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Life sciences · Journal article
Life Science Alliance · November 4, 2026
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SNORD116 is a small nucleolar RNA deficient in Prader-Willi syndrome individuals. The mechanisms by which SNORD116 conveys its effects are unknown. Here, transcriptomic analysis showed that diacylglycerol kinase kappa (Dgkk) expression was elevated in the hypothalamus of Snord116-deficient mice. In silico analyses predicted a strong RNA:RNA interaction between Snord116 and Dgkk mRNA that is fully conserved in mouse and human. In vitro experiments in human cellular models demonstrated that SNORD116 mediates 2'-O-methylation of DGKK mRNA and regulates DGKK mRNA and protein expression. In Snord116-deficient mouse neurons, increased Dgkk expression was associated with attenuated diacylglycerol-mediated activation of ERK and PKC, critical elements in neuronal signaling cascades. In mice, brain Dgkk expression peaks during late embryonic and early postnatal periods, coinciding with peak rates of neurogenesis; its expression in adults is restricted mainly to brain regions implicated in Prader-Willi syndrome pathophysiology, including the arcuate nucleus of the hypothalamus. Fasting acutely decreased hypothalamic Dgkk expression in wild-type mice. Increased Dgkk expression in Snord116-deficient mice could reflect derangements in this pathway that affects both brain development and cell-specific functions.