Molecular signature of the imprintosome complex at the mating-type locus in fission yeast
Authors:Célia Raimondi1, Bernd Jagla2, Caroline Proux3, Hervé Waxin4, Serge Gangloff1, Benoit Arcangioli1
doi: 10.15698/mic2018.04.623
Volume 5, pp. 169 to 183, published 16/01/2018.
1 Genomes and Genetics department, Genome Dynamics Unit, UMR 3525 CNRS, Institut Pasteur, 25-28 rue du docteur Roux, Paris, France. Sorbonne Universités, Université Pierre et Marie Curie, Institut de Formation Doctorale, 75252 Paris Cedex 05, France.
2 Center for Human Immunology, CRT & Hub de Bioinformatique et Biostatistiques, C3BI, Institut Pasteur, 25-28 rue du Docteur Roux, Paris, France.
3 Genomes and Genetics department, Plate-forme Transcriptome & Epigenome, Biomics, Centre d’Innovation et Recherche Technologique (Citech), Institut Pasteur, 25-28 rue du Docteur Roux, Paris, France.
4 Enseignement, Institut Pasteur, 25-28 rue du Docteur Roux, Paris, France.
Keywords:
imprint, mating type switching, epigenetics, replication, Lsd1, Lsd2, Sap1
Corresponding Author(s):
Conflict of interest statement:
The authors declare that no competing interests exist.
Please cite this article as:
Célia Raimondi, Bernd Jagla, Caroline Proux, Hervé Waxin, Serge Gangloff, Benoit Arcangioli (2018). Molecular signature of the imprintosome complex at the mating-type locus in fission yeast. Microbial Cell 5(4): 169-183. doi: 10.15698/mic2018.04.623
© 2018 Raimondi et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
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.