The mre11 A470 alleles influence the hereditability and the segregation of telosomes in Saccharomyces cerevisiae

Telomeres, the nucleoprotein complexes at the termini of linear chromosomes, are essential for the processes of end replication, end protection, and chromatin segregation. The Mre11 complex is involved in multiple cellular roles in DNA repair and structure in the regulation and function of telomere...

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Autores principales: Baek, In-Joon, Moss, Daniel S., Lustig, Arthur J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5590830/
https://www.ncbi.nlm.nih.gov/pubmed/28886051
http://dx.doi.org/10.1371/journal.pone.0183549
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author Baek, In-Joon
Moss, Daniel S.
Lustig, Arthur J.
author_facet Baek, In-Joon
Moss, Daniel S.
Lustig, Arthur J.
author_sort Baek, In-Joon
collection PubMed
description Telomeres, the nucleoprotein complexes at the termini of linear chromosomes, are essential for the processes of end replication, end protection, and chromatin segregation. The Mre11 complex is involved in multiple cellular roles in DNA repair and structure in the regulation and function of telomere size homeostasis. In this study, we characterize yeast telomere chromatin structure, phenotypic heritability, and chromatin segregation in both wild-type [MRE11] and A470 motif alleles. MRE11 strains confer a telomere size of 300 base pairs of G+T irregular simple sequence repeats. This DNA and a portion of subtelomeric DNA is embedded in a telosome: a MNase-resistant non-nucleosomal particle. Chromatin immunoprecipitation shows a three to four-fold lower occupancy of Mre11A470T proteins than wild-type proteins in telosomes. Telosomes containing the Mre11A470T protein confer a greater resistance to MNase digestion than wild-type telosomes. The integration of a wild-type MRE11 allele into an ectopic locus in the genome of an mre11A470T mutant and the introduction of an mre11A470T allele at an ectopic site in a wild-type strain lead to unexpectedly differing results. In each case, the replicated sister chromatids inherit telosomes containing only the protein encoded by the genomic mre11 locus, even in the presence of protein encoded by the opposing ectopic allele. We hypothesize that the telosome segregates by a conservative mechanism. These data support a mechanism for the linkage between sister chromatid replication and maintenance of either identical mutant or identical wild-type telosomes after replication of sister chromatids. These data suggest the presence of an active mechanism for chromatin segregation in yeast.
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spelling pubmed-55908302017-09-15 The mre11 A470 alleles influence the hereditability and the segregation of telosomes in Saccharomyces cerevisiae Baek, In-Joon Moss, Daniel S. Lustig, Arthur J. PLoS One Research Article Telomeres, the nucleoprotein complexes at the termini of linear chromosomes, are essential for the processes of end replication, end protection, and chromatin segregation. The Mre11 complex is involved in multiple cellular roles in DNA repair and structure in the regulation and function of telomere size homeostasis. In this study, we characterize yeast telomere chromatin structure, phenotypic heritability, and chromatin segregation in both wild-type [MRE11] and A470 motif alleles. MRE11 strains confer a telomere size of 300 base pairs of G+T irregular simple sequence repeats. This DNA and a portion of subtelomeric DNA is embedded in a telosome: a MNase-resistant non-nucleosomal particle. Chromatin immunoprecipitation shows a three to four-fold lower occupancy of Mre11A470T proteins than wild-type proteins in telosomes. Telosomes containing the Mre11A470T protein confer a greater resistance to MNase digestion than wild-type telosomes. The integration of a wild-type MRE11 allele into an ectopic locus in the genome of an mre11A470T mutant and the introduction of an mre11A470T allele at an ectopic site in a wild-type strain lead to unexpectedly differing results. In each case, the replicated sister chromatids inherit telosomes containing only the protein encoded by the genomic mre11 locus, even in the presence of protein encoded by the opposing ectopic allele. We hypothesize that the telosome segregates by a conservative mechanism. These data support a mechanism for the linkage between sister chromatid replication and maintenance of either identical mutant or identical wild-type telosomes after replication of sister chromatids. These data suggest the presence of an active mechanism for chromatin segregation in yeast. Public Library of Science 2017-09-08 /pmc/articles/PMC5590830/ /pubmed/28886051 http://dx.doi.org/10.1371/journal.pone.0183549 Text en © 2017 Baek et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Baek, In-Joon
Moss, Daniel S.
Lustig, Arthur J.
The mre11 A470 alleles influence the hereditability and the segregation of telosomes in Saccharomyces cerevisiae
title The mre11 A470 alleles influence the hereditability and the segregation of telosomes in Saccharomyces cerevisiae
title_full The mre11 A470 alleles influence the hereditability and the segregation of telosomes in Saccharomyces cerevisiae
title_fullStr The mre11 A470 alleles influence the hereditability and the segregation of telosomes in Saccharomyces cerevisiae
title_full_unstemmed The mre11 A470 alleles influence the hereditability and the segregation of telosomes in Saccharomyces cerevisiae
title_short The mre11 A470 alleles influence the hereditability and the segregation of telosomes in Saccharomyces cerevisiae
title_sort mre11 a470 alleles influence the hereditability and the segregation of telosomes in saccharomyces cerevisiae
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5590830/
https://www.ncbi.nlm.nih.gov/pubmed/28886051
http://dx.doi.org/10.1371/journal.pone.0183549
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