To survive and spread, many mobile genetic elements must be expressed by their hosts. This requires both regulatory activity, and subversion of host defence mechanisms. How retrotransposons, such as human LINE1, meet these requirements remains unclear. Here, we perform saturating mutagenesis of the ~1kb human LINE1 promoter across 8 cellular contexts, which coupled with ORF screens, provides a comprehensive picture of how LINE1 achieves expression in the host. We identify a set of 3 regulatory regions that are essential irrespective of cellular context, and a variety of cell-type specific transcription factor binding sites with important contributions to activity. The universally most important site has been previously reported to be a RUNX binding site. We demonstrate that it is, in fact, a U1 splice donor site. Despite containing no introns, human LINE1 requires a U1 donor site to subvert transcriptional surveillance by the Restrictor complex, which in its absence, triggers premature termination of RNA Pol II. To minimise detrimental splicing, the U1 donor is sub-optimal, and the LINE1 sequence is devoid of strong splice acceptors. Importantly, the acquisition of a U1 site appears to be a general requirement for retrotransposons, and consequently, splice donors have evolved convergently in non-LTR retrotransposons from a variety of species. Altogether, this suggests that mobile genetic elements evolve mechanisms to subvert host transcriptional surveillance pathways, which may have evolved to help defend against transposon invasion and activity.