The Caenorhabditis elegans gene ham-2 links Hox patterning to migration of the HSN motor neuron (original) (raw)
- Paul D. Baum,
- Catherine Guenther,
- C. Andrew Frank,
- Binh V. Pham, and
- Gian Garriga
- Department of Molecular and Cell Biology, University of California, Berkeley, California 94720-3204 USA
Abstract
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.
Footnotes
↵Corresponding author.
E-MAIL garriga{at}peregrine.berkley.edu; FAX (510) 642-7000.
- Received August 5, 1998.
- Accepted December 29, 1998.
Cold Spring Harbor Laboratory Press