Reestablishing the epigenetic ground state of the Caenorhabditis elegans (C. elegans) zygote is required for normal development and ensures that information is transferred properly from one generation to the next. Two epigenetic enzymes, the H3K4me2 demethylase, SPR-5, and the H3K9 methyltransferase, MET-2, are maternally deposited into the oocyte and cooperate to reestablish the epigenetic ground state by modifying histone methylation. Progeny of worms lacking spr-5 and met-2 rapidly accumulate H3K4me2 resulting in somatic expression of spermatogenesis genes and sterility, while worms that lack both SPR-5 and MET-2 exhibit a maternal effect sterile phenotype. Compared to Wildtype, these double mutants display multiple developmental defects including, developmental delay, perturbed vulva formation, and defects in oogenesis. Despite this, the mechanisms by which SPR-5 and MET-2 transgenerationally regulate development is unclear. Here, we show that spr-5;met-2 mutant worm progeny exhibit a severe L2 developmental delay in both the germline and soma. This phenotype hints that there could be feedback between germline and soma. In addition, we discuss experimental approaches to examine the mechanisms by which SPR-5 and MET-2 regulate cell fate decisions during C. elegans development.