Question

Read the following passage carefully.

While the phenotypic plasticity observed in *Daphnia magna* in response to predator kairomones has long been documented, the exact molecular mechanisms underlying this transgenerational defense strategy have only recently been elucidated. Historically, evolutionary biologists hypothesized that maternal stress hormones directly altered embryonic development. However, recent transcriptomic analyses demonstrate that kairomone exposure does not primarily affect hormone synthesis. Instead, the perception of predator-specific chemical cues by maternal olfactory receptors triggers a localized neuroendocrine signaling cascade that upregulates the expression of specific DNA methyltransferases in the germline. This enzymatic activity hypermethylates promoter regions of genes associated with carapace formation in the developing oocytes. Crucially, it is this precise epigenetic silencing of growth-regulating genes—rather than the presence of the kairomone itself or maternal stress hormones—that causes the morphological shift towards a hardened, defensive morphotype in the subsequent generation. Furthermore, the persistence of this phenotype relies entirely on the delayed demethylation of these loci during embryogenesis; if demethylation occurs prematurely, the default morphological pathway resumes, leaving the offspring vulnerable despite the initial maternal neuroendocrine response.

According to the passage, which one of the following most directly causes the morphological shift toward a defensive phenotype in the offspring of *Daphnia magna* exposed to predator kairomones?