title: Overproduction of elongation factor 1alpha, an essential translational component, causes aberrant cell morphology by affecting the control of growth polarity in fission yeast.
abstract: BACKGROUND
  Elongation factor 1alpha (EF1alpha), 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 EF1alpha with respect to these various biochemical or biological activities remains limited. Here we report the identification of EF1alpha-encoding genes as genes whose over-expression causes aberrant cell morphology in fission yeast.
  
  
  RESULTS
  Overproduction of EF1alpha caused aberrant cell morphology-elliptic, curved or branched-and growth defects in yeast cells at high temperatures. EF1alpha-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 EF1alpha 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 EF1alpha was bound to G-actin. Indeed, the fission yeast actin was immunoprecipitated along with EF1alpha. Moreover, the temperature sensitivity caused by the overproduction of EF1alpha was restored by co-overproduction of actin.
  
  
  CONCLUSIONS
  Fission yeast EF1alpha has the ability to alter the cell morphology of yeast by affecting the control of actin and microtubule cytoskeletons.
authors.affiliation: Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University.
authors.forename: M
authors.initials: M
authors.lastname: Suda
authors.forename: M
authors.initials: M
authors.lastname: Fukui
authors.forename: Y
authors.initials: Y
authors.lastname: Sogabe
authors.forename: K
authors.initials: K
authors.lastname: Sato
authors.forename: A
authors.initials: A
authors.lastname: Morimatsu
authors.forename: R
authors.initials: R
authors.lastname: Arai
authors.forename: F
authors.initials: F
authors.lastname: Motegi
authors.forename: T
authors.initials: T
authors.lastname: Miyakawa
authors.forename: I
authors.initials: I
authors.lastname: Mabuchi
authors.forename: D
authors.initials: D
authors.lastname: Hirata
mesh_terms: D000199:Actins / Q000378:metabolism; D000595:Amino Acid Sequence; D001483:Base Sequence; D015153:Blotting, Western; D018797:Cell Cycle Proteins / Q000235:genetics; D017931:DNA Primers; D008826:Microbial Sensitivity Tests; D008969:Molecular Sequence Data; D020648:Peptide Elongation Factor 1 / Q000096:biosynthesis* / Q000378:metabolism; D011485:Protein Binding; D014176:Protein Biosynthesis; D012568:Schizosaccharomyces / Q000166:cytology* / Q000187:drug effects / Q000235:genetics / Q000254:growth & development; D013696:Temperature
chemical_list: D000199:Actins; D018797:Cell Cycle Proteins; D017931:DNA Primers; D020648:Peptide Elongation Factor 1