Drosophila MBF1 is a co-activator for Tracheae Defective and contributes to the formation of tracheal and nervous systems

• Published in: Development (Cambridge) Vol. 130; no. 4; pp. 719 - 728
• Main Authors: Liu, Qing-Xin, Jindra, Marek, Ueda, Hitoshi, Hiromi, Yasushi, Hirose, Susumu
• Format: Journal Article
• Language: English
• Published: England The Company of Biologists Limited 01.02.2003
• Subjects: Amino Acid Sequence; Animals; Animals, Genetically Modified; Binding Sites; Cloning, Molecular; DNA-Binding Proteins; Drosophila - embryology; Drosophila - genetics; Drosophila Proteins - genetics; Drosophila Proteins - metabolism; Embryo, Nonmammalian; Gene Expression Regulation, Developmental; Molecular Sequence Data; Nervous System - embryology; Nuclear Proteins - genetics; Nuclear Proteins - metabolism; Sequence Homology, Amino Acid; TATA-Box Binding Protein - genetics; TATA-Box Binding Protein - metabolism; Trachea - embryology; Trans-Activators - genetics; Trans-Activators - metabolism; Transcription Factors - genetics; Transcription Factors - metabolism; Transcription, Genetic; Transcriptional Activation
• ISSN: 0950-1991; 1477-9129
• DOI: 10.1242/dev.00297

During gene activation, the effect of binding of transcription factors to cis-acting DNA sequences is transmitted to RNA polymerase by means of co-activators. Although co-activators contribute to the efficiency of transcription, their developmental roles are poorly understood. We used Drosophila to conduct molecular and genetic dissection of an evolutionarily conserved but unique co-activator, Multiprotein Bridging Factor 1 (MBF1), in a multicellular organism. Through immunoprecipitation, MBF1 was found to form a ternary complex including MBF1, TATA-binding protein (TBP) and the bZIP protein Tracheae Defective (TDF)/Apontic. We have isolated a Drosophila mutant that lacks the mbf1 gene in which no stable association between TBP and TDF is detectable, and transcription of a TDF-dependent reporter gene is reduced by 80%. Although the null mutants of mbf1 are viable, tdf becomes haploinsufficient in mbf1 -deficient background, causing severe lesions in tracheae and the central nervous system, similar to those resulting from a complete loss of tdf function. These data demonstrate a crucial role of MBF1 in the development of tracheae and central nervous system.