LINE 1 (L1) is a successful retrotransposon that has amplified to high copy number in the mammalian genome; it makes up ∼17% of the human genome, and ∼19% of the mouse genome. In addition to constituting a large portion of the genome, it also plays an important role in the evolution of the genome, and has been implicated in a number of diseases. However, the details of its replication mechanism are incompletely understood. L1 encodes two proteins that are required for retrotransposition. These two proteins are both translated from a single dicistronic mRNA, yet are stoichiometrically required in different amounts. The 5' cistron on the mouse L1 mRNA, open reading frame 1 (ORF1), is unlikely to be translationally initiated by the conventional cap-dependent translation initiation because of the 1.8kb long and 62% G/C 5'UTR. The downstream cistron in mouse L1 mRNA, ORF2, cannot be translated by the conventional cap-dependent translation as it is 2942nt away from the cap and preceded by 17 AUG start codons. Using the dicistronic reporter assay, sequences upstream of the two open reading frames (ORFs) were found to have internal ribosome entry site (IRES) activities. Additional control experiments such as promoterless reporter assays and transfections of in vitro transcribed RNA confirmed that the apparent IRES activities were not due to artifacts of the assay. Various truncations suggested that the ORF1 IRES is modular, while the minimal ORF2 IRES was localized to a 53nt region within the coding sequence of ORF1. RNA secondary structure probing using selective 2'-hydroxyl acylation analyzed by primer extension (SHAPE) revealed that the two IRESes are relatively unstructured, with single-stranded regions that can potentially base pair with the 18S rRNA. Four nuclear proteins (hnRNP-R, nucleolin, syncrip, and hnRNP-L) were found to interact specifically with the ORF2 IRES using affinity chromatography and mass spectrometry. In summary, my thesis work has identified and characterized two IRESes of mouse L1, enhancing our understanding of L1 biology, particularly the role of translation control during L1 retrotransposition.