The Cell Cycle-regulated Protein Human GTSE-1 Controls DNA Damage-induced Apoptosis by Affecting p53 Function

GTSE-1 (G2 and S phase-expressed-1) protein is specifically expressed during S and G2 phases of the cell cycle. It is mainly localized to the microtubules and when overexpressed delays the G2 to M transition. Here we report that human GTSE-1 (hGTSE-1) protein can negatively regulate p53 transactivation function, protein levels, and p53-dependent apoptosis. We identified a physical interaction between the C-terminal regulatory domain of p53 and the C-terminal region of hGTSE-1 that is necessary and sufficient to down-regulate p53 activity. Furthermore, we provide evidence that hGTSE-1 is able to control p53 function in a cell cycle-dependent fashion. hGTSE-1 knock-down by small interfering RNA resulted in a S/G2-specific increase of p53 levels as well as cell sensitization to DNA damage-induced apoptosis during these phases of the cell cycle. Altogether, this work suggests a physiological role of hGTSE-1 in apoptosis control after DNA damage during S and G2 phases through regulation of p53 function. GTSE-1 (G2 and S phase-expressed-1) protein is specifically expressed during S and G2 phases of the cell cycle. It is mainly localized to the microtubules and when overexpressed delays the G2 to M transition. Here we report that human GTSE-1 (hGTSE-1) protein can negatively regulate p53 transactivation function, protein levels, and p53-dependent apoptosis. We identified a physical interaction between the C-terminal regulatory domain of p53 and the C-terminal region of hGTSE-1 that is necessary and sufficient to down-regulate p53 activity. Furthermore, we provide evidence that hGTSE-1 is able to control p53 function in a cell cycle-dependent fashion. hGTSE-1 knock-down by small interfering RNA resulted in a S/G2-specific increase of p53 levels as well as cell sensitization to DNA damage-induced apoptosis during these phases of the cell cycle. Altogether, this work suggests a physiological role of hGTSE-1 in apoptosis control after DNA damage during S and G2 phases through regulation of p53 function. Cellular response to DNA damage efficiently induces cell growth arrest or apoptosis through a complex network of regulatory pathways. A key element in the integration of these pathways is the tumor suppressor protein p53. The function of p53 as tumor suppressor is mainly ascribable to its activity as a transcription factor that specifically activates genes in response to various of DNA and cell the p53 response is genes can mainly growth the of or apoptosis The that p53 activity to the protein regulation of p53 protein control of its and as well as that of the of p53 The key of p53 is the The by negatively p53 function to the region of p53 and its p53 and through the GTSE-1 G2 and S human C-terminal small interfering in G2 and S human C-terminal small interfering in (G2 and S in during a of genes a cell that a p53 p53 induces GTSE-1 transcription by in the to p53 GTSE-1 is by DNA damage of p53 of GTSE-1 protein that is mainly localized to the microtubules evidence of of the protein in and in and in GTSE-1 protein is cell during S and G2 It in and in of GTSE-1 resulted in a of the G2 to M of p53 The cell and the to the G2 the GTSE-1 human hGTSE-1 we report that hGTSE-1 can control DNA damage-induced apoptosis by p53 and function. 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