<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE125703" accession="SRP182143">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP182143</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA517274</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE125703</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Inducible histone K-to-M mutations are dynamic tools to probe the physiological role of site-specific histone methylation in vitro and in vivo</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>Here, we developed mouse models expressing inducible lysine to methionine mutants of histone H3, which function as dominant negative inhibitors of methylation at their respective sites. Upon induction of H3K9M or H3K36M, we observed potent differentiation defects in stem cells and regenerative tissues. This work covers ChIP-seq in this model system for H3K9me3, H3K36me3, and H3K27me3. Overall design: Examination of H3K9me3 in hemaotpoietic stem and progenitor cells expressing H3K9M.Examination of H3K27me3 and H3K36me3 in hemaotpoietic stem and progenitor cells expressing H3K36M.H3K9M.Examination of H3K9me3, H3K27me3, and H3K36me3 in hemaotpoietic stem and progenitor cells expressing WT H3.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE125703</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>31659274</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
