title: Translation from nonautonomous type IAP retrotransposon is a critical determinant of transposition activity: implication for retrotransposon-mediated genome evolution.
abstract: Retrotransposons constitute a major component of the genome and their proliferation significantly impacts genome evolution. Retrotransposons can propagate autonomously or nonautonomously. Nonautonomous type transposition occurs through trans-complementation by autonomous type retrotransposons. While autonomous type retrotransposons have been studied extensively, the translation products from nonautonomous type retrotransposons are not well characterized. In a previous study, we isolated both autonomous and nonautonomous type intracisternal A particle (IAP) elements from the mouse genome and established a tissue culture assay to examine trans-complementation of nonautonomous type IAP element. Using this system in the present study, we determined an active role for the translation product from nonautonomous type IAP element. Point mutations that either eliminated or truncated the IAP protein were introduced and their effects on trans-complementation were examined. Trans-complementation efficiency correlated with the expression of nonautonomous type IAP protein. The effect of nonautonomous type IAP protein was observed only when it was provided in cis, suggesting an interaction of nonautonomous type IAP protein and its transcript immediately after transcription. Interaction of autonomous and nonautonomous type IAP proteins was demonstrated by immunostaining and coimmunoprecipitation assay. Based on these findings, we propose a model in which nonautonomous type IAP protein associates with its transcript, recruits autonomous type IAP protein, and promotes the assembly of transposition competent IAP particle. The active role of the nonautonomous type IAP protein revealed in this study may provide a new insight into retrotransposon proliferation within the genome.
authors.affiliation: Department of Social and Environmental Medicine, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.
authors.forename: Ei-Suke
authors.initials: ES
authors.lastname: Saito
authors.forename: Vincent W
authors.initials: VW
authors.lastname: Keng
authors.forename: Junji
authors.initials: J
authors.lastname: Takeda
authors.forename: Kyoji
authors.initials: K
authors.lastname: Horie
mesh_terms: D000818:Animals; D004252:DNA Mutational Analysis; D019143:Evolution, Molecular; D007426:Genes, Intracisternal A-Particle; D005816:Genetic Complementation Test; D005822:Genetic Vectors; D016678:Genome; D006367:HeLa Cells; D006801:Humans; D051379:Mice; D014176:Protein Biosynthesis; D054730:Protein Interaction Domains and Motifs; D011506:Proteins / Q000737:chemistry / Q000235:genetics; D017384:Sequence Deletion
chemical_list: D011506:Proteins