<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE168699" accession="SRP310232">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP310232</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA713547</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE168699</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Time series data of chromatin and transcription throughout the cell cycle</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>The occupancy states of DNA-binding nucleosomes and subnucleosome-sized proteins (e.g.  transcription factors, replication proteins, etc.) determine the chromatin accessibility landscape and provide additional regulatory context for DNA-templated processes including transcription and DNA replication. Throughout the mitotic cell division cycles, the transcriptome undergoes periodic reprogramming along with replication- and mitosis-induced global chromatin reconfiguration; however, profiling of the cell cycle-specific chromatin dynamics and understandings of its regulatory mechanisms remain limited. Here we employed high-resolution MNase-seq to factor-agnostically map the genome-wide chromatin occupancy with synchronized Saccharomyces cerevisiae cell populations, in parallel with transcriptome profiling by RNA-seq. Throughout the cell cycles, the occupancy of gene-body nucleosomes and promoter subnucleosomes (presumably TFs and polymerase) exhibit both transcription- dependent and independent periodicity, suggesting a decoupling between transcription and chromatin occupancy dynamics. The “phased” positioning of nucleosomes within gene bodies, however, is pervasively disorganized by replication fork progression, and also regulated by the intensity and cell cycle phase of transcriptional activation. Finally, we profiled the chromatin organization around replication origins throughout the complete cell cycle and revealed the chromatin context for origin efficiency. Overall design: Time course of yeast released from a-factor and collected every 10 min from T=0 min (prior to release) to 150 min (Replicate 1) or 140 min (Replicate 2) post release. Because the recovery time from a-factor arrest for Replicate 1 is about one time point longer than Replicate 2, T=10 min for Replicate 1 is discarded and all later time points are shifted one time point earlier when  aligning the cell cycle timeline with Replicate 2.  Two biological replicates are conducted which include 30 samples of MNase chromatin and 29 samples of RNA (T=110 min for Replicate 2 is of bad quality and discarded).</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE168699</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>34946946</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
