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First published online 22 October 2003
doi: 10.1242/dev.00818

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Bar homeodomain proteins are anti-proneural in the Drosophila eye: transcriptional repression of atonal by Bar prevents ectopic retinal neurogenesis

¹ Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
² Program in Developmental Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
³ Department of Ophthalmology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA

^* Author for correspondence (e-mail: kchoi{at}bcm.tmc.edu)

Accepted 26 August 2003

Atonal (Ato)/Math (Mammalian atonal homolog) family proneural proteins are key regulators of neurogenesis in both vertebrates and invertebrates. In the Drosophila eye, Ato is essential for the generation of photoreceptor neurons. Ato expression is initiated at the anterior ridge of the morphogenetic furrow but is repressed in the retinal precursor cells behind the furrow to prevent ectopic neurogenesis. We show that Ato repression is mediated by the conserved homeobox proteins BarH1 and BarH2. Loss of Bar causes cell-autonomous ectopic Ato expression, resulting in excess photoreceptor clusters. The initial ommatidial spacing at the furrow occurs normally in the absence of Bar, suggesting that the ectopic neurogenesis within Bar mutant clones is not due to the lack of Notch (N)-dependent lateral inhibition. Targeted misexpression of Bar is sufficient to repress ato expression. Furthermore, we provide evidence that Bar represses ato expression at the level of transcription without affecting the expression of an ato activator, Cubitus interruptus (Ci). Thus, we propose that Bar is essential for transcriptional repression of ato and the prevention of ectopic neurogenesis behind the furrow.

Key words: Bar homeodomain protein, atonal, Proneural, Retinal neurogenesis, Drosophila eye

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