TY - JOUR
T1 - A pedigree-based map of recombination in the domestic dog genome
AU - Campbell, Christopher L.
AU - Bhérer, Claude
AU - Morrow, Bernice E.
AU - Boyko, Adam R.
AU - Auton, Adam
N1 - Funding Information:
We thank Yu Kong and Anthony Marcketta for their helpful discussions and assistance in the analysis of this data. We thank Liz Corey and the Cornell Veterinary Biobank for their assistance in pedigree analysis of the colony. C.L.C. was supported by a Training Program in Cellular and Molecular Biology and Genetics, T32 GM007491. C.B. was supported by a postdoctoral fellowship from the Fonds de la Recherche en Santé du Québec. Data in this paper are from a thesis to be submitted in partial fulfillment of the requirements for the Degree of Doctor of Philosophy in the Graduate Division of Medical Sciences, Albert Einstein College of Medicine, Yeshiva University for C.L.C.
Publisher Copyright:
© 2016 Campbell et al.
PY - 2016
Y1 - 2016
N2 - Meiotic recombination in mammals has been shown to largely cluster into hotspots, which are targeted by the chromatin modifier PRDM9. The canid family, including wolves and dogs, has undergone a series of disrupting mutations in this gene, rendering PRDM9 inactive. Given the importance of PRDM9, it is of great interest to learn how its absence in the dog genome affects patterns of recombination placement. We have used genotypes from domestic dog pedigrees to generate sex-specific genetic maps of recombination in this species. On a broad scale, we find that placement of recombination events in dogs is consistent with that in mice and apes, in that the majority of recombination occurs toward the telomeres in males, while female crossing over is more frequent and evenly spread along chromosomes. It has been previously suggested that dog recombination is more uniform in distribution than that of humans; however, we found that recombination in dogs is less uniform than in humans. We examined the distribution of recombination within the genome, and found that recombination is elevated immediately upstream of the transcription start site and around CpG islands, in agreement with previous studies, but that this effect is stronger in male dogs. We also found evidence for positive crossover interference influencing the spacing between recombination events in dogs, as has been observed in other species including humans and mice. Overall our data suggests that dogs have similar broad scale properties of recombination to humans, while fine scale recombination is similar to other species lacking PRDM9.
AB - Meiotic recombination in mammals has been shown to largely cluster into hotspots, which are targeted by the chromatin modifier PRDM9. The canid family, including wolves and dogs, has undergone a series of disrupting mutations in this gene, rendering PRDM9 inactive. Given the importance of PRDM9, it is of great interest to learn how its absence in the dog genome affects patterns of recombination placement. We have used genotypes from domestic dog pedigrees to generate sex-specific genetic maps of recombination in this species. On a broad scale, we find that placement of recombination events in dogs is consistent with that in mice and apes, in that the majority of recombination occurs toward the telomeres in males, while female crossing over is more frequent and evenly spread along chromosomes. It has been previously suggested that dog recombination is more uniform in distribution than that of humans; however, we found that recombination in dogs is less uniform than in humans. We examined the distribution of recombination within the genome, and found that recombination is elevated immediately upstream of the transcription start site and around CpG islands, in agreement with previous studies, but that this effect is stronger in male dogs. We also found evidence for positive crossover interference influencing the spacing between recombination events in dogs, as has been observed in other species including humans and mice. Overall our data suggests that dogs have similar broad scale properties of recombination to humans, while fine scale recombination is similar to other species lacking PRDM9.
KW - Canine genetics crossover
KW - Interference hotspots PRDM9 recombination
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U2 - 10.1534/g3.116.034678
DO - 10.1534/g3.116.034678
M3 - Article
AN - SCOPUS:84996486919
SN - 2160-1836
VL - 6
SP - 3517
EP - 3524
JO - G3 (Bethesda, Md.)
JF - G3 (Bethesda, Md.)
IS - 11
ER -