Is somatic retrotransposition a parasitic or symbiotic phenomenon?

Abstract

The extraordinary evolutionary success of transposable elements (TEs) invites us to question the nature of the co-evolutionary dynamics between TE and host. Although sometimes assumed to be wholly parasitic, TEs have penetrated and spread throughout eukaryotic genomes at a rate unparalleled by other parasites. This near-ubiquity, occurring despite the potentially deleterious effects of insertional mutagenesis, raises the possibility that a counterbalancing benefit exists for the host. Such a benefit may act at the population level to generate genomic diversity within a species and hence greater adaptability under new selective pressures, or at the level of primary gain for the individual. Recent studies have highlighted the occurrence of retrotransposition events in the germline and discovered a surprisingly high rate of mobilization in somatic cells. Here we examine the available evidence for somatic retrotransposition and discuss how this phenomenon may confer a selective advantage upon an individual or species.

Figure 1. L1 is the main driver of retrotransposition in human cells. (A) L1 structure. ORF1 encodes an RNA-packaging protein and ORF2 encodes a protein (ORF2p) with endonuclease and reverse transcriptase domains.^, (B) Expression of L1 is limited by transcriptional repression and (C) post transcriptional regulation. (D) L1 ORF1p and ORF2p form an RNP with a marked cis preference, but ORF2p can also mobilize other RNAs with a polyA tail in trans. (E) Diverse effects of L1 insertional mutagenesis on gene expression. (F) L1 is known to be highly active during embryogenesis, and in neural cells (G), resulting in somatic mosaicism. Somatic retrotransposition in other adult tissues may also occur.