Opposite effects of GCN5 and PCAF knockdowns on the alternative mechanism of telomere maintenance
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Maya Jeitany1,2,3,4,*, Dalal Bakhos-Douaihy1,2,3,4,*, David C. Silvestre1,2,3,4, Jose R. Pineda1,2,3,4, Nicolas Ugolin5, Angela Moussa1,2,3,4, Laurent R. Gauthier1,2,3,4, Didier Busso2,6, Marie-Pierre Junier7,8,9,*, Hervé Chneiweiss7,8,9,*, Sylvie Chevillard5, Chantal Desmaze1,2,3,4, François D. Boussin1,2,3,4
1Laboratoire de Radiopathologie, CEA, Institut de Radiobiologie Cellulaire et Moléculaire, Fontenay-aux-Roses, France
2INSERM UMR967, Fontenay-aux-Roses, France
3Université Paris VII, UMR967, Fontenay-aux-Roses, France
4Université Paris XI, UMR967, Fontenay-aux-Roses, France
5Laboratoire de Cancérologie Expérimentale, iRCM, DSV, CEA, Fontenay-aux-Roses, France
6CIGEx, IRCM, Fontenay-aux-Roses, France
7CNRS UMR8246 Neuroscience Paris Seine-IBPS, Team Glial Plasticity, Paris, France
8Inserm U1130, Neuroscience Paris Seine-IBPS, Team Glial Plasticity, Paris, France
9University Pierre and Marie Curie UMCR18, Neuroscience Paris Seine-IBPS, Team Glial Plasticity, Paris, France
*These authors contributed equally to this work
François D. Boussin, email: email@example.com
Maya Jeitany, email: firstname.lastname@example.org
Keywords: PCAF, GCN5, telomere recombination, ALT
Received: June 07, 2016 Accepted: February 06, 2017 Published: February 17, 2017
Cancer cells can use a telomerase-independent mechanism, known as alternative lengthening of telomeres (ALT), to elongate their telomeres. General control non-derepressible 5 (GCN5) and P300/CBP-associated factor (PCAF) are two homologous acetyltransferases that are mutually exclusive subunits in SAGA-like complexes. Here, we reveal that down regulation of GCN5 and PCAF had differential effects on some phenotypic characteristics of ALT cells. Our results suggest that GCN5 is present at telomeres and opposes telomere recombination, in contrast to PCAF that may indirectly favour them in ALT cells.
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