As a critical phase transition in plant development, seed germination is sensitive to salt stress. Several phytohormones including abscisic acid (ABA) and gibberellin (GA) are involved in the suppression of seed germination by salt stress. Emerging evidence suggests that long noncoding RNAs (lncRNAs) play a regulatory role in the response of plants to varying abiotic stresses. Many salt stress-responsive lncRNAs have been identified in different plant species; however, the molecular mechanisms underlying the epigenetic regulation of plant response to salt stress by lncRNAs remain largely unexplored. Here, we identified a salt stress-induced MtCIR2, a lncRNA in legume species Medicago truncatula, and found that overexpression and mutation of MtCIR2 led to reduced and enhanced seed germination under salt stress, respectively. The MtCIR2-dependent seed germination under salt stress was accounted for by an increase in the endogenous concentration of ABA and a decrease in the endogenous GA concentration. We further discovered that MtCIR2 interacted with BMI1, a core component of Polycomb Repressive Complex 1, which in turn enhanced H2A ubiquitination at the loci encoding ABA catabolic enzyme gene CYP707A2 and GA biosynthesis gene GA20ox1/2. This epigenetic silencing by MtCIR2 led to an increase in endogenous ABA and a decrease in GA concentration of germinating seeds, thereby suppressing seed germination under salt stress. These findings elucidate a novel mechanism by which lncRNA epigenetically regulates plant response to abiotic stress via histone ubiquitination, and highlight an intricate interplay between the lncRNA and epigenetic machinery in response to salt stress during seed germination.