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SETDB1-dependent heterochromatin stimulates alternative lengthening of telomeres.


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SETDB1-dependent heterochromatin stimulates alternative lengthening of telomeres.
Sci Adv. 2019 May 8;5(5):eaav3673.
Mathilde Gauchier, Sophie Kan, Amandine Barral, Sandrine Sauzet, Eneritz Agirre, Erin Bonnell, Nehmé Saksouk, Teresa K Barth, Satoru Ide, Serge Urbach, Raymund J Wellinger, Reini F Luco, Axel Imhof, Jérôme Déjardin
DOI: 10.1126/sciadv.aav3673
PubMed publication date (edat): 5/16/2019

Abstract

Alternative lengthening of telomeres, or ALT, is a recombination-based process that maintains telomeres to render some cancer cells immortal. The prevailing view is that ALT is inhibited by heterochromatin because heterochromatin prevents recombination. To test this model, we used telomere-specific quantitative proteomics on cells with heterochromatin deficiencies. In contrast to expectations, we found that ALT does not result from a lack of heterochromatin; rather, ALT is a consequence of heterochromatin formation at telomeres, which is seeded by the histone methyltransferase SETDB1. Heterochromatin stimulates transcriptional elongation at telomeres together with the recruitment of recombination factors, while disrupting heterochromatin had the opposite effect. Consistently, loss of SETDB1, disrupts telomeric heterochromatin and abrogates ALT. Thus, inhibiting telomeric heterochromatin formation in ALT cells might offer a new therapeutic approach to cancer treatment.

PMID: 31086817
Free Full-Text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6506250/

Maximus Peto

Max Peto is a longevity researcher and founder of Long Life Labs. A biochemist by training, he studies the biochemistry of aging and longevity and has worked with research organizations such as SENS Research Foundation, Methuselah Foundation, BioAge Labs, Life Extension Foundation, and Ichor Therapeutics. His work at Long Life Labs is focused on empowering people to understand and manage the most critical factors for better health and longer life.

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