Post-Transcriptional Control of LINE-1 Retrotransposition by Cellular Host Factors in Somatic Cells
Abstract
Long INterspersed Element-1 (LINE-1 or L1) retrotransposons form the only autonomously active family of transposable elements in humans. They are expressed and mobile in the germline, in embryonic stem cells and in the early embryo, but are silenced in most somatic tissues. Consistently, they play an important role in individual genome variations through insertional mutagenesis and sequence transduction, which occasionally lead to novel genetic diseases. In addition, they are reactivated in nearly half of the human epithelial cancers, contributing to tumor genome dynamics. The L1 element codes for two proteins, ORF1p and ORF2p, which are essential for its mobility. ORF1p is an RNA-binding protein with nucleic acid chaperone activity and ORF2p possesses endonuclease and reverse transcriptase activities. These proteins and the L1 RNA assemble into a ribonucleoprotein particle (L1 RNP), considered as the core of the retrotransposition machinery. The L1 RNP mediates the synthesis of new L1 copies upon cleavage of the target DNA and reverse transcription of the L1 RNA at the target site. The L1 element takes benefit of cellular host factors to complete its life cycle, however several cellular pathways also limit the cellular accumulation of L1 RNPs and their deleterious activities. Here, we review the known cellular host factors and pathways that regulate positively or negatively L1 retrotransposition at post-transcriptional level, in particular by interacting with the L1 machinery or L1 replication intermediates; and how they contribute to control L1 activity in somatic cells.
Related
- Nuclear NPR1 Modulates Salicylic Acid/Jasmonic Acid Crosstalk via Transcriptional Control of WRKY Transcription Factors
- Suppression of meiotic double-strand break formation in somatic cells by DREAM factors TCX5/6 maintains genome stability
- Cellular, chromatin-accessibility, and spatial contextualization of bulk transcriptional patterns linked to positive peritoneal cytology in endometrial cancer
- Assessment of the transcriptional and cellular effects of CRISPRa targeting Dopa decarboxylase and GTP cyclohydrolase 1 in HEK293 and SH-SY5Y cellular models of Parkinsonian neurotoxicity.
- Divergent transcriptional responses of conserved cellular machinery to warming and phosphorus limitation in freshwater phytoplankton
BibTeX
@article{pizarro2026posttranscriptional,
title = {{Post-Transcriptional Control of LINE-1 Retrotransposition by Cellular Host Factors in Somatic Cells}},
author = {Javier G Pizarro and Gaël Cristofari},
journal = {Frontiers in Cell and Developmental Biology},
year = {2026},
month = oct,
doi = {10.3389/fcell.2016.00014},
url = {https://hal.science/hal-05794249v1},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Post-Transcriptional Control of LINE-1 Retrotransposition by Cellular Host Factors in Somatic Cells
AU - Javier G Pizarro
AU - Gaël Cristofari
PY - 2026
DA - 2026/10/12
JO - Frontiers in Cell and Developmental Biology
DO - 10.3389/fcell.2016.00014
UR - https://hal.science/hal-05794249v1
AB - Long INterspersed Element-1 (LINE-1 or L1) retrotransposons form the only autonomously active family of transposable elements in humans. They are expressed and mobile in the germline, in embryonic stem cells and in the early embryo, but are silenced in most somatic tissues. Consistently, they play an important role in individual genome variations through insertional mutagenesis and sequence transduction, which occasionally lead to novel genetic diseases. In addition, they are reactivated in nearly half of the human epithelial cancers, contributing to tumor genome dynamics. The L1 element codes for two proteins, ORF1p and ORF2p, which are essential for its mobility. ORF1p is an RNA-binding protein with nucleic acid chaperone activity and ORF2p possesses endonuclease and reverse transcriptase activities. These proteins and the L1 RNA assemble into a ribonucleoprotein particle (L1 RNP), considered as the core of the retrotransposition machinery. The L1 RNP mediates the synthesis of new L1 copies upon cleavage of the target DNA and reverse transcription of the L1 RNA at the target site. The L1 element takes benefit of cellular host factors to complete its life cycle, however several cellular pathways also limit the cellular accumulation of L1 RNPs and their deleterious activities. Here, we review the known cellular host factors and pathways that regulate positively or negatively L1 retrotransposition at post-transcriptional level, in particular by interacting with the L1 machinery or L1 replication intermediates; and how they contribute to control L1 activity in somatic cells.
SN - 2296-634X
ER -