Opposite effects of GCN5 and PCAF knockdowns on the alternative mechanism of telomere maintenance

Maya Jeitany; Dalal Bakhos-Douaihy; David C. Silvestre; Jose R. Pineda; Nicolas Ugolin; Angela Moussa; Laurent R. Gauthier; Didier Busso; Marie-Pierre Junier; Hervé Chneiweiss; Sylvie Chevillard; Chantal Desmaze; François D. Boussin

doi:10.18632/oncotarget.15447

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Research Papers:

Opposite effects of GCN5 and PCAF knockdowns on the alternative mechanism of telomere maintenance

Maya Jeitany, Dalal Bakhos-Douaihy, David C. Silvestre, Jose R. Pineda, Nicolas Ugolin, Angela Moussa, Laurent R. Gauthier, Didier Busso, Marie-Pierre Junier, Hervé Chneiweiss, Sylvie Chevillard, Chantal Desmaze and François D. Boussin _

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Oncotarget. 2017; 8:26269-26280. https://doi.org/10.18632/oncotarget.15447

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Abstract

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

Correspondence to:

François D. Boussin, email: [email protected]

Maya Jeitany, email: [email protected]

Keywords: PCAF, GCN5, telomere recombination, ALT

Received: June 07, 2016 Accepted: February 06, 2017 Published: February 17, 2017

ABSTRACT

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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Research Papers:

Opposite effects of GCN5 and PCAF knockdowns on the alternative mechanism of telomere maintenance

Abstract