Seed germination, an initial stage of the plant life cycle, is sensitive to salt stress. Phytohormones such as abscisic acid (ABA) and gibberellins (GA) are involved in the suppression of seed germination by salt stress. Despite identification of numerous salt stress-responsive long noncoding RNAs (lncRNAs) in different vascular plants, the mechanisms by which lncRNAs regulate seed germination under salt stress at transcriptional and post-transcriptional levels are being deciphered. In the present study, we identified an intergenic lncRNA from Medicago truncatula, referred to as MtCIR1, and functionally characterized its role in response of seed germination to salt stress by over-expressing, anti-sensing and mutating MtCIR1 in M. truncatula. We found that MtCIR1 negatively regulated seed germination under salt stress, such that over-expressing and anti-sensing/mutating MtCIR21 reduced and enhanced seed germination, respectively. The MtCIR2-dependent seed germination was found to be accounted for by increases in endogenous ABA and decreases in GA levels of seeds due to down-regulating expression of ABA catabolic gene CYP707A4 and GA biosynthesis gene GA20ox1. We further found that MtCIR1 specifically interacted with SmD1b, a core spliceosomal component, which in turn may alter the stability of genes CYP707A2 and GA20ox1. These results suggest that MtCIR1 mediates seed germination under salt stress by remotely modulating alternative splicing of key downstream genes, thus disrupting endogenous ABA and GA homeostasis in seeds under salt stress. These findings highlight that alternative splicing is involved in regulation of lncRNA MtCIR1-dependent seed germination under salt stress by targeting ABA and GA metabolism.