ArticleMolecular biology of the cell2015
Ccq1-Tpz1TPP1 interaction facilitates telomerase and SHREC association with telomeres in fission yeast.
Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Fission yeast RPA-TERT-Tpz1TPP1 complex promotes telomere extension and suppresses telomere recombination.PLoS genetics · 2026Article
- Fission yeast RPA-TERT-Tpz1bioRxiv : the preprint server for biology · 2026Article
- Ccq1 restrains Mre11-mediated degradation to distinguish short telomeres from double-strand breaks.Nucleic acids research · 2024Article
- Structural insights into Pot1-ssDNA, Pot1-Tpz1 and Tpz1-Ccq1 Interactions within fission yeast shelterin complex.PLoS genetics · 2022Article
- Ccq1-Raf2 interaction mediates CLRC recruitment to establish heterochromatin at telomeres.Life science alliance · 2021Article
- Subtelomeric Chromatin in the Fission YeastMicroorganisms · 2021Review
- TASks for subtelomeres: when nucleosome loss and genome instability are favored.Current genetics · 2019Review
- Tpz1Communications biology · 2019Article
- Shelterin and subtelomeric DNA sequences control nucleosome maintenance and genome stability.EMBO reports · 2019Article
- LARP7-like protein Pof8 regulates telomerase assembly and poly(A)+TERRA expression in fission yeast.Nature communications · 2018Article
- Fission yeast Ccq1 is a modulator of telomerase activity.Nucleic acids research · 2018Article
- CTC1-mediated C-strand fill-in is an essential step in telomere length maintenance.Nucleic acids research · 2017Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Evolutionarily conserved shelterin complex is essential for telomere maintenance in the fission yeast Schizosaccharomyces pombe. Elimination of the fission yeast shelterin subunit Ccq1 causes progressive loss of telomeres due to the inability to recruit telomerase, activates the DNA damage checkpoint, and loses heterochromatin at telomere/subtelomere regions due to reduced recruitment of the heterochromatin regulator complex Snf2/histone deacetylase-containing repressor complex (SHREC). The shelterin subunit Tpz1(TPP1) directly interacts with Ccq1 through conserved C-terminal residues in Tpz1(TPP1), and tpz1 mutants that fail to interact with Ccq1 show telomere shortening, checkpoint activation, and loss of heterochromatin. While we have previously concluded that Ccq1-Tpz1(TPP1) interaction contributes to Ccq1 accumulation and telomerase recruitment based on analysis of tpz1 mutants that fail to interact with Ccq1, another study reported that loss of Ccq1-Tpz1(TPP1) interaction does not affect accumulation of Ccq1 or telomerase. Furthermore, it remained unclear whether loss of Ccq1-Tpz1(TPP1) interaction affects SHREC accumulation at telomeres. To resolve these issues, we identified and characterized a series of ccq1 mutations that disrupt Ccq1-Tpz1(TPP1) interaction. Characterization of these ccq1 mutants established that Ccq1-Tpz1(TPP1) interaction contributes to optimal binding of the Ccq1-SHREC complex, and is critical for Rad3(ATR)/Tel1(ATM)-dependent Ccq1 Thr93 phosphorylation and telomerase recruitment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.