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Abstract Five to ten percent of mammalian genomes is occupied by multiple clades of endogenous retroviruses (ERVs), that may count thousands of members. New ERV clades arise by retroviral infection of the germline followed by expansion by reinfection and/or retrotransposition. ERV mobilization is a source of deleterious variation, driving the emergence of ERV silencing mechanisms, leaving “DNA fossils”. Here we show that the ERVK2-1-LTR clade is still active in the bovine and a source of disease-causing alleles. We develop a method to measure the rate of ERVK2-1-LTR mobilization, finding an average of 1 per ~150 sperm cells, with >10-fold difference between animals. We perform a genome-wide association study and identify eight loci affecting ERVK2-1-LTR mobilization. We provide evidence that polymorphic ERVK2-1-LTR elements in four of these loci cause the association. We generate a catalogue of full length ERVK2-1-LTR elements, and show that it comprises 15% of C -type autonomous elements, and 85% of D -type non-autonomous elements lacking functional genes. We show that >25% of the variance of mobilization rate is determined by the number of C -type elements, yet that de novo insertions are dominated by D -type elements. We propose that D -type elements act as parasite-of-parasite gene drives that may contribute to the observed demise of ERV elements.
Tang et al. (Sat,) studied this question.