Control of neuronal fate by the XXXX segmentation gene even-skipped.

@entity238 @entity19235 @entity19234
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 @entity238 embryogenesis. Interestingly, most of the segmentation and homoeotic genes in @entity238 , 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 @entity19234 (ftz) and showed that ftz CNS expression is involved in the determination of an identified neuron. Here we show that another segmentation gene, even-skipped ( @entity19235 ), is expressed in a different but overlapping subset of neurons. Temperature-sensitive inactivation of the @entity19235 protein during neurogenesis alters the fate of two of these neurons. Our results indicate that the nuclear protein products of the @entity19235 and ftz segmentation genes are components of the mechanism controlling cell fate during neuronal development.
