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Development, Vol 117, Issue 3 1017-1029, Copyright © 1993 by Company of Biologists


JOURNAL ARTICLES

Expression of the Drosophila optomotor-blind gene transcript in neuronal and glial cells of the developing nervous system

B Poeck, A Hofbauer and GO Pflugfelder
Theodor Boveri Institut, Lehrstuhl fur Genetik, Wurzburg, Germany.

Mutations in the complex gene locus optomotor-blind (omb) can lead to defects in the development of both the optic lobes and external features of the adult fly. We describe here the expression of omb in the developing and adult nervous system using in situ hybridization. During embryogenesis, omb expression is first observed in the optic lobe anlagen. It later expands to a larger part of the developing larval brain and to the gnathal lobes. Cells in the ventral and peripheral nervous systems begin to express omb after completion of germ band extension. Later in embryonic development, expression declines and only persists in the antennomaxillary complex and in part of the brain hemispheres. During the larval and pupal stages, omb expression in the brain is confined to the developing optic lobes and contiguous regions of the central brain. At these stages, only a few cells show expression in the ventral ganglion. In the eye imaginal disc, transcript accumulation is most conspicuous in a group of presumptive glia precursor cells posterior to the morphogenetic furrow and in the optic stalk. In the adult brain, expression is prominent in several regions of the optic lobe cortex and along the border between central brain and optic lobes. In the mutation In(1)ombH31, 40 kb of regulatory DNA, downstream from the transcription unit, are removed from the omb gene. In(1)ombH31 is characterized by the lack of a set of giant interneurons from the lobula plate of the adult optic lobes. We find that, already during embryogenesis, there is a drastic difference between wild type and In(1)ombH31 in the level of the omb transcript in the optic lobe primordia. The adult mutant phenotype may thus be caused by omb misexpression during embryonic development.


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© The Company of Biologists Ltd 1993