ABSTRACT
We report the identification and characterization of transcriptional silencing at native telomeres in the budding yeast Kluyveromyces lactis. We show that K. lactis telomeres are able to repress the transcription of a gene located at the junction between the telomeric repeat tract and the subtelomeric domain. As in Saccharomyces cerevisiae, switching between the repressed and derepressed transcriptional states occurs. C-terminal truncation of the telomere binding protein Rap1p, which leads to a regulated alteration in telomere length, reduces telomeric silencing. In addition, telomeric silencing is reduced dramatically in telomerase RNA mutants in which telomere length control has been lost. This is consistent with the possibility that the structure of the entire telomere affects the silencing functions exhibited by its internal domain.
Subject(s)
Gene Silencing , Kluyveromyces/genetics , Mutation , Telomere/genetics , Base Sequence , DNA, Fungal/genetics , Fungal Proteins/genetics , Genes, Fungal , Saccharomyces cerevisiae/genetics , Saccharomyces cerevisiae Proteins/genetics , Shelterin Complex , Telomere-Binding Proteins/genetics , Transcription Factors/geneticsABSTRACT
Telomeres, the natural ends of eukaryotic chromosomes, are essential for the protection of chromosomes from end-to-end fusions, recombination, and shortening. Here we explore their role in the process of meiotic division in the budding yeast, Kluyveromyces lactis. Telomerase RNA mutants that cause unusually long telomeres with deregulated structure led to severely defective meiosis. The severity of the meiotic phenotype of two mutants correlated with the degree of loss of binding of the telomere binding protein Rap1p. We show that telomere size and the extent of potential Rap1p binding to the entire telomere are irrelevant to the process of meiosis. Moreover, we demonstrate that extreme difference in telomere size between two homologous chromosomes is compatible with the normal function of telomeres during meiosis. In contrast, the structure of the most terminal telomeric repeats is critical for normal meiosis. Our results demonstrate that telomeres play a critical role during meiotic division and that their terminal cap structure is essential for this role.
