P-ELEMENT INSERTION-DEPENDENT GENE ACTIVATION IN THE DROSOPHILA EYE

Citation
Ba. Hay et al., P-ELEMENT INSERTION-DEPENDENT GENE ACTIVATION IN THE DROSOPHILA EYE, Proceedings of the National Academy of Sciences of the United Statesof America, 94(10), 1997, pp. 5195-5200
Citations number
37
Categorie Soggetti
Multidisciplinary Sciences
ISSN journal
00278424
Volume
94
Issue
10
Year of publication
1997
Pages
5195 - 5200
Database
ISI
SICI code
0027-8424(1997)94:10<5195:PIGAIT>2.0.ZU;2-4
Abstract
Insights into the function of a gene can be gained in multiple ways, i ncluding loss-of-function phenotype, sequence similarity, expression p attern, and by the consequences of its misexpression. Analysis of the phenotypes produced by expression of a gene at an abnormal time, place , or level may provide clues to a gene's function when other approache s are not illuminating. Here we report that an eye-specific, enhancer- promoter present in the P element expression vector pGMR is able to dr ive high level expression in the eye of genes near the site of P eleme nt insertion. Cell fate determination, differentiation, proliferation, and death are essential for normal eye development. Thus the ability to carry out eye-specific misexpression of a significant fraction of g enes in the genome, given the dispensability of the eye for viability and fertility of the adult, should provide a powerful approach for ide ntifying regulators of these processes. To test this idea we carried o ut two overexpression screens for genes that function to regulate cell death. We screened for insertion-dependent dominant phenotypes in a w ild-type background, and for dominant modifiers of a reaper overexpres sion-induced small eye phenotype. Multiple chromosomal loci were ident ified, including an insertion 5' to hid, a potent inducer of apoptosis , and insertions 5' to DIAP1, a cell death suppressor. To facilitate t he cloning of genes near the P element insertion new misexpression vec tors were created. A screen with one of these vectors identified eagle as a suppressor of a rough eye phenotype associated with overexpressi on of an activated Ras1 gene.