the posterior body region, move to a central posi- 
tion along the animal's length, near its gonad. Mu- 
tations in two genes cause the SMs to terminate 
their migrations prematurely. These mutations ap- 
pear to alter an intercellular signaling system that 
controls SM migration by causing the SMs to be re- 
pelled by rather than attracted to a gonadal signal 
that normally directs the SM migration. 
IV Cell Differentiation. 
Genes involved in the differentiation of nerves 
and muscles have been identified. For example, 
many mutations have been shown to affect the de- 
velopment of the axon of the serotonergic her- 
maphrodite-specific neuron (HSN) motor neuron, 
which innervates the vulval muscles and stimulates 
egg laying. The HSN axon normally first grows ven- 
trally and then grows anteriorly; a single branch de- 
velops from this axon. These different aspects of 
HSN axonal outgrowth seem to be under separate 
genetic control: four genes affect ventral grovvT;h, 
PUBLICATIONS 
seven genes affect anterior growth, and, because 
the vulva induces HSN branch formation, a variety 
of genes identified on the basis of their function in 
vulval development (see above) affect branching. 
One of the genes involved in anterior HSN axonal 
outgrowth, unc-76, defines a component specifi- 
cally required for HSN growth within the ventral 
nerve cord. 
Muscle differentiation has been examined by 
identifying mutants abnormal in muscle structure 
and function. Five interacting genes involved in the 
regulation of muscle contraction have been identi- 
fied. One of these genes {unc-93) has been cloned 
and found to encode a novel protein with multiple 
putative transmembrane domains. The other four 
genes known to interact with unc-93 niay define 
other muscle membrane proteins or may define 
proteins that regulate the activity of unc-93- 
Dr. Horvitz is also Professor of Biology at the 
Massachusetts Institute of Technology and Neurobi- 
ologist at Massachusetts General Hospital. 
Articles 
Desai, C., Garriga, G., Mclntire, S., and Horvitz, H.R. 1988. A genetic pathway for the development of the 
Caenorhabditis elegans HSN motor neurons. Nature 336:638-646. 
Desai, C, and Horvitz, H.R. 1989. Caenorhabditis elegans mutants defective in the functioning of the motor 
neurons responsible for egg laying. Genetics 121:703-721. 
Finney, M., Ruvkun, G., and Horvitz, H.R. 1988. The C. elegans cell lineage and differentiation gene unc-86 
encodes a protein with a homeodomain and extended similarity to transcription factors. Cell 55:757-769. 
Herr, W, Sturm, R.A., Clerc, R.G., Corcoran, L.M., Baltimore, D., Sharp, P.A., Ingraham, H.A., Rosenfeld, M.G. , 
Finney, M., Ruvkun, G., and Horvitz, H.R. 1988. The POU domain: a large conserved region in the mamma- 
lian pit-1, oct-1, oct-2 and Caenorhabditis elegans unc-86 gene products. Genes Dev 2:1513-1516. 
Ruvkun, G., Ambros, V, Coulson, A., Waterston, R., Sulston, J., and Horvitz, H.R. 1989. Molecular genetics of 
the Caenorhabditis elegans heterochronic gene lin-14. Genetics 121:501-516. 
Sternberg, PW, and Horvitz, H.R. 1988. /m-i 7 mutations of Caenorhabditis elegans disrupt certain asymmet- 
ric cell divisions. Dev Biol 130:67-73. 
Sternberg, RW, and Horvitz, H.R. 1989. The combined action of two intercellular signaling pathways speci- 
fies three cell fates during vulval induction in C. elegans. Cell 58:679-693. 
Trent, C, Wood, WB., and Horvitz, H.R. 1988. A novel dominant transformer allele of the sex-determining 
gene her-1 of Caenorhabditis elegans. Genetics 120:145-^51 . 
492 
