The modification of transcriptional regulation is a well-documented evolutionary mechanism in both plants and animals, but post-transcriptional controls have received less attention. The derived hermaphrodite of C. elegans has regulated spermatogenesis in an otherwise female body. PUF family RNA-binding proteins FBF-1 and FBF-2 limit XX spermatogenesis by repressing the male-promoting proteins FEM-3 and GLD-1. For my dissertation research, I examine the function of PUF homologs from other Caenorhabditis species, with emphasis on C. briggsae, which evolved selfing convergently. C. briggsae lacks a bona fide fbf-1/2 ortholog, but two members of the related PUF-2 subfamily, Cbr-puf-2 and Cbr-puf-1.2, do have a redundant germline sex determination role. Surprisingly, this is to promote, rather than limit, hermaphrodite spermatogenesis. I provide genetic, molecular, and biochemical evidence that Cbr-puf-2 and Cbr-puf-1.2 repress Cbr-gld-1 by a conserved mechanism. However, Cbr-gld-1 acts to limit, rather than promote, XX spermatogenesis. As with gld-1, no sex determination function for fbf or puf-2 orthologs is observed in gonochoristic Caenorhabditis. These results indicate that PUF family genes were coopted for sex determination in each hermaphrodite via their long-standing association with gld-1, and that their precise sex-determining roles depend on the species-specific context in which they act. Finally, I document non-redundant roles for Cbr-puf-2 in several aspects of somatic development. I show Cbr-puf-2 is required for reliable embryonic development, and that it is essential for vulval development and normal progression from early larval stage. I provide evidence suggesting that this latter role is related to pharyngeal muscle physiology. Thus, recently duplicated PUF paralogs, while redundant for some roles, can also rapidly acquire distinct non-redundant functions. This is consistent with theoretical models for the preservation of gene duplicates.