Rough eye Is a Gain-of-Function Allele of amos That Disrupts Regulation of the Proneural Gene atonal During Drosophila Retinal Differentiation

Rough eye Is a Gain-of-Function Allele of amos That Disrupts Regulation of the Proneural Gene atonal During Drosophila Retinal Differentiation

Françoise Chanut^a, Katherine Woo^a, Shalini Pereira^b, Terrence J. Donohoe^b, Shang-Yu Chang^d, Todd R. Laverty^e, Andrew P. Jarman^f, and Ulrike Heberlein^a,c
^a Department of Anatomy, University of California, San Francisco, California 94143,
^b Gallo Center, University of California, San Francisco, California 94143,
^c Program in Neuroscience and Developmental Biology, University of California, San Francisco, California 94143,
^d Cornell Graduate School of Medical Sciences, Sloan-Kettering Research Institute, New York, New York 10021,
^e Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, California 94720
^f Wellcome Trust Center for Cell Biology, Institute of Cell and Molecular Biology, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom

Corresponding author: Françoise Chanut, S1334, Box 0452, University of California, 513 Parnassus Ave., San Francisco, CA 94143., chanut{at}itsa.ucsf.edu (E-mail)

Communicating editor: T. SCHÜPBACH

The regular organization of the ommatidial lattice in the Drosophilaeye originates in the precise regulation of the proneural geneatonal (ato), which is responsible for the specification ofthe ommatidial founder cells R8. Here we show that Rough eye(Roi), a dominant mutation manifested by severe roughening ofthe adult eye surface, causes defects in ommatidial assemblyand ommatidial spacing. The ommatidial spacing defect can beascribed to the irregular distribution of R8 cells caused bya disruption of the patterning of ato expression. Disruptionsin the recruitment of other photoreceptors and excess Hedgehogproduction in differentiating cells may further contribute tothe defects in ommatidial assembly. Our molecular characterizationof the Roi locus demonstrates that it is a gain-of-functionmutation of the bHLH gene amos that results from a chromosomalinversion. We show that Roi can rescue the retinal developmentaldefect of ato¹ mutants and speculate that amos substitutes forsome of ato's function in the eye or activates a residual functionof the ato¹ allele.

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