The cohesin acetyltransferase Eco1 coordinates rDNA replication and transcription
Eco1 is the acetyltransferase that establishes sister‐chromatid cohesion during DNA replication. A budding yeast strain with an eco1 mutation that genocopies Roberts syndrome has reduced ribosomal DNA (rDNA) transcription and a transcriptional signature of starvation. We show that deleting FOB1—a ge...
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Veröffentlicht in: | EMBO reports 2014-05, Vol.15 (5), p.609-617 |
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Sprache: | eng |
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Zusammenfassung: | Eco1 is the acetyltransferase that establishes sister‐chromatid cohesion during DNA replication. A budding yeast strain with an eco1 mutation that genocopies Roberts syndrome has reduced ribosomal DNA (rDNA) transcription and a transcriptional signature of starvation. We show that deleting FOB1—a gene that encodes a replication fork‐blocking protein specific for the rDNA region—rescues rRNA production and partially rescues transcription genome‐wide. Further studies show that deletion of FOB1 corrects the genome‐wide replication defects, nucleolar structure, and rDNA segregation that occur in the eco1 mutant. Our study highlights that the presence of cohesin at the rDNA locus has a central role in controlling global DNA replication and gene expression.
Synopsis
Cohesin affects gene expression and DNA replication genome‐wide through the control of processes at the rDNA region in budding yeast. Replication defects at the rDNA in a cohesin acetyltransferase mutant lead to global defects that could contribute to human disease.
A cohesin acetyltransferase mutant in budding yeast has global defects in gene expression and DNA replication.
Recovery of DNA replication at the ribosomal DNA (fob1Δ) rescues local and global defects in replication and transcription.
Global defects in gene expression and DNA replication in Roberts syndrome could stem in part from the ribosomal DNA.
Graphical Abstract
Cohesin affects gene expression and DNA replication genome‐wide by controlling processes at the rDNA region. Replication defects at the rDNA in a cohesin acetyltransferase mutant lead to global defects that could contribute to human disease. |
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ISSN: | 1469-221X 1469-3178 |
DOI: | 10.1002/embr.201337974 |