The two somatic gonadal progenitors (SGPs) of Caenorhabditis elegans are multipotent progenitor cells that give rise to all somatic tissues of the reproductive system, including uterus, sheath, spermatheca, distal tip cells and the anchor cell. Their sister cells are head mesodermal cells (hmcs), one undergoes programmed cell death and the other terminally differentiates shortly after it is born. We use this cell fate decision – SGP versus hmc – as a simple and genetically tractable model to understand the determinants of multipotency. Forward and reverse genetic approaches have identified hnd-1/dHand, let-381/FoxF and three different subunits of the SWI/SNF chromatin remodeling complex (swsn-1, swsn-4, and pbrm-1) as regulators of the SGP/hmc cell fate decision. Loss-of-function mutants in any of these genes have fewer than the normal number of SGPs and when the SGPs are present, they often express a marker that is characteristic of the hmc, suggesting that mutant SGPs are partially transformed into hmcs. We examined hnd-1; pbrm-1 double mutants and found that they have a synergistic phenotype, indicating that hnd-1 and SWI/SNF act in parallel. We also found that let-381 is co-expressed with hnd-1 in the SGPs and hnd-1 promoter deletions that remove three predicted LET-381 binding sites abolish expression of a rescuing hnd-1::GFP reporter in SGPs. Taken together, our data support a model in which let-381 acts upstream of hnd-1 and the SWI/SNF complex acts in parallel to hnd-1 to regulate gene expression in SGPs. HND-1 is a transcription factor and SWI/SNF chromatin remodeling complexes influence gene expression by altering chromatin structure. Therefore, a simple model is that SWI/SNF acts by facilitating the binding of HND-1 to its target genes to regulate gene expression in SGPs. SWI/SNF chromatin remodeling complexes are important for the proliferation of mammalian multipotent progenitors. The identification of downstream targets of SWI/SNF in the SGP/hmc cell fate decision may therefore uncover conserved molecular mechanisms regulating multipotency in diverse species.