GWAS reveals determinants of mobilization rate and dynamics of an active endogenous retrovirus of cattle

Lijing Tang (), Benjamin Swedlund, Sébastien Dupont, Chad Harland, Gabriel Costa Monteiro Moreira, Keith Durkin, Maria Artesi, Eric Mullaart, Arnaud Sartelet, Latifa Karim, Wouter Coppieters, Michel Georges () and Carole Charlier ()
Additional contact information
Lijing Tang: University of Liège
Benjamin Swedlund: University of Liège
Sébastien Dupont: University of Liège
Chad Harland: University of Liège
Gabriel Costa Monteiro Moreira: University of Liège
Keith Durkin: University of Liège
Maria Artesi: University of Liège
Eric Mullaart: CRV
Arnaud Sartelet: University of Liège
Latifa Karim: University of Liège
Wouter Coppieters: University of Liège
Michel Georges: University of Liège
Carole Charlier: University of Liège

Nature Communications, 2024, vol. 15, issue 1, 1-18

Abstract: 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 ERVK[2-1-LTR] clade is still active in the bovine and a source of disease-causing alleles. We develop a method to measure the rate of ERVK[2-1-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 ERVK[2-1-LTR] mobilization. We provide evidence that polymorphic ERVK[2-1-LTR] elements in four of these loci cause the association. We generate a catalogue of full length ERVK[2-1-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.

Date: 2024
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-024-46434-1 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-46434-1

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-024-46434-1

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().