Center for RNA Biology: From Genome to Therapeutics, Department of Biochemistry and Biophysics, Department of Urology, University of Rochester Medical Center, Rochester, United States
Li Huitong Xie
Center for RNA Biology: From Genome to Therapeutics, Department of Biochemistry and Biophysics, Department of Urology, University of Rochester Medical Center, Rochester, United States
Department of Genetics, Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, United States
Qiang Chen
Center for RNA Biology: From Genome to Therapeutics, Department of Biochemistry and Biophysics, Department of Urology, University of Rochester Medical Center, Rochester, United States
Dalia Ghoneim
Center for RNA Biology: From Genome to Therapeutics, Department of Biochemistry and Biophysics, Department of Urology, University of Rochester Medical Center, Rochester, United States
Bin Zhang
Department of Pathology and Laboratory Medicine, Department of Pediatrics, University of Rochester Medical Center, Rochester, United States
Jarra Jagne
Animal Health Diagnostic Center, Cornell University College of Veterinary Medicine, Ithaca, United States
Chengbo Yang
Department of Animal Science, University of Manitoba, Winnipeg, Canada
Center for RNA Biology: From Genome to Therapeutics, Department of Biochemistry and Biophysics, Department of Urology, University of Rochester Medical Center, Rochester, United States
PIWI-interacting RNAs (piRNAs) protect the germ line by targeting transposable elements (TEs) through the base-pair complementarity. We do not know how piRNAs co-evolve with TEs in chickens. Here we reported that all active TEs in the chicken germ line are targeted by piRNAs, and as TEs lose their activity, the corresponding piRNAs erode away. We observed de novo piRNA birth as host responds to a recent retroviral invasion. Avian leukosis virus (ALV) has endogenized prior to chicken domestication, remains infectious, and threatens poultry industry. Domestic fowl produce piRNAs targeting ALV from one ALV provirus that was known to render its host ALV resistant. This proviral locus does not produce piRNAs in undomesticated wild chickens. Our findings uncover rapid piRNA evolution reflecting contemporary TE activity, identify a new piRNA acquisition modality by activating a pre-existing genomic locus, and extend piRNA defense roles to include the period when endogenous retroviruses are still infectious.
