The mre11 A470 alleles influence the hereditability and the segregation of telosomes in Saccharomyces cerevisiae (original with corrected raw data)

TL;DR

This study investigates how MRE11 A470 alleles affect telomere structure, heritability, and segregation in yeast, revealing a potential active chromatin segregation mechanism linked to sister chromatid replication.

Contribution

It demonstrates the influence of MRE11 A470 alleles on telosome composition, heritability, and segregation, suggesting a conservative segregation mechanism in yeast telomeres.

Findings

MRE11 A470 alleles alter telosome resistance to MNase.

Telomere size is approximately 300 base pairs with G+T repeats.

Telosomes segregate with a conservative mechanism, maintaining allele-specific composition.

Abstract

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.