Format: ORAL

Trude Schwarzacher1, Katja R. Richert-Poeggeler2, Osamah Alisaw3, Gilbert Chofong2, Kitty Vijverberg4, Pat Heslop- Harrison1

1 Department of Genetics and Genome Biology, Institute for Environmental Futures, University of Leicester, Leicester, United Kingdom 2 Julius Kuehn Institute, Federal Research Centre for Cultivated Plants, Institute for Epidemiology and Pathogen Diagnostics, Braunschweig, Germany 3 Department of Plant Protection, Faculty of Agriculture, University of Kufa, Kufa, Iraq 4 Radboud University, Institute for Water and Wetland Research (IWWR), Nijmegen, Netherlands

Pararetroviruses (PRVs) share a common origin with retroviruses and LTR retrotransposons employing reverse transcription for genome replication. In plants, both episomal and chromosomal (endogenous; EPRVs) forms are present. Pararetrovirus evolution most likely occurred through recombination of an ancestral genomic retroelement with exogenous RNA viruses and resulted in horizontal gene transfer. Illegitimate recombination probably also facilitated pararetrovirus integration into the host genomes using virus sequences instead of homologous host genomic sequences on the sister chromatid (during mitosis) or homologous chromosome (during meiosis). RNA interference initiated in the host, regulates episomal and chromosomal pararetrovirus forms, while pararetroviruses themselves have evolved suppressors against this plant defense. Analysing genome and raw read sequences as well as small (sm)RNA databases revealed three types of EPRV clusters comprising petuvirus-, florendovirus- and caulimovirus-like sequences along with two distinct variants of Petunia vein clearing virus (ePVCV-1 and -2) in wild and hybrid petunia. Both ePVCV variants increased in copy number in P. hybrida, a diploid hybrid of P. axillaris and P. inflata, while exhibiting differences in sequences, organization and activity patterns. ePVCV-1 shared 99% sequence identity with the known episomal PVCV and host smRNAs mapped throughout its genome, likely serving as template for initiating episomal PVCV replication in P. hybrida.  ePVCV-2, with only 74% similarity, lacked some regulatory elements and homologous smRNAs, rendering it replication incompetent. In the permissive genomes P. axillaris and P. hybrida, we found the pericentromeric regions to be hot spots for EPRV integration. In PVCV infected P. parodii, with no detectable ePVCV but episomally replicating PVCV, de novo integration of PVCV in the telomeric regions of a single chromosome was identified.  We postulate that the pericentromeric insertions are older and silenced while telomeric ePVCV localizations of some P. hybrida lines indicate recent, transient activation of ePVCV-1 and de novo integration.