PMID- 9144214
OWN - NLM
STAT- MEDLINE
DCOM- 19970605
LR  - 20190524
IS  - 0027-8424 (Print)
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 94
IP  - 10
DP  - 1997 May 13
TI  - P element insertion-dependent gene activation in the Drosophila eye.
PG  - 5195-200
AB  - Insights into the function of a gene can be gained in multiple ways, including 
      loss-of-function phenotype, sequence similarity, expression pattern, 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 approaches are not illuminating. Here we report that 
      an eye-specific, enhancer-promoter present in the P element expression vector 
      pGMR is able to drive high level expression in the eye of genes near the site of 
      P element 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 genes in the genome, 
      given the dispensability of the eye for viability and fertility of the adult, 
      should provide a powerful approach for identifying regulators of these processes. 
      To test this idea we carried out two overexpression screens for genes that 
      function to regulate cell death. We screened for insertion-dependent dominant 
      phenotypes in a wild-type background, and for dominant modifiers of a reaper 
      overexpression-induced small eye phenotype. Multiple chromosomal loci were 
      identified, including an insertion 5' to hid, a potent inducer of apoptosis, and 
      insertions 5' to DIAP1, a cell death suppressor. To facilitate the cloning of 
      genes near the P element insertion new misexpression vectors were created. A 
      screen with one of these vectors identified eagle as a suppressor of a rough eye 
      phenotype associated with overexpression of an activated Ras1 gene.
FAU - Hay, B A
AU  - Hay BA
AD  - Department of Molecular and Cell Biology and Howard Hughes Medical Institute, 
      University of California, Berkeley, CA 94720-3200, USA.
FAU - Maile, R
AU  - Maile R
FAU - Rubin, G M
AU  - Rubin GM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (DNA Primers)
RN  - 0 (DNA Transposable Elements)
RN  - 0 (Drosophila Proteins)
RN  - 0 (Genetic Markers)
RN  - 0 (Peptides)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (rpr protein, Drosophila)
SB  - IM
MH  - Animals
MH  - Animals, Genetically Modified
MH  - Apoptosis
MH  - *Chromosome Mapping
MH  - DNA Primers
MH  - *DNA Transposable Elements
MH  - Drosophila/*genetics
MH  - *Drosophila Proteins
MH  - Enhancer Elements, Genetic
MH  - Eye/*cytology/ultrastructure
MH  - *Gene Expression Regulation, Developmental
MH  - Genes, Dominant
MH  - *Genes, Insect
MH  - Genes, Suppressor
MH  - Genetic Markers
MH  - Genotype
MH  - Microscopy, Electron, Scanning
MH  - *Ocular Physiological Phenomena
MH  - Organ Specificity
MH  - Peptide Biosynthesis
MH  - Peptides/genetics
MH  - Plasmids
MH  - Polymerase Chain Reaction
MH  - Promoter Regions, Genetic
MH  - Recombinant Fusion Proteins/biosynthesis
MH  - Transcriptional Activation
PMC - PMC24655
EDAT- 1997/05/13 00:00
MHDA- 1997/05/13 00:01
PMCR- 1997/11/13
CRDT- 1997/05/13 00:00
PHST- 1997/05/13 00:00 [pubmed]
PHST- 1997/05/13 00:01 [medline]
PHST- 1997/05/13 00:00 [entrez]
PHST- 1997/11/13 00:00 [pmc-release]
AID - 0486 [pii]
AID - 10.1073/pnas.94.10.5195 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 1997 May 13;94(10):5195-200. doi: 
      10.1073/pnas.94.10.5195.