Longevity is a complex trait influenced by environmental, genetic, and epigenetic factors. WDR-5, a member of the COMPASS complex, methylates histone 3 at lysine 4 (H3K4). Previously, the Brunet lab has shown that wdr-5 mutants are long-lived, and this longevity is inherited by wild-type descendants. We demonstrate that longevity in this background is a transgenerational phenotype that takes several generations to manifest after the loss of WDR-5. Consistent with the gradual appearance of longevity in wdr-5 mutant populations, we see that lifespan correlates with levels of dimethylation of histone 3 at lysine 9 (H3K9me2), a mark associated with repressive chromatin. This result suggests that H3K9me2 may be inherited transgenerationally and confer longevity in wdr-5 mutants. To examine this possibility, we mutated met-2, the methyltransferase required for all germline H3K9me2, in wdr-5 mutants. We show that the extended lifespan of wdr-5 mutants is dependent on met-2, further implicating H3K9me2 in the mechanism of longevity. Moreover, our finding that H3K9me2 is heritable indicates that it may also be involved in the inheritance of longevity in wdr-5 mutants. To test this possibility, we deleted met-2 in descendants of wdr-5 mutants, and find that the loss of met-2 abolishes the inheritance of longevity. Taken together, these data support a model in which H3K9me2 facilitates longevity and its epigenetic inheritance.