Journal
MICROBIAL CELL
Volume 5, Issue 4, Pages 169-183Publisher
SHARED SCIENCE PUBLISHERS OG
DOI: 10.15698/mic2018.04.623
Keywords
imprint; mating type switching; epigenetics; replication; Lsd1; Lsd2; Sap1
Categories
Funding
- Fondation ARC for Cancer Research
- Fondation pour la Recherche Medicale (FRM)
- Pasteur Institute
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Genetic and molecular studies have indicated that an epigenetic imprint at mat1, the sexual locus of fission yeast, initiates mating type switching. The polar DNA replication of mat1 generates an imprint on the Watson strand. The process by which the imprint is formed and maintained through the cell cycle remains unclear. To understand better the mechanism of imprint formation and stability, we characterized the recruitment of early players of mating type switching at the mat1 region. We found that the switch activating protein 1 (Sap1) is preferentially recruited inside the mat1M allele on a sequence (SS13) that enhances the imprint. The lysine specific demethylases, Lsd1/2, that control the replication fork pause at MPS1 and the formation of the imprint are specifically drafted inside of mat1, regardless of the allele. The CENP-B homolog, Abp1, is highly enriched next to mat1 but it is not required in the process. Additionally, we established the computational signature of the imprint. Using this signature, we show that both sides of the imprinted molecule are bound by Lsd1/2 and Sap1, suggesting a nucleoprotein protective structure defined as imprintosome.
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