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Vol. 13, No. 4, pp. 472-483, February 15, 1999
Department of Molecular and Cell Biology, University of California,
Berkeley, California 94720-3204 USA
The Caenorhabditis elegans HSN motor neurons permit genetic
analysis of neuronal development at single-cell resolution. The egl-5 Hox gene, which patterns the posterior of the embryo, is required for both early (embryonic) and late (larval) development of
the HSN. Here we show that ham-2 encodes a zinc finger protein that acts downstream of egl-5 to direct HSN cell migration, an early differentiation event. We also demonstrate that the EGL-43 zinc
finger protein, also required for HSN migration, is expressed in the
HSN specifically during its migration. In an egl-5 mutant background, the HSN still expresses EGL-43, but expression is no longer
down-regulated at the end of the cell's migration. Finally, we find a
new role in early HSN differentiation for UNC-86, a POU homeodomain
transcription factor shown previously to act downstream of
egl-5 in the regulation of late HSN differentiation. In an unc-86; ham-2 double mutant the HSNs are defective in EGL-43
down-regulation, an egl-5-like phenotype that is absent in
either single mutant. Thus, in the HSN, a Hox gene, egl-5,
regulates cell fate by activating the transcription of genes encoding
the transcription factors HAM-2 and UNC-86 that in turn individually
control some differentiation events and combinatorially affect others.
[Key Words: ham-2; egl-5; unc-86; Hox; neuronal migration; zinc finger]
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