Abstract
LINE-1 (long interspersed element 1) is an autonomous non-long terminal repeat retrotransposon. Its replication often causes mutation and rearrangement of host genomic DNA. Accordingly, host cells have evolved mechanisms to control LINE-1 mobility. Here, we report that a helicase named MOV10 effectively suppresses LINE-1 transposition. Mutating the helicase motifs impairs this function of MOV10, suggesting that MOV10 requires its helicase activity to suppress LINE-1 replication. Further studies show that MOV10 post-transcriptionally diminishes the level of LINE-1 RNA. The association of MOV10 with both LINE-1 RNA and ORF1 suggests that MOV10 interacts with LINE-1 RNP and consequently causes its RNA degradation. These data demonstrate collectively that MOV10 contributes to the cellular control of LINE-1 replication.
Highlights
Retrotransposon LINE-1 causes dozens of genetic diseases
Moloney leukemia virus type 10 protein (MOV10) Overexpression Diminishes LINE-1 Retrotransposition— To monitor LINE-1 activity, we used in the following experiments a CMV-L1-neoRT reporter construct that has a neomycin resistance gene inserted in the 3Ј-UTR of LINE-1 in the opposite direction from the LINE-1 coding sequence (Fig. 1A) [45]
Such a design ensures that a functional neomycin resistance mRNA can only be produced from the reverse transcribed LINE-1 DNA in which the intron should have been removed during RNA splicing
Summary
Retrotransposon LINE-1 causes dozens of genetic diseases. Results: Human MOV10 diminishes the level of LINE-1 RNA by acting at a post-transcriptional stage. We report that a helicase named MOV10 effectively suppresses LINE-1 transposition. Mutating the helicase motifs impairs this function of MOV10, suggesting that MOV10 requires its helicase activity to suppress LINE-1 replication. To control massively activated LINE-1, germ line cells express a special type of small RNA named piRNA (piwi-interacting RNA) that arms Piwi (P-element induced wimpy testis) proteins to suppress LINE-1 [25, 26]. Several reports have demonstrated that MOV10 inhibits the replication of lentiviruses including human immunodeficiency virus type 1 (HIV-1) This inhibition depends on the incorporation of MOV10 into HIV-1 particles and the impediment of viral reverse transcription [42,43,44]. We report that MOV10 restricts the mobilization of LINE-1, which further demonstrates MOV10 as an important player in host defense against exogenous and endogenous parasitic genetic elements
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
