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A role for Ebi in neuronal cell cycle control
Author(s) -
Boulton Simon J.,
Brook Adam,
StaehlingHampton Karen,
Heitzler Pascal,
Dyson Nick
Publication year - 2000
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/19.20.5376
Subject(s) - biology , ectopic expression , microbiology and biotechnology , phenotype , mutant , cellular differentiation , enhancer , cell cycle , mitosis , mutation , genetic screen , e2f , genetics , cell , transcription factor , cell culture , gene
Mutations in ebi were isolated as enhancers of an over‐proliferation phenotype generated by elevated E2F/DP activity in the Drosophila eye. ebi alleles also strongly suppress a phenotype caused by the cyclin‐dependent kinase inhibitor p21, restoring S phases in the second mitotic wave of the developing eye disk. ebi mutant embryos display ectopic S phases within the peripheral nervous system and central nervous system at a time in development when neuronal precursor cells would normally begin to differentiate. Consistent with this, we find that ebi mutants have a reduced capacity to undergo neuronal differentiation, that Ebi physically interacts with Sina and phyllopod, and that Ebi promotes Ttk88 degradation in vitro and in S2 cells. Ectopic expression of Ttk88 inhibited differentiation in embryos and eye discs; however, this block to differentiation was insufficient to promote S phase entry in either of the situations where ebi mutations gave this effect. We conclude that Ebi has two distinct functions; it promotes the degradation of a repressor of neuronal differentiation (Ttk88), and has a second independent function that limits S phase entry.