To begin a study of pattern formation in the early embryo, I have been analysing the role of an even-skipped homolog identified in the genomic sequence. eve homologs have been found in animals ranging from coral to human, and they are usually expressed at the posterior during gastrulation, in mesodermal (and sometimes ectodermal) tissue. The role of this posterior expression is not known in any organism. I found that vab-7 encodes this even-skipped homolog. Lack of vab-7 function results in gross posterior disorganization and uncoordinated behavior. By in situ hybridization, vab-7 RNA is first expressed during gastrulation in four cells at the extreme posterior end. Two of these cells are the right posterior muscle precursors Cppa and Cppp. By lineaging vab-7 mutant embryos, I found that about half of the Cppa and Cppp muscle cells are transformed into what appear to be hypodermal cells, the fate of some of the anterior C descendants. No defects were found in left posterior muscle cells. This left/right difference in vab-7 function in posterior muscle cells may be related to the more posterior location of right, versus left muscle precursors. Cpap is also defective: though it produces hypodermal cells as in wild-type, some are positioned too far anteriorly. These defects suggest that vab-7 may act to help blastomeres choose between anterior and posterior fates. What directs the early expression of vab-7 RNA? These cells could respond to a signal from neighboring cells, or they could inherit the ability to express vab-7. To distinguish between these models, I am examining the expression of vab-7 in mutant backgrounds in which neighboring blastomeres are transformed to different fates, and in which certain cells have been ablated. Preliminary results suggest that the early expression of vab-7 is at least partly governed by inherited factors. In L1 larvae, a vab-7/lacZ fusion gene is expressed in dorsal (but not ventral) posterior muscle cells, posterior hypodermal cells, and the posterior four P cells. This expression both overlaps and is posterior to that from the HOM-C genes mab-5 and egl-5, suggesting that vab-7 may function with them in anterior/posterior patterning. Consistent with this, egl-5 expression is reduced in vab-7 mutant embryos. To address this further, I have begun to look for other interactions between vab-7 and the HOM-C genes.