MAPK target sites of eyes absent are not required for eye development or survival in Drosophila.

TitleMAPK target sites of eyes absent are not required for eye development or survival in Drosophila.
Publication TypeJournal Article
Year of Publication2012
AuthorsJusiak, B, Abulimiti, A, Haelterman, N, Chen, R, Mardon, G
JournalPLoS One
Date Published2012
KeywordsAnimals, Compound Eye, Arthropod, Drosophila, Drosophila Proteins, Eye Proteins, Gene Expression Regulation, Developmental, Mitogen-Activated Protein Kinases, Mutation, Phenotype, Phosphorylation, Signal Transduction

Eyes absent (Eya) is a highly conserved transcription cofactor and protein phosphatase that plays an essential role in eye development and survival in Drosophila. Ectopic eye induction assays using cDNA transgenes have suggested that mitogen activated protein kinase (MAPK) activates Eya by phosphorylating it on two consensus target sites, S402 and S407, and that this activation potentiates the ability of Eya to drive eye formation. However, this mechanism has never been tested in normal eye development. In the current study, we generated a series of genomic rescue transgenes to investigate how loss- and gain-of-function mutations at these two MAPK target sites within Eya affect Drosophila survival and normal eye formation: eya(+)GR, the wild-type control; eya(SA)GR, which lacks phosphorylation at the two target residues; and eya(SDE)GR, which contains phosphomimetic amino acids at the same two residues. Contrary to the previous studies in ectopic eye development, all eya genomic transgenes tested rescue both eye formation and survival equally effectively. We conclude that, in contrast to ectopic eye formation, MAPK-mediated phosphorylation of Eya on S402 and S407 does not play a role in normal development. This is the first study in Drosophila to evaluate the difference in outcomes between genomic rescue and ectopic cDNA-based overexpression of the same gene. These findings indicate similar genomic rescue strategies may prove useful for re-evaluating other long-standing Drosophila developmental models.

Alternate JournalPLoS One
PubMed ID23251383
PubMed Central IDPMC3520925
Grant ListP30 EY002520 / EY / NEI NIH HHS / United States
R01 EY011232 / EY / NEI NIH HHS / United States
EY-002520 / EY / NEI NIH HHS / United States

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