REGULATORY AUTONOMY AND MOLECULAR CHARACTERIZATION OF THE DROSOPHILA OUT AT FIRST GENE

Citation
De. Bergstrom et al., REGULATORY AUTONOMY AND MOLECULAR CHARACTERIZATION OF THE DROSOPHILA OUT AT FIRST GENE, Genetics, 139(3), 1995, pp. 1331-1346
Citations number
67
Categorie Soggetti
Genetics & Heredity
Journal title
ISSN journal
00166731
Volume
139
Issue
3
Year of publication
1995
Pages
1331 - 1346
Database
ISI
SICI code
0016-6731(1995)139:3<1331:RAAMCO>2.0.ZU;2-D
Abstract
Our previous work has shown that the expression of the Drosophila deca pentaplegic (dpp) gene in imaginal disks is controlled by a 30 kb arra y of enhancers located 3' of the dpp coding region. Here, we describe the cloning and characterization of out at first (oaf), a gene located near this enhancer region. Transcription of oaf results in three clas ses of alternatively polyadenylated RNAs whose expression is developme ntally regulated. All oaf transcripts contain two adjacent open readin g frames separated by a single UGA stop codon. Suppression of the UGA codon during translation, as seen previously in Drosophila, could lead to the production of different proteins from the same RNA. During oog enesis, oaf RNA is expressed in nurse cells of all ages and maternally contributed to the egg. During embryonic development, zygotic transcr iption of the gene occurs in small clusters of cells in most or all se gments at the time of germband extension and subsequently in a segment ally repeated pattern in the developing central nervous system. The ge ne is also expressed in the embryonic, larval and adult gonads of both sexes. We also characterize an enhancer trap line with its transposon inserted within the oaf gene and use it to generate six recessive oaf mutations. All six cause death near the beginning of the first larval instar, with two characterized lines showing nervous system defects. Last, we discuss our data in light of the observation that the enhance rs controlling dpp expression in the imaginal disks have no effect on the relatively nearby oaf gene.