ArticlePLoS genetics2015
The Analysis of Pendolino (peo) Mutants Reveals Differences in the Fusigenic Potential among Drosophila Telomeres.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Impact of diffused versus vasculature targeted DNA damage on the heart of mice depleted of telomeric factor Ft1.Aging cell · 2023Article
- Technologies, strategies, and cautions when deconvoluting genome-wide association signals: FTO in focus.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023Review
- Low dose rate γ-irradiation protects fruit fly chromosomes from double strand breaks and telomere fusions by reducing the esi-RNA biogenesis factor Loquacious.Communications biology · 2022Article
- AKTIP interacts with ESCRT I and is needed for the recruitment of ESCRT III subunits to the midbody.PLoS genetics · 2021Article
- Interplay of the nuclear envelope with chromatin in physiology and pathology.Nucleus (Austin, Tex.) · 2020Review
- Insights into HP1a-Chromatin Interactions.Cells · 2020Review
- The Telomere Paradox: Stable Genome Preservation with Rapidly Evolving Proteins.Trends in genetics : TIG · 2020Review
- Mice with reduced expression of the telomere-associated protein Ft1 develop p53-sensitive progeroid traits.Aging cell · 2018Article
- The Drosophila telomere-capping protein Verrocchio binds single-stranded DNA and protects telomeres from DNA damage response.Nucleic acids research · 2017Article
- Article
- Life and cancer without telomerase: ALT and other strategies for making sure ends (don't) meet.Critical reviews in biochemistry and molecular biology · 2017Review
- Recurrent Innovation at Genes Required for Telomere Integrity in Drosophila.Molecular biology and evolution · 2017Article
- The telomeric protein AKTIP interacts with A- and B-type lamins and is involved in regulation of cellular senescence.Open biology · 2016Article
- Mammalian telomeres and their partnership with lamins.Nucleus (Austin, Tex.) · 2016Review
- A role for Separase in telomere protection.Nature communications · 2016Article
- AKTIP/Ft1, a New Shelterin-Interacting Factor Required for Telomere Maintenance.PLoS genetics · 2015Article
- Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drosophila telomeres are sequence-independent structures that are maintained by transposition to chromosome ends of three specialized retroelements (HeT-A, TART and TAHRE; collectively designated as HTT) rather than telomerase activity. Fly telomeres are protected by the terminin complex (HOAP-HipHop-Moi-Ver) that localizes and functions exclusively at telomeres and by non-terminin proteins that do not serve telomere-specific functions. Although all Drosophila telomeres terminate with HTT arrays and are capped by terminin, they differ in the type of subtelomeric chromatin; the Y, XR, and 4L HTT are juxtaposed to constitutive heterochromatin, while the XL, 2L, 2R, 3L and 3R HTT are linked to the TAS repetitive sequences; the 4R HTT is associated with a chromatin that has features common to both euchromatin and heterochromatin. Here we show that mutations in pendolino (peo) cause telomeric fusions (TFs). The analysis of several peo mutant combinations showed that these TFs preferentially involve the Y, XR and 4th chromosome telomeres, a TF pattern never observed in the other 10 telomere-capping mutants so far characterized. peo encodes a non-terminin protein homologous to the E2 variant ubiquitin-conjugating enzymes. The Peo protein directly interacts with the terminin components, but peo mutations do not affect telomeric localization of HOAP, Moi, Ver and HP1a, suggesting that the peo-dependent telomere fusion phenotype is not due to loss of terminin from chromosome ends. peo mutants are also defective in DNA replication and PCNA recruitment. However, our results suggest that general defects in DNA replication are unable to induce TFs in Drosophila cells. We thus hypothesize that DNA replication in Peo-depleted cells results in specific fusigenic lesions concentrated in heterochromatin-associated telomeres. Alternatively, it is possible that Peo plays a dual function being independently required for DNA replication and telomere capping.
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