Neuroectodermal transcription of the Drosophila neurogenic genes E(spl) and HLH-m5 is regulated by proneural genes

• Published in: Development (Cambridge) Vol. 120; no. 4; pp. 815 - 826
• Main Authors: KRAMATSCHEK, B, CAMPOS-ORTEGA, J. A
• Format: Journal Article
• Language: English
• Published: Cambridge The Company of Biologists Limited 01.04.1994; Company of Biologists
• Subjects: Animals; Base Sequence; Basic Helix-Loop-Helix Transcription Factors; Biological and medical sciences; DNA-Binding Proteins - genetics; Drosophila; Drosophila - embryology; Drosophila - genetics; Ectoderm - physiology; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation, Developmental; Genes, Insect; Insecta; Invertebrates; Life cycle. Embryology. Development; Models, Genetic; Molecular Sequence Data; Mutagenesis, Site-Directed; Nervous System - embryology; Physiology. Development; Transcription Factors - genetics; Transcription, Genetic; Helix loop helix structure; Embryonic development; Transcription; Insecta; Drosophila; Drosophilidae; Regulation(control); Arthropoda; Trans acting regulatory factor; Regulatory sequence; Cis effect; Nervous tissue; Invertebrata; Diptera
• ISSN: 0950-1991; 1477-9129
• DOI: 10.1242/dev.120.4.815

The Enhancer of split gene complex (E(SPL)-C) of Drosophila comprises seven genes encoding bHLH proteins, which are required by neuroectodermal cells for epidermal development. Using promoter and gene fusions with the lacZ gene, we determined the location of cis-acting sequences necessary for normal expression of two of the genes of the E(SPL)-C, E(spl) and HLH-m5. About 0.46 kb of E(spl) and 1.9 kb of HLH-m5 upstream sequences are necessary to reproduce the normal transcription pattern of these genes. The gene products of achaete, scute and lethal of scute, together with that of ventral nervous system condensation defective, act synergistically to specify the neuroectodermal E(spl) and HLH-m5 expression domains. Negative cross- and autoregulatory interactions of the E(SPL)-C on E(spl) contribute, directly or indirectly, to this regulation. Interactions involve DNA binding, since mutagenesis of binding sites for bHLH proteins in the E(spl) promoter abolishes neuroectodermal expression and activates ectopic expression in neuroblasts. A model for activation and repression of E(spl) in the neuroectoderm and neuroblasts, respectively, is proposed.