Figure 7.

Full-length active Hmg2p^s causes a growth defect in strains deficient in the methylation pathway, but not the Kennedy pathway. (A) Diagram of the two major phospholipid biosynthetic pathways in S. cerevisiae. The Kennedy pathway is highlighted in blue, and the CDP-DAG/methylation pathway is highlighted in pink. (B) Live cell imaging of Hmg2p^s-TM-hN-GFP in wild-type, cki1·, cpt1·, and ept1· null strains. Log phase cells were grown in SC-URA. Arrows indicate membrane structures. (C) Live cell imaging of Hmg2p^s-TM-hN-GFP in wild-type, psd1·, cho2·, and opi3· null strains. Log phase cells were grown in SC-URA. Arrows indicate membrane structures. (D) Representative growth experiment of cells inoculated into synthetic complete liquid media lacking uracil and grown for ∼55 h at 30°C. Strains deficient in the methylation pathway do not grow to as high a density as wild-type strains in synthetic complete media (data not shown). When Hmg2p^s is overexpressed (light bars) in psd1·, cho2·, or opi3· null strains, cells display a significant growth defect. This phenotype is not observed in cki1·, cpt1·, or ept1· null strains. Overexpression of Hmg2p^s-TM-hN-GFP (dark bars) does not affect growth in any of the null strains tested.