<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE178873" accession="SRP325546">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP325546</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA741268</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE178873</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>A stress-induced error prone 3' flap-based Okazaki fragment maturation pathway creates internal tandem duplications for cell survival (RNA-seq)</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Faithful and efficient Okazaki fragment maturation is the key to maintain the genome integrity. In addition, this process is coupled with deposition of histone proteins. Therefore, functional deficiency in Okazaki fragment maturation may cause genome instablities as well and epigenetic alterations. We conduct WGS of WT and rad27 knockout yeast strains to define the DNA mutations caused by defective Okazaki fragment muturaton and conduct RNA-seq to define the changes in gene expression profiling due to defetive Okazaki fragment muturations.. Overall design: We conduct WGS of WT and rad27 knockout yeast strains (n=1 for each sample) to define the genome-wide DNA mutation frequence and spectrum caused by defective Okazaki fragment muturaton. We conduct RNA-seq (n = 2 for each sample) to define the changes in gene expression profiling due to defetive Okazaki fragment muturations..</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE178873</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>34855483</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
    <STUDY_ATTRIBUTES>
      <STUDY_ATTRIBUTE>
        <TAG>parent_bioproject</TAG>
        <VALUE>PRJNA741273</VALUE>
      </STUDY_ATTRIBUTE>
    </STUDY_ATTRIBUTES>
  </STUDY>
</STUDY_SET>
