Mutations in histone modifying enzymes have dramatic effects on transmitting epigenetic information between generations. In C. elegans, the H3K4me2 demethylase, spr-5, and the H3K9me2 methyltransferase, met-2, synergize at fertilization to reprogram the epigenetic landscape and prevent the inappropriate expression of germ specific genes in the early zygote. If either enzyme is lost, developmental defects occur; both spr-5 and met-2 mutants display a progressive sterility phenotype. This phenotype is even more exacerbated in spr-5; met-2 double mutants, which exhibit maternal effect sterility and a severe developmental delay after a single generation. In mammals, orthologs of SPR-5, LSD1, and SPR-1, CoREST, physically associate, and in the absence of CoREST, LSD1 demethylase activity is impaired. In C. elegans, SPR-5 and SPR-1 interact in vitro, and worms deficient in SPR-5 or SPR-1 rescue the egg-laying defect observed in se1-12 mutants. These findings suggest that a more complex co-regulatory mechanism may exist where SPR-1 interacts with and regulates SPR-5 function. We hypothesize that this interaction is required at fertilization to ensure proper epigenetic reprogramming and development of the zygote. To test this hypothesis, we first compared progressive sterility in spr-1 vs. spr-5 mutants. Unlike spr-5 mutants, spr-1 worms do not become progressively sterile over many generations nor do they display any obvious morphological defects. Taking advantage of the severe developmental delay and sterility phenotypes observed in spr-5; met-2 mutants, we assessed whether these same phenotypes were present in met-2; spr-1 mutants. Interestingly, similar to spr-5; met-2 progeny, met-2; spr-1 progeny display sterility and developmental delay in a single generation, albeit not as severe as spr-5; met-2 mutants. While ~ 20% of met-2; spr-1 progeny are sterile in a single generation, we observe an increase to ~ 60% by generation 8, and this increase in sterility is accompanied by a decline in the total number of progeny. By generation 10, we observe an increase in the number met-2; spr-1 adult germlines that phenocopy the disorganized and under developed germline morphology that we observe in spr-5; met-2 mutants. Taken together, our data suggest SPR-1 regulates SPR-5 function, but also leaves open the possibility SPR-5 may interact with other proteins/complexes to program the epigenetic landscape at fertilization. With this, spr-1 emerges as an epigenetic player with implications for regulating epigenetic reprogramming and development.