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Division of Neurosciences, Beckman Research Institute, City of Hope National Medical Center, Duarte, CA 91010, USA.
We analyzed the distribution of long interspersed nuclear elements (LINE)-1 (L1) along mouse autosomes at a 1-Mb scale, and found a unique combination of high density and strand asymmetry of L1 elements at the imprinted Prader-Willi syndrome/Angelman syndrome (PWS/AS) locus on mouse chromosome 7. This L1 signature overlaps the paternally expressed domain of the locus, excluding the maternally expressed Ube3a gene, and is conserved in rat and human. Unlike the PWS/AS locus, other instances of high L1 density and strand asymmetry in the mouse are not associated with imprinted regions and are not evolutionarily conserved in human. The evolutionary conservation of the L1 signature at the PWS/AS locus despite differences in composition of L1 elements between rodent and human, requires a mechanism for active perpetuation of L1 asymmetry during bursts of L1 activity, and indicates a possible functional role for L1 elements at this locus. Aside from the PWS/AS locus, rodents have a far greater correlation of L1 densities between DNA strands than do humans; we provide evidence that this difference in interstrand correlation between the two taxa is due largely to the difference in average age of the dominant L1 families.
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