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Citation
Fan, Y., Schlierf, M., Gaspar, A.C., Dreux, C., Kpebe, A., Chaney, L., Mathieu, A., Hitte, C., Grémy, O., Sarot, E., Horn, M., Zhao, Y., Kinzy, T.G., Rabinow, L. (2010). Drosophila translational elongation factor-1{gamma} is modified in response to DOA kinase activity and is essential for cellular viability.  Genetics 184(1): 141--154.
FlyBase ID
FBrf0209673
Publication Type
Research paper
Abstract

Drosophila translational elongation factor-1gamma (EF1gamma) interacts in the yeast two-hybrid system with DOA, the LAMMER protein kinase of Drosophila. Analysis of mutant EF1gamma alleles reveals that the locus encodes a structurally conserved protein essential for both organismal and cellular survival. Although no genetic interactions were detected in combinations with mutations in EF1alpha, an EF1gamma allele enhanced mutant phenotypes of Doa alleles. A predicted LAMMER kinase phosphorylation site conserved near the C terminus of all EF1gamma orthologs is a phosphorylation site in vitro for both Drosophila DOA and tobacco PK12 LAMMER kinases. EF1gamma protein derived from Doa mutant flies migrates with altered mobility on SDS gels, consistent with it being an in vivo substrate of DOA kinase. However, the aberrant mobility appears to be due to a secondary protein modification, since the mobility of EF1gamma protein obtained from wild-type Drosophila is unaltered following treatment with several nonspecific phosphatases. Expression of a construct expressing a serine-to-alanine substitution in the LAMMER kinase phosphorylation site into the fly germline rescued null EF1gamma alleles but at reduced efficiency compared to a wild-type construct. Our data suggest that EF1gamma functions in vital cellular processes in addition to translational elongation and is a LAMMER kinase substrate in vivo.

PubMed ID
PubMed Central ID
PMC2815912 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Genetics
    Title
    Genetics
    Publication Year
    1916-
    ISBN/ISSN
    0016-6731
    Data From Reference
    Aberrations (3)
    Alleles (18)
    Genes (11)
    Physical Interactions (2)
    Natural transposons (1)
    Insertions (6)
    Experimental Tools (2)
    Transgenic Constructs (7)