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(1-5). LINE-1 expression is low in most differentiated cells but high in some cancer cells, in testis and during embryonic development(6-12). To minimize the negative impact on their hosts genomes,, many mobile elements strategically limit their amplification potential, particularly in somatic cells(13-15). 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(16).
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