<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE99674" accession="SRP108608">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP108608</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA389283</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE99674</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Transcriptome analysis of whole hippocampus from wild-type and TET1-deficient mice after electroconvulsive shock</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>We examined the effect of TET1 deletion on activity-dependent gene regulation by comparing RNA-seq expression profiles from the hippocampus of ECS-treated Tet1?e4-/- and Tet1+/+ mice. We discovered that 34 genes were significantly upregulated and 184 genes were downregulated, suggesting a primary role for TET1 in activating gene expression. In order to test the hypothesis that TET1 is responsible for regulating activity-dependent genes, we cataloged a dataset of activity-dependent genes based on a literature review. While there was not significant enrichment for activity-dependent genes disrupted in Tet1-deficient mice, dysregulation of several activity-dependent genes were identified including the master memory gene regulator, Npas4. Gene Ontology analyses of the dysregulated genes detected a significant enrichment for genes involved in the extracellular region/matrix/space. Interestingly, RNA-seq revealed downregulation of Oxtr, the receptor which binds oxytocin. Overall design: RNA-sequencing of whole hippocampus from 3 Tet1?e4-/- and 3 Tet1+/+ mice 1.5-2 hours after electroconvulsive shock</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE99674</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>30518695</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
