tion of the embryonic axonal tracks. The otd muta- 
tions that completely eliminate gene activity result 
in the fusion of pairs of horizontal axonal commis- 
sures present in each segment of the embryo. Most 
likely this defect is secondary to the abnormal dif- 
ferentiation of a small subset of neurons that are 
normally located at the ventral midline in wild-type 
embryos. Less-severe mutations in this gene do not 
'affect the embryonic CNS but act later in develop- 
ment, causing a deletion of specific visual struc- 
tures, the ocelli, in the adult fly. In collaboration 
with Dr. Allan C. Spradling (HHMI, The Carnegie 
Institution of Washington), this laboratory has 
cloned the otd gene. The otd gene encodes one 
major 5 kb message that is expressed in precursor 
cells along the ventral midline. Sequence analysis 
indicates that otd encodes a protein with a highly 
repeated structure that contains a homeodomain 
that has been implicated in DNA-binding activities. 
The analysis of otd is providing insights about a 
gene product that is essential not only for embry- 
onic axonal patterning but also for the determina- 
tion of eye structures during imaginal development. 
ly Targeting Gene Expression in Drosophila. 
Although most of the work in Dr. Perrimon's lab- 
oratory has been focused on the analysis of devel- 
opmental genes, a system is also being developed 
that will allow the controlled expression of specific 
genes in predetermined cells or groups of cells. 
The approach taken utilizes the activation proper- 
ties of the yeast GAL4 protein, which activates only 
those genes bearing a GAL4-binding site within 
their promoters. It has been shown by others that 
GAL4 can also activate transcription in Drosophila. 
This approach involves the expression of GAL4 in a 
subset of cells and the subsequent introduction of 
genes whose transcription is driven by GAL4-bind- 
ing sites. Some of the applications of this system 
will involve the analysis of pattern regulation after 
selective killing of specific cells and the analysis of 
ectopic expression of "switch" genes, which control 
cell fate or identity. 
Dr. Perrimon is also Assistant Professor of Genet- 
ics at the Harvard Medical School. 
PUBLICATIONS 
Articles 
Ambrosio, L., Mahowald, A.R, and Perrimon, N. 1989. l(l)pole hole is required maternally for pattern forma- 
tion in the terminal regions of the embryo. Development 106:145-158. 
Klingensmith, J., Noll, E. , and Perrimon, N. 1989. The segment polarity phenotype oi Drosophila involves dif- 
ferential tendencies toward transformation and cell death. Dev Biol 134:130-145. 
Ng, S.-C., Perkins, L.A., Conboy, G., Perrimon, N., and Fishman, M. 1989. KDrosophila gene expressed in the 
embryonic CNS shares one conserved domain with the mammalian GAP-43. Development 105:629-638. 
Oliver, B., Perrimon, N. , and Mahowald, A.P 1988. Genetic evidence that the sans fille locus is involved in 
Drosophila sex determination. Genetics 120:159-171. 
Perrimon, N., Engstrom, L., and Mahowald, A.P 1989- Zygotic lethals with specific maternal effect phenotypes 
in Drosophila melanogaster . I. Loci on the X chromosome. Genetics 121:333-352. 
Perrimon, N. , Smouse, D., and Miklos, G.L.G. 1989. Developmental genetics of loci at the base of the X chro- 
mosome Drosophila melanogaster. Genetics 121:313-331. 
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