ABSTRACT
Retrotransposons are ubiquitous and major components of plant genomes, and are characteristically retroviral-like in their genomic structure and in the major proteins encoded. Nevertheless, few have been directly demonstrated to be transcribed or reverse transcribed. The BARE-1 retrotransposon family of barley (Hordeum vulgare) is highly prevalent, actively transcribed, and contains well conserved functional regions. Insertion sites for BARE-1 are highly polymorphic in the barley genome. Here we show that BARE-1 is translated and the capsid protein (GAG) and integrase (IN) components of the predicted polyprotein are processed into polypeptides of expected size. Some of the GAG sediments as virus-like particles together with IN and with BARE-1 cDNA. Reverse transcriptase activity is also present in gradient fractions containing BARE-1 translation products. Virus-like particles have also been visualized in fractions containing BARE-1 components. Thus BARE-1 components necessary for carrying out the life cycle of an active retrotransposon appear to be present in vivo, and to assemble. This would suggest that post-translational mechanisms may be at work to prevent rapid genome inflation through unrestricted integration.
ABSTRACT
The replicative retrotransposon life cycle offers the potential for explosive increases in copy number and consequent inflation of genome size. The BARE-1 retrotransposon family of barley is conserved, disperse, and transcriptionally active. To assess the role of BARE-1 in genome evolution, we determined the copy number of its integrase, its reverse transcriptase, and its long terminal repeat (LTR) domains throughout the genus Hordeum. On average, BARE-1 contributes 13.7 x 10(3) full-length copies, amounting to 2.9% of the genome. The number increases with genome size. Two LTRs are associated with each internal domain in intact retrotransposons, but surprisingly, BARE-1 LTRs were considerably more prevalent than would be expected from the numbers of intact elements. The excess in LTRs increases as both genome size and BARE-1 genomic fraction decrease. Intrachromosomal homologous recombination between LTRs could explain the excess, removing BARE-1 elements and leaving behind solo LTRs, thereby reducing the complement of functional retrotransposons in the genome and providing at least a partial "return ticket from genomic obesity."
