Background and Aims Endogenous pararetroviruses (EPRVs) are widespread components of plant genomes that originated from episomal DNA viruses of the Caulimoviridae family. Due to fragmentation and rearrangements, most EPRVs have lost their ability to replicate through reverse transcription and to initiate viral infection. Similar to the closely related retrotransposons, extant EPRVs were retained and often amplified in plant genomes for several million years. Here, we characterize the complete genomic EPRV fraction of the crop sugar beet (Beta vulgaris, Amaranthaceae) to understand how they shaped the beet genome and to suggest explanations for their absent virulence. Methods Using next- and third-generation sequencing data and genome assembly, we reconstructed full-length in silico representatives for the three host-specific EPRVs (beetEPRVs) in the B. vulgaris genome. Focusing on the endogenous caulimovirid beetEPRV3, we investigated its chromosomal localization, abundance and distribution by fluorescent in situ and Southern hybridization. Key Results Full-length beetEPRVs range between 7.5 and 10.7 kb in size, are heterogeneous in structure and sequence, and occupy about 0.3 % of the beet genome. Although all three beetEPRVs were assigned to the florendoviruses, they showed variably arranged protein-coding domains, different fragmentation, and preferences for diverse sequence contexts. We observed small RNAs that specifically target the individual beetEPRVs, indicating stringent epigenetic suppression. BeetEPRV3 sequences occur along all sugar beet chromosomes, preferentially in the vicinity of each other and are associated with heterochromatic, centromeric and intercalary satellite DNAs. BeetEPRV3 members also exist in genomes of related wild species, indicating an initial beetEPRV3 integration 13.4–7.2 million years ago. Conclusions Our study in beet illustrates the variability of EPRV structure and sequence in a single host genome. Evidence of sequence fragmentation and epigenetic silencing implies possible plant strategies to cope with long-term persistence of EPRVs, including amplification, fixation in the heterochromatin, and containment of EPRV virulence.

中文翻译：

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破碎、沉默和隐藏：驯服的内源性副逆转录病毒逃脱了从甜菜（Beta vulgaris）基因组中的消除

背景和目的内源性副逆转录病毒 (EPRV) 是植物基因组的广泛组成部分，起源于花茎病毒科的附加型 DNA 病毒。由于断裂和重排，大多数 EPRV 失去了通过逆转录复制和启动病毒感染的能力。与密切相关的逆转录转座子类似，现存的 EPRV 在植物基因组中保留并经常扩增数百万年。在这里，我们表征了作物甜菜（甜菜，苋科）的完整基因组 EPRV 部分，以了解它们如何塑造甜菜基因组，并对其缺乏毒力提出解释。方法使用下一代和第三代测序数据和基因组组装，我们在计算机中重建了普通小菜属基因组中三种宿主特异性 EPRV（甜菜EPRV）的全长代表。针对内源花椰菜病毒属甜菜EPRV3，我们通过荧光原位杂交和Southern杂交研究了其染色体定位、丰度和分布。主要结果 全长甜菜EPRV 大小在 7.5 至 10.7 kb 之间，结构和序列异质，约占甜菜基因组的 0.3%。尽管所有三种甜菜EPRV都属于弗洛伦多病毒，但它们表现出不同排列的蛋白质编码结构域、不同的片段化以及对不同序列背景的偏好。我们观察到专门针对单个甜菜EPRV 的小RNA，表明严格的表观遗传抑制。BeetEPRV3 序列沿着所有甜菜染色体出现，优先彼此相邻，并与异染色质、着丝粒和居间卫星 DNA 相关。BeetEPRV3 成员也存在于相关野生物种的基因组中，表明甜菜EPRV3 的初始整合发生在 13.4-720 万年前。结论 我们对甜菜的研究说明了单一宿主基因组中 EPRV 结构和序列的变异性。序列断裂和表观遗传沉默的证据表明植物可能采取应对 EPRV 长期存在的策略，包括扩增、固定在异染色质中以及遏制 EPRV 毒力。