In:
PLOS Genetics, Public Library of Science (PLoS), Vol. 19, No. 5 ( 2023-5-1), p. e1010566-
Abstract:
Transposable elements constitute nearly half of the mammalian genome and play important roles in genome evolution. While a multitude of both transcriptional and post-transcriptional mechanisms exist to silence transposable elements, control of transposition in vivo remains poorly understood. MOV10, an RNA helicase, is an inhibitor of mobilization of retrotransposons and retroviruses in cell culture assays. Here we report that MOV10 restricts LINE1 retrotransposition in mice. Although MOV10 is broadly expressed, its loss causes only incomplete penetrance of embryonic lethality, and the surviving MOV10-deficient mice are healthy and fertile. Biochemically, MOV10 forms a complex with UPF1, a key component of the nonsense-mediated mRNA decay pathway, and primarily binds to the 3′ UTR of somatically expressed transcripts in testis. Consequently, loss of MOV10 results in an altered transcriptome in testis. Analyses using a LINE1 reporter transgene reveal that loss of MOV10 leads to increased LINE1 retrotransposition in somatic and reproductive tissues from both embryos and adult mice. Moreover, the degree of LINE1 retrotransposition inhibition is dependent on the Mov10 gene dosage. Furthermore, MOV10 deficiency reduces reproductive fitness over successive generations. Our findings demonstrate that MOV10 attenuates LINE1 retrotransposition in a dosage-dependent manner in mice.
Type of Medium:
Online Resource
ISSN:
1553-7404
DOI:
10.1371/journal.pgen.1010566
DOI:
10.1371/journal.pgen.1010566.g001
DOI:
10.1371/journal.pgen.1010566.g002
DOI:
10.1371/journal.pgen.1010566.g003
DOI:
10.1371/journal.pgen.1010566.g004
DOI:
10.1371/journal.pgen.1010566.g005
DOI:
10.1371/journal.pgen.1010566.g006
DOI:
10.1371/journal.pgen.1010566.s001
DOI:
10.1371/journal.pgen.1010566.s002
DOI:
10.1371/journal.pgen.1010566.s003
DOI:
10.1371/journal.pgen.1010566.s004
DOI:
10.1371/journal.pgen.1010566.s005
DOI:
10.1371/journal.pgen.1010566.s006
DOI:
10.1371/journal.pgen.1010566.s007
DOI:
10.1371/journal.pgen.1010566.s008
DOI:
10.1371/journal.pgen.1010566.s009
DOI:
10.1371/journal.pgen.1010566.s010
DOI:
10.1371/journal.pgen.1010566.s011
DOI:
10.1371/journal.pgen.1010566.s012
DOI:
10.1371/journal.pgen.1010566.r001
DOI:
10.1371/journal.pgen.1010566.r002
DOI:
10.1371/journal.pgen.1010566.r003
DOI:
10.1371/journal.pgen.1010566.r004
DOI:
10.1371/journal.pgen.1010566.r005
DOI:
10.1371/journal.pgen.1010566.r006
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2023
detail.hit.zdb_id:
2186725-2
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