NDLI: A Role for Human DNA Polymerase λ in Alternative Lengthening of Telomeres

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A Role for Human DNA Polymerase λ in Alternative Lengthening of Telomeres

Content Provider	MDPI
Author	Ulrich, Hübscher Mentegari, Elisa Bertoletti, Federica Kissova, Miroslava Zucca, Elisa Galli, Silvia Tagliavini, Giulia Garbelli, Anna Maffia, Antonio Bione, Silvia Ferrari, Elena Fagagna, Fabrizio D’Adda di Francia, Sofia Sabbioneda, Simone Chen, Liuh-Yow Lingner, Joachim Bergoglio, Valerie Hoffmann, Jean-Sébastien Crespan, Emmanuele Maga, Giovanni
Copyright Year	2021
Description	Telomerase negative cancer cell types use the Alternative Lengthening of Telomeres (ALT) pathway to elongate telomeres ends. Here, we show that silencing human DNA polymerase (Pol λ) in ALT cells represses ALT activity and induces telomeric stress. In addition, replication stress in the absence of Pol λ, strongly affects the survival of ALT cells. In vitro, Pol λ can promote annealing of even a single G-rich telomeric repeat to its complementary strand and use it to prime DNA synthesis. The noncoding telomeric repeat containing RNA TERRA and replication protein A negatively regulate this activity, while the Protection of Telomeres protein 1 (POT1)/TPP1 heterodimer stimulates Pol λ. Pol λ associates with telomeres and colocalizes with TPP1 in cells. In summary, our data suggest a role of Pol λ in the maintenance of telomeres by the ALT mechanism.
Starting Page	2365
e-ISSN	14220067
DOI	10.3390/ijms22052365
Journal	International Journal of Molecular Sciences
Issue Number	5
Volume Number	22
Language	English
Publisher	MDPI
Publisher Date	2021-02-27
Access Restriction	Open
Subject Keyword	International Journal of Molecular Sciences Cell Biology Alternative Lengthening of Telomeres (alt) Dna Polymerase Λ Dna Double-strand Breaks (dsbs) Extra-chromosomal Telomeric Repeats (ectrs) Promyelocytic Leukemia (pml) Bodies Telomere Dysfunction-induced Foci (tifs) Telomere Stress Microhomology-mediated Strand Transfer (mmst) Activity
Content Type	Text
Resource Type	Article

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