An active murine transposon family pair: Retrotransposition of "master" MusD copies and ETn trans-mobilization

摘要: LTR-retrotransposons have been found in all mammals which they sought, and can represent several percent of the genome mass (Boeke Stoye 1997; Lander et al. 2001; Waterston 2002). The complete sequencing human has left only a remote possibility that some might still be active, with exception few fully coding elements from HERV-K(HML2) family endogenous retroviruses (Lower 1996; Mayer 1999; Reus Turner 2001). In contrast, mouse genome, it long shown such as IAP sequences ETn (Early Transposon) are mobile, because responsible for most insertional mutagenesis events revealed by phenotypic mutations vivo (for review, see Kuff Lueders 1988; 1990; Ostertag Kazazian Jr. Baust Recently, gag, pro, pol genes autonomous transposition identified characterized their mobility ex assays (Dewannieux 2004). Conversely, involved numerous germ-line somatic mutations, indicating recent retrotransposition, although do not harbor full-length retroviral (Sonigo 1987). comprises 5.7-kb classified into two groups differing 3′-half LTR 5′-internal region (Shell 1990): I 200 copies per haploid C57BL/6J mice, II 40 (Baust 2003). Their expression is limited to embryos, peaking between embryonic days 3.5 (E3.5) E7.5 (Brulet 1985), well cell lines 1983; Shell 1987; Tanaka Ishihara related MusD elements, another murine LTR-retrotransposon (Mager Freeman 2000). hundred 7.5-kb-long containing similarities betaretroviruses. They share almost identical LTRs similar 3′ internal downstream gene, including polypurine tract (Fig. 1A). also 5′ upstream gag an intact primer binding site tRNALys—also (Kaghad 1985; 2003)—and possible packaging signal (described Mager It proposed derive recombinatory replacement unknown origin, colonized retrotransposition via complementation trans active present study was aimed at search characterization “master” copies, is, encode enzymatic structural proteins necessary own mobility, possibly mobilization elements. A genome-wide silico resulted identification nine we cloned assayed functionality. Interestingly, three tested proved transposition-competent behave high-efficiency mobile heterologous cells. We further demonstrate triggered thus strengthening “parasitic” relationship these classes elements. Figure 1. Structure rationale assay retrotransposition. (A) Genomic organization MusD, type (dark gray box) U3-R-U5 border ORFs homologous ...