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The activity of the Drosophila morphogenetic protein Bicoid is inhibited by a domain located outside its homeodomain

Chen Zhao¹, Allen York¹, Fan Yang^1,*, David J. Forsthoefel², Vrushank Dave¹, Dechen Fu¹, Dongyi Zhang¹, Maria S. Corado³, Stephen Small³, Mark A. Seeger² and Jun Ma^1,

¹ Division of Developmental Biology, Children’s Hospital Research Foundation, University of Cincinnati College of Medicine, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
² Department of Molecular Genetics and the Neurobiotechnology Center, The Ohio State University, 125 Rightmire Hall, 1060 Carmack Road, Columbus, OH 43210, USA
³ Department of Biology, New York University, 100 Washington Square East, New York, NY 10003, USA*Present address: Department of Molecular Genetics, University of Cincinnati College of Medicine, 231 Sabin Drive, Cincinnati, OH 45267, USA

Author for correspondence (e-mail: jun.ma{at}chmcc.org)

Accepted 4 January 2002

The Drosophila morphogenetic protein Bicoid (Bcd) is a homeodomain-containing activator that stimulates the expression of target genes during early embryonic development. We demonstrate that a small domain of Bcd located immediately N-terminally of the homeodomain represses its own activity in Drosophila cells. This domain, referred to as a self-inhibitory domain, works as an independent module that does not rely on any other sequences of Bcd and can repress the activity of heterologous activators. We further show that this domain of Bcd does not affect its properties of DNA binding or subcellular distribution. A Bcd derivative with point mutations in the self-inhibitory domain severely affects pattern formation and target gene expression in Drosophila embryos. We also provide evidence to suggest that the action of the self-inhibitory domain requires a Drosophila co-factor(s), other than CtBP or dSAP18. Our results suggest that proper action of Bcd as a transcriptional activator and molecular morphogen during embryonic development is dependent on the downregulation of its own activity through an interaction with a novel co-repressor(s) or complex(es).

Key words: Drosophila, Bicoid, Transcription

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