SETDB1-dependent heterochromatin stimulates alternative lengthening of telomeres

• Published in: Science advances Vol. 5; no. 5; p. eaav3673
• Main Authors: Gauchier, Mathilde, Kan, Sophie, Barral, Amandine, Sauzet, Sandrine, Agirre, Eneritz, Bonnell, Erin, Saksouk, Nehmé, Barth, Teresa K., Ide, Satoru, Urbach, Serge, Wellinger, Raymund J., Luco, Reini F., Imhof, Axel, Déjardin, Jérôme
• Format: Journal Article
• Language: English
• Published: United States American Association for the Advancement of Science (AAAS) 01.05.2019; American Association for the Advancement of Science
• Subjects: Animals; Biochemistry, Molecular Biology; Cancer; Cell Line, Tumor; Heterochromatin - metabolism; Histone Chaperones - metabolism; Histone-Lysine N-Methyltransferase - antagonists & inhibitors; Histone-Lysine N-Methyltransferase - deficiency; Histone-Lysine N-Methyltransferase - genetics; Histone-Lysine N-Methyltransferase - metabolism; Humans; Life Sciences; Methyltransferases - deficiency; Methyltransferases - genetics; Mice; Mice, Inbred C57BL; Molecular biology; Mouse Embryonic Stem Cells - cytology; Mouse Embryonic Stem Cells - metabolism; Repressor Proteins - deficiency; Repressor Proteins - genetics; RNA Interference; RNA, Small Interfering - metabolism; SciAdv r-articles; Telomere - metabolism; Telomere Shortening; Telomeric Repeat Binding Protein 2 - metabolism; X-linked Nuclear Protein - metabolism
• ISSN: 2375-2548; 2375-2548
• DOI: 10.1126/sciadv.aav3673

Atypical heterochromatin forms on telomeres and correlates with ALT activities. 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 hetero...