The short interspersed elements (SINEs) comprise a significant portion of mammalian genomes and regulate gene expression through a variety of mechanisms. We found that 4.5SH, a rodent-specific abundant nuclear noncoding RNA that is highly homologous to the retrotransposon SINE B1, controls the expression of multiple genes containing the antisense insertion of SINE B1 through nuclear retention independently of the A-to-I editing. The depletion of endogenous 4.5SH with antisense oligonucleotides changes the subcellular distribution of these target transcripts containing the antisense SINE B1. We also found that the 4.5SH RNA binds to the nuclear ds-RNA binding protein NF110, which is required for the nuclear retention mediated by 4.5SH. We propose that the amplification of the 4.5SH cluster in specific rodent species rapidly released hidden genetic diversity accumulated through the antisense insertion of SINE B1, having delineated the course of their evolution.