The homeobox-containing mec-3 gene of C. elegans is expressed in 10 mechanosensory neurons and is necessary for these cells to acquire their fate. All the mec-3-expressing cells are anterior daughters from an asymmetric cell division. In this paper, we examine the expression of a mec-3--lacZ fusion in the presence of mutations that may disrupt asymmetric cell division or anterior-posterior positional information, as well as mutations that may specifically alter mec-3 expression. A mutation in lin-17 causes production of additional mec-3-expressing cells and can have its effect on the cell division that produces a mec-3-expressing cell. In a lin-5 mutant, in which postembryonic blast cells do not complete cell division and become polyploid, blast cells that would give rise to mec-3-expressing daughters instead express mec-3 themselves. In a lin-12 glp-1 double mutant, which is disrupted for many cell interactions in which two cells compete for the same fate, mec-3 expression is unaffected. These results are consistent with a model for asymmetric cell division in which the mec-3-expressing cell and its sister are different immediately upon cell division, rather than acquiring differences through later interaction with each other or their surroundings. lin-17 mutant animals also show defects in the position of the PVM cell and the PLM axons. Animals mutant in unc-73 and unc-40, known to have axon outgrowth defects, also show errors in PVM position and a low frequency of additional mec-3-expressing cells, as well as occasional secondary vulval protrusions, a common phenotype of lin-17 animals. Many other mutations have either no effect on mec-3 expression or an effect that can be largely predicted from previously known phenotypes: these include mab-5, mig-1, unc-53, egl-5, lin-32, and egl-27. unc-11 shows an unexpected and specific defect in mec-3 expression in the PVD neurons, but not in the other mec-3-expressing cells. Two mutations that suppress the egg-laying defect of unc-86 have no effect on the mec-3 expression defect in an unc-86 mutant.