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 , Herve Chneiweiss (1) , Sylvie Chevillard , Chantal Desmaze , Francois D. Boussin

1 NPS-04 - Plasticité gliale et neuro-oncologie = Glial Plasticity

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.

Mots clés: PCAF; GCN5; telomere recombination; ALT

Domaines: Neurosciences [q-bio.NC]

Maya Jeitany, Dalal Bakhos-Douaihy, David C. Silvestre, Jose R. Pineda, Nicolas Ugolin, et al.. Opposite effects of GCN5 and PCAF knockdowns on the alternative mechanism of telomere maintenance. Oncotarget, 2017, 8 (16), pp.26269-26280. ⟨10.18632/oncotarget.15447⟩. ⟨hal-01541412⟩