Over the last several years we have been characterizing the NK-2 homeodomain family in C. elegans. During the course of this work we have also studied a related homeobox gene, since named
ceh-29. CEH-29 is a member of the bsh (brain specific homeobox) family (thanks to T. Burglin for help in classification). The founding member of this family, Drosophila bsh, is expressed exclusively in the brain where it is thought to play a highly specialized role in the determination and function of brain cell types (Jones and McGinnis, 1993).
ceh-29 was initially identified by the genome sequencing project. The gene maps to chromosome II (cosmid F31E8) between
dpy-10 and
cyp-10 with the gene
snt-1 located ~7kb downstream. As a starting point in our analysis of
ceh-29 we used phage libraries to isolate genomic DNA and a putative full length cDNA. The cDNA clone allowed us to determine that CEH-29 was a relatively small protein (190aa), containing a homeodomain and a number of acidic regions. To determine where the
ceh-29 promoter was active, we created
ceh-29::gfp and lacZ fusions. In transgenic lines, reporter expression was first detected during early embryogenesis (~100 cells) in what appeared to be neuronal precursors. Reporter expression continued in neuronal cells reaching very high levels. In early larval development, cell proccesses of numerous neural cells could be clearly observed. To determine the consequences of loss of function of
ceh-29, we carried out
ceh-29 RNAi in wild-type animals. The F1 offspring of injected animals were then scored for visible phenotypes. In these animals we observed a low penetrance L1 scrawny arrest phenotype, with the majority appearing wild-type We have not characterized this gene further. Anyone interested in analyzing the neuronal
ceh-29::gfp expression pattern, or further investigating the
ceh-29 loss of function phenotype should contact us. B. Jones and W. McGinnis (1993). A new Drosophila homeobox gene, bsh, is expressed in a subset of brain cells during embryogenesis. Development 117, 793-806.