, whereas significant amygdala activity was present following aversion learning at PN13-14. Overall, the mouse results parallel behavioral and neural results in the rat model of attachment, and provide the foundation for the use of transgenic and knockout models to assess the impact of both genetic (biological vulnerabilities) and environmental factors (abusive) on attachment-related behaviors and behavioral development.
    Full-text · Article · Aug 2013 · Genes Brain and Behavior
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    ABSTRACT: Etiology is unknown in the majority of individuals with autism spectrum disorder (ASD). One strategy to investigate pathogenesis is to stratify this heterogeneous disorder based on a prominent phenotypic feature that enriches for homogeneity within population strata. Co-occurring gastrointestinal dysfunction (GID) characterizes a subset of children with ASD. Our current objective was to investigate a potential pathophysiological measure to test the hypothesis that children with both ASD and GID have a more severe metabolic dysfunction than children with ASD-only, given that the highly metabolically active brain and gastrointestinal system may additively contribute measurable impairment. Plasma levels of F2t-Isoprostanes (F2-IsoPs), a gold standard biomarker of oxidative stress, were measured in 87 children in four groups: ASD-GID, ASD-only, GID-only and Unaffected. F2-IsoP levels were elevated in all 3 clinical groups compared to the Unaffected group, with the ASD-GID group significantly elevated above the ASD-only group (mean, SD in pg/mg: ASD-GID 53.6, 24.4; ASD-only 36.5, 13.3; p = 0.007). Adjusting for age, sex, and triglyceride levels, F2-IsoP levels remained significantly different between study groups, with a moderate effect size of ηp (2) = 0.187 (p = 0.001). Elevation in peripheral oxidative stress is consistent with, and may contribute to, the more severe functional impairments in the ASD-GID group. With unique medical, metabolic, and behavioral features in children with ASD-GID, the present findings serve as a compelling rationale for both individualized approaches to clinical care and integrated studies of biomarker enrichment in ASD subgroups that may better address the complex etiology of ASD.
    Full-text · Article · Jul 2013 · PLoS ONE
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    ABSTRACT: Background Several proteins involved in epigenetic regulation cause syndromic neurodevelopmental disorders when human genes are mutated. More general involvement of epigenetic mechanisms in neurodevelopmental phenotypes is unclear. Methods In an attempt to determine whether DNA methylation differentiates clinical subgroups, profiling was performed on bisulfite converted DNA from lymphoblastoid cell lines (LCLs) in discovery (n = 20) and replication (n = 40) cohorts of females with Rett syndrome (RTT; n = 18), autism (AUT; n = 17), seizure disorder (SEZ; n = 6), and controls (CTL; n = 19) using Illumina HumanMethylation27 arrays. TAC1 CpGs were validated using a Sequenom EpiTYPER assay and expression was measured in LCLs and postmortem brain. Chromatin immunoprecipitation was performed in HEK cells. Cells were treated with valproic acid and MeCP2 binding was assessed. Results Two female-only cohorts were analyzed. DNA methylation profiling in a discovery cohort identified 40 CpGs that exhibited statistically significant differential methylation (≥15%) between clinical groups (P <0.01). Hierarchical clustering and principal components analysis suggested neurodevelopmental groups were distinct from CTL, but not from each other. In a larger and more heterogeneous replication cohort, these 40 CpG sites suggested no clear difference between clinical groups. Pooled analysis of DNA methylation across all 60 samples suggested only four differentially methylated CpG sites (P <0.0005), including TAC1. TAC1 promoter CpG hypermethylation was validated in AUT and SEZ (P <0.005). Analyzed for the first time in postmortem brain, TAC1 expression was reduced in cingulate cortex in RTT and AUT+SEZ (P = 0.003). However, no significant difference in TAC1 promoter CpG methylation was detected in RTT and AUT+SEZ brains. Additional molecular analyses revealed that MeCP2 binds directly to the TAC1 promoter and is sensitive to antiepileptic drug treatment. Conclusion These data suggest that DNA methylation is not widely altered in RTT, consistent with subtle changes in gene expression previously observed. However, TAC1 may be an important target for further functional analyses in RTT. Studies of larger sample cohorts using primary cells that also consider shared clinical features and drug treatments may be required to address apparent subtle disruptions of DNA methylation in neurodevelopmental disorders.
    Full-text · Article · Jun 2013 · Journal of Neurodevelopmental Disorders
  • Pat Levitt · A. Bonnin

    No preview · Article · May 2013 · Neurotoxicology and Teratology

Publication Stats

11k Citations
1,209.91 Total Impact Points


  • 2003-2016
    • Vanderbilt University
      • • Department of Pharmacology
      • • Vanderbilt Kennedy Center (VKC)
      Нашвилл, Michigan, United States
  • 2013-2015
    • Children's Hospital Los Angeles
      • Vision Development Institute
      Los Ángeles, California, United States
  • 2009-2015
    • University of California, Los Angeles
      Los Ángeles, California, United States
  • 2011-2013
    • University of Southern California
      • Department of Cell and Neurobiology
      Los Angeles, California, United States
    • Keck School of Medicine USC
      Los Angeles, California, United States
    • University of North Carolina at Chapel Hill
      • Department of Cell Biology and Physiology
      North Carolina, United States
  • 2010
    • Meharry Medical College
      • Department of Neuroscience and Pharmacology
      Nashville, TN, United States
  • 1993-2006
    • University of Pittsburgh
      • • Department of Psychiatry
      • • Department of Neurobiology
      Pittsburgh, Pennsylvania, United States
    • Philadelphia ZOO
      Filadelfia, Pennsylvania, United States
  • 2002
    • Federal University of Rio de Janeiro
      • Programa de Glicobiologia
      Rio de Janeiro, Rio de Janeiro, Brazil
  • 1995-1997
    • Robert Wood Johnson University Hospital
      New Brunswick, New Jersey, United States
  • 1996
    • Philadelphia University
      Philadelphia, Pennsylvania, United States