scholarly journals Drosophila telomere capping protein HOAP interacts with DSB sensor proteins Mre11 and Nbs

2021 ◽  
Author(s):  
Kinyo On ◽  
Gilles Crevel ◽  
Sue Cotterill ◽  
Masanobu Itoh ◽  
Yasuko Kato
Keyword(s):  
Capping Protein ◽  
Telomere Capping ◽  
Sensor Proteins

scholarly journals The Drosophila telomere-capping protein Verrocchio binds single-stranded DNA and protects telomeres from DNA damage response

2016 ◽  
Vol 45 (6) ◽  
pp. 3068-3085 ◽  
Author(s):  
Alessandro Cicconi ◽  
Emanuela Micheli ◽  
Fiammetta Vernì ◽  
Alison Jackson ◽  
Ana Citlali Gradilla ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Single Stranded Dna ◽  
Capping Protein ◽  
Damage Response ◽  
Telomere Capping

scholarly journals Genome-wide Control of Heterochromatin Replication by the Telomere Capping Protein TRF2

2018 ◽  
Vol 70 (3) ◽  
pp. 449-461.e5 ◽  
Author(s):  
Aaron Mendez-Bermudez ◽  
Liudmyla Lototska ◽  
Serge Bauwens ◽  
Marie-Josèphe Giraud-Panis ◽  
Olivier Croce ◽  
...  
Keyword(s):  
Capping Protein ◽  
Genome Wide ◽  
Telomere Capping

scholarly journals Yeast telomere capping protein Stn1 overrides DNA replication control through the S phase checkpoint

2009 ◽  
Vol 106 (7) ◽  
pp. 2206-2211 ◽  
Author(s):  
H. J. Gasparyan ◽  
L. Xu ◽  
R. C. Petreaca ◽  
A. E. Rex ◽  
V. Y. Small ◽  
...  
Keyword(s):  
Dna Replication ◽  
S Phase ◽  
Capping Protein ◽  
Replication Control ◽  
Telomere Capping ◽  
Yeast Telomere ◽  
S Phase Checkpoint

scholarly journals “Mitotic Slippage” and Extranuclear DNA in Cancer Chemoresistance: A Focus on Telomeres

2020 ◽  
Vol 21 (8) ◽  
pp. 2779 ◽  
Author(s):  
Kristine Salmina ◽  
Agnieszka Bojko ◽  
Inna Inashkina ◽  
Karolina Staniak ◽  
Magdalena Dudkowska ◽  
...  
Keyword(s):  
Giant Cells ◽  
Telomere Maintenance ◽  
Holocentric Chromosomes ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Capping Protein ◽  
Mitotic Slippage ◽  
Alternative Lengthening ◽  
Telomere Capping ◽  
Cancer Chemoresistance

Mitotic slippage (MS), the incomplete mitosis that results in a doubled genome in interphase, is a typical response of TP53-mutant tumors resistant to genotoxic therapy. These polyploidized cells display premature senescence and sort the damaged DNA into the cytoplasm. In this study, we explored MS in the MDA-MB-231 cell line treated with doxorubicin (DOX). We found selective release into the cytoplasm of telomere fragments enriched in telomerase reverse transcriptase (hTERT), telomere capping protein TRF2, and DNA double-strand breaks marked by γH2AX, in association with ubiquitin-binding protein SQSTM1/p62. This occurs along with the alternative lengthening of telomeres (ALT) and DNA repair by homologous recombination (HR) in the nuclear promyelocytic leukemia (PML) bodies. The cells in repeated MS cycles activate meiotic genes and display holocentric chromosomes characteristic for inverted meiosis (IM). These giant cells acquire an amoeboid phenotype and finally bud the depolyploidized progeny, restarting the mitotic cycling. We suggest the reversible conversion of the telomerase-driven telomere maintenance into ALT coupled with IM at the sub-telomere breakage sites introduced by meiotic nuclease SPO11. All three MS mechanisms converging at telomeres recapitulate the amoeba-like agamic life-cycle, decreasing the mutagenic load and enabling the recovery of recombined, reduced progeny for return into the mitotic cycle.

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