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Citation
Chanut, F., Woo, K., Pereira, S., Donohoe, T.J., Chang, S.Y., Laverty, T.R., Jarman, A.P., Heberlein, U. (2002). Rough eye Is a Gain-of-Function Allele of amos That Disrupts Regulation of the Proneural Gene atonal During Drosophila Retinal Differentiation.  Genetics 160(2): 623--635.
FlyBase ID
FBrf0144903
Publication Type
Research paper
Abstract

The regular organization of the ommatidial lattice in the Drosophila eye originates in the precise regulation of the proneural gene atonal (ato), which is responsible for the specification of the ommatidial founder cells R8. Here we show that Rough eye (Roi), a dominant mutation manifested by severe roughening of the adult eye surface, causes defects in ommatidial assembly and ommatidial spacing. The ommatidial spacing defect can be ascribed to the irregular distribution of R8 cells caused by a disruption of the patterning of ato expression. Disruptions in the recruitment of other photoreceptors and excess Hedgehog production in differentiating cells may further contribute to the defects in ommatidial assembly. Our molecular characterization of the Roi locus demonstrates that it is a gain-of-function mutation of the bHLH gene amos that results from a chromosomal inversion. We show that Roi can rescue the retinal developmental defect of ato1 mutants and speculate that amos substitutes for some of ato's function in the eye or activates a residual function of the ato1 allele.

PubMed ID
PubMed Central ID
PMC1461986 (PMC) (EuropePMC)
DOI
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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