Function of the interaction between RAD2, a yeast homolog of human XPG, and TEF2, a translational elongation factor

초록

Mutations in the human XPG gene cause Cockayne syndrome (CS) and xeroderma pigmentosum (XP). Transcription defects have been suggested as the fundamental cause of CS; however, defining CS as a transcription syndrome is inconclusive. Previously, we provided evidence for the involvement of RAD2, the Saccharomyces cerevisiae counterpart of XPG, in cell cycle regulation and efficient actin assembly following ultraviolet irradiation. RAD2 C-terminal deletion, which resembles the XPG mutation found in XPG/CS cells, caused cell growth arrest, the cell cycle stalling, a defective α-factor response, shortened lifespan, cell polarity defect, and misregulated actin-dynamics after DNA damage. Recently, we performed pull-down binding assay using Rad2p and rad2C?p as the bates, and found that Tfe2p protein interacts with Rad2p C-terminal region. In order to study the role of Rad2p-Tef2p interaction, we generated tef2 deletion mutant and examined various phenotypes including cell growth, actin dynamics, lifespan, % survival, and mutagenesis after UV irradiation. These results might provide insights into the role of RAD2 in post-UV irradiation cell cycle regulation and actin assembly, which may be an underlying cause of XPG/CS.