Nature 333, 376 - 378 (26 May 1988); doi:10.1038/333376a0

Control of neuronal fate by the Drosophila segmentation gene even-skipped

Chris Q. Doe^*, David Smouse^* & Corey S. Goodman^†

Department of Biological Sciences, Stanford University, Stanford, California 94305, USA
^*Present address: Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, Colorado 80309, USA (C. Q. D. ) and Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA (D. S.)
^†To whom correspondence should be addressed at Department of Biochemistry, University of California, Berkeley, California 94720, USA

The central nervous system (CNS) contains a remarkable diversity of cell types. The molecular basis for generating this neuronal diversity is poorly understood. Much is known, however, about the regulatory genes which control segmentation and segment identity during early Drosophila embryogenesis1,2. Interestingly, most of the segmentation and homoeotic genes in Drosophila, as well as many of their vertebrate homologues, are expressed during the development of the nervous system (for example, ref. 3). Are these genes involved in specifying the identity of individual neurons during neurogenesis, just as they specify the identity of cells during segmentation? We previously described the CNS expression of the segmentation gene fushi tarazu (ftz) and showed that ftz CNS expression is involved in the determination of an identified neuron³. Here we show that another segmentation gene, even-skipped (eve), is expressed in a different but overlapping subset of neurons. Temperature-sensitive inactivation of the eve protein during neurogenesis alters the fate of two of these neurons. Our results indicate that the nuclear protein products of the eve and ftz segmentation genes are components of the mechanism controlling cell fate during neuronal development.

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