Research Paper Volume 1, Issue 2 pp 219—233
WRN helicase defective in the premature aging disorder Werner syndrome genetically interacts with topoisomerase 3 and restores the top3 slow growth phenotype of sgs1 top3
Figure 3. WRN expression induces S/G2 arrest in sgs1 top3 cells. Logarithmically growing cultures of sgs1 top3 strain transformed with YEp112SpGAL, YEp112SpGAL-WRN, or YEp112SpGAL-SGS1, and the vector-transformed wild-type parental strain were induced at 2% gal concentration for 6 h. Cultures were harvested, processed for DAPI staining as described in "Materials and Methods" and were observed using Axiovert 200 M microscope(Zeiss; 100x lens). Shown is the DAPI staining of the sgs1 top3 transformed with YEp112SpGAL (upper left) and with YEp112SpGAL-WRN (upper right). Arrows show cells with undivided nuclei. Distribution of the cells in G1 (single cells) and S/G2 (budded cells) is shown in lower panel.