FEBS Letters
FEBS Letters
5 years ago

The Gpn3 Q279* cancer-associated mutant inhibits Gpn1 nuclear export and is deficient in RNA polymerase II nuclear targeting

Sonia G. Peña-Gómez, Bárbara Lara Chacón, Roberto Sánchez-Olea, Violeta Romero, Lucía E. Méndez-Hernández, Angel A. Barbosa-Camacho, Rogelio González-González, Mónica R. Calera, Angélica Y. Robledo-Rivera, José A. Guerra-Moreno
Gpn3 is required for RNA polymerase II (RNAPII) nuclear targeting. Here, we investigated the effect of a cancer-associated Q279* nonsense mutation in Gpn3 cellular function. Employing RNAi, we replaced endogenous Gpn3 by wt or Q279* RNAi-resistant Gpn3R in epithelial model cells. RNAPII nuclear accumulation and transcriptional activity are markedly decreased in cells expressing only Gpn3R Q279*. Wild-type Gpn3R localizes to the cytoplasm but a fraction of Gpn3R Q279* enters the cell nucleus and inhibits Gpn1-EYFP nuclear export. This property and the transcriptional deficit in Gpn3R Q279*-expressing cells requires a PDZ-binding motif generated by the Q279* mutation. We conclude that this PDZ-binding motif resulting from the Q279* mutation causes Gpn3 nuclear entry, inhibits Gpn1 nuclear export and Gpn3-mediated RNAPII nuclear targeting. This article is protected by copyright. All rights reserved.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1002/1873-3468.12856

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