<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE141068" accession="SRP233367">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP233367</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA591917</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE141068</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Repression of damaged and intact rDNA by the SUMO pathway</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Ribosomal RNAs (rRNAs) are essential components of the ribosome and are among the  most abundant macromolecules in the cell. To ensure high rRNA level, eukaryotic  genomes contain dozens to hundreds of rDNA genes, however, only a fraction of the rRNA  genes seems to be active, while others are transcriptionally silent. In Drosophila rDNA  units damaged by insertions of retrotransposons are repressed by an unknown  mechanism. Here, we established a new model to study regulation of rDNA expression  using molecularly marked rDNA transgenes. Using this model, we show that insertion of  any heterologous sequence into rDNA leads to transcriptional repression. We found that  SUMO (Small Ubiquitin-like Modifier) is required for efficient repression of damaged rDNA  units. Surprisingly, SUMO also controls expression of intact rDNA, demonstrating that a  single pathway is responsible for both selective repression of damaged units and silencing  of surplus rDNA. Overall design: Transposons profiling by high throughput sequencing</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE141068</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>33164748</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
