Mushroom body defect, a gene involved in the control of neuroblast proliferation in Drosophila, encodes a coiled–coil protein
- Zhonghui Guan*†,
- Antonio Prado†‡,
- Jörg Melzig‡,
- Martin Heisenberg‡,
- Howard A. Nash*, and
- Thomas Raabe‡§
- *Laboratory of Molecular Biology, Section on Molecular Genetics, National Institute of Mental Health, Bethesda, MD 20892-4034; and ‡Theodor-Boveri-Institut für Biowissenschaften, Lehrstuhl für Genetik, Universität Würzburg, Am Hubland, D-97074 Würzburg, Germany
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Contributed by Howard A. Nash
Abstract
Neurogenesis relies on the establishment of the proper number and precisely controlled proliferation of neuroblasts, the neuronal precursor cells. A role for the mushroom body defect (mud) gene in both of these aspects of neuroblast behavior, as well as possible roles in other aspects of fruit fly biology, is implied by phenotypes associated with mud mutations. We have localized mud by determining the sequence change in one point mutant, identifying a predicted ORF affected by the mutation, and showing that an appropriate segment of the genome rescues mud mutant phenotypes. An analysis of mud cDNAs and a survey of mud transcripts by Northern blotting indicate that the gene is subject to differential splicing and is expressed primarily during embryogenesis but also, at lower levels, during subsequent developmental stages in a sexually dimorphic manner. The gene is predicted to encode a polypeptide without obvious homologs but with two prominent structural features, a long coiled coil that constitutes the central core of the protein and a carboxyl-terminal transmembrane domain.
Footnotes
Abbreviations
- KC,
- Kenyon cell;
- mud,
- mushroom body defect gene;
- MB,
- mushroom body;
- Nb,
- neuroblast;
- TM,
- transmembrane
- Accepted May 10, 2000.
- Copyright © 2000, The National Academy of Sciences
