Background and Aims The genus Fritillaria
(Liliaceae) comprises species with extremely large genomes (1C ¼ 30 000–127 000 Mb) and a bicontinental distribution. Most North American species (subgenus Liliorhiza) differ from Eurasian Fritillaria species by their distinct phylogenetic position and increased amounts of heterochromatin. This study examined the contribution of major repetitive elements to the genome obesity found in Fritillaria
and identified repeats contributing to the heterochromatin arrays in Liliorhiza species.
Methods Two Fritillaria
species of similar genome size were selected for detailed analysis, one from each phylogeographical clade: F. affinis
(1C ¼ 45.6 pg, North America) and F. imperialis
(1C ¼ 43.0 pg, Eurasia). Fosmid libraries were constructed from their genomic DNAs and used for identification, sequence characterization, quantification and chromosome localization of clones containing highly repeated sequences.
Key Results and Conclusions Repeats corresponding to 6.7 and 4.7% of the F. affinis
and F. imperialis
genome, respectively, were identified. Chromoviruses and the Tat lineage of Ty3/gypsy group long terminal repeat retrotransposons were identified as the predominant components of the highly repeated fractions in the F. affinis
and F. imperialis
genomes, respectively. In addition, a heterogeneous, extremely AT-rich satellite repeat was isolated from F. affinis
The FriSAT1 repeat localized in heterochromatic bands makes up approx. 26% of the F. affinis
genome and substantial genomic fractions in several other Liliorhiza species. However, no evidence of a relationship between heterochromatin content and genome size variation was observed. Also, this study was unable to reveal any predominant repeats which tracked the increasing/decreasing trends of genome size evolution in Fritillaria
. Instead, the giant Fritillaria genomes seem to be composed of many diversified families of transposable elements. We hypothesize that the genome obesity may be partly determined by the failure of removal mechanisms to counterbalance effectively the retrotransposon amplification.