Abstract
Long interspersed elements (LINE-1s, also called L1s) are the only active members of the autonomous, non-long terminal repeat (LTR) retrotransposon family, which reshapes mammalian genomes in many different ways. LINE-1 expression is low in most differentiated cells but high in some cancer cells, in testis and during embryonic development. To minimize the negative impact on their hosts' genomes, many mobile elements strategically limit their amplification potential, particularly in somatic cells. Here we show that the A-rich coding strand of the human LINE-1 contains multiple functional canonical and noncanonical polyadenylation (poly(A)) signals, resulting in truncation of full-length transcripts by premature polyadenylation. This attenuation lowers the rate of retrotransposition in assays using HeLa cells. It probably also increases the negative effects of LINE-1 insertions into genes.
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