Background: Elongation factor lo (EF1 alpha), an essential component of the eukaryotic translational machinery, has been shown to possess various biochemical and biological activities, including F-actin-binding and -bundling, microtubule-severing, and the activity of making fibroblasts highly susceptible to transformation. However, our understanding of the biological significance of EF1 alpha with respect to these various biochemical or biological activities remains Limited. Here we report the identification of EF1 alpha-encoding genes as genes whose over-expression causes aberrant cell morphology in fission yeast.
Results: Overproduction of EF1 alpha caused aberrant cell morphology-elliptic, curved or branched-and growth defects in yeast cells at high temperatures. EF1 alpha-overproducing cells showed a supersensitivity to the actin inhibitor cytochalasin D and to the tubulin inhibitor thiabendazole. Genetic analyses using cdc mutants suggested that excess EF1 alpha disturbed the establishment and the maintenance of growth polarity in the G1 phase by preventing the localization of F-actin to the polarized growing site and the organization of microtubules. Results from DNase I column chromatography indicated that EF1 alpha was bound to G-actin. Indeed, the fission yeast actin was immunoprecipitated along with EF1 alpha. Moreover, the temperature sensitivity caused by the overproduction of EF1 alpha was restored by co-overproduction of actin.
Conclusions: Fission yeast EF1 alpha has the ability to alter the cell morphology of yeast by affecting the control of actin and microtubule cytoskeletons.