Overproduction of elongation factor 1α, an essential translational component, causes aberrant cell morphology by affecting the control of growth polarity in fission yeast

Background Elongation factor 1α (EF1α), 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 EF1α with respect to these various biochemical or biological activities remains limited. Here we report the identification of EF1α‐encoding genes as genes whose over‐expression causes aberrant cell morphology in fission yeast. Results Overproduction of EF1α caused aberrant cell morphology—elliptic, curved or branched—and growth defects in yeast cells at high temperatures. EF1α‐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 EF1α disturbed the establishment and the maintenance of growth polarity in the G1 phase by pre‐ venting the localization of F‐actin to the polarized growing site and the organization of microtubules. Results from DNase I column chromatography indicated that EF1α was bound to G‐actin. Indeed, the fission yeast actin was immunoprecipitated along with EF1α. Moreover, the temperature sensitivity caused by the overproduction of EF1α was restored by co‐overproduction of actin. Conclusions Fission yeast EF1α has the ability to alter the cell morphology of yeast by affecting the control of actin and microtubule cytoskeletons.