Repeated losses of PRDM9-directed recombination despite the conservation of PRDM9 across vertebrates

Author:

Baker Zachary1ORCID,Schumer Molly234ORCID,Haba Yuki5,Bashkirova Lisa6,Holland Chris47,Rosenthal Gil G47,Przeworski Molly12ORCID

Affiliation:

1. Department of Systems Biology, Columbia University, New York City, United States

2. Department of Biological Sciences, Columbia University, New York City, United States

3. Harvard Society of Fellows, Harvard University, Cambridge, United States

4. Centro de Investigaciones Científicas de las Huastecas 'Aguazarca', Hidalgo, Mexico

5. Department of Evolution, Ecology and Environmental Biology, Columbia University, New York City, United States

6. Department of Biochemistry and Molecular Biophysics, Columbia University, New York City, United States

7. Department of Biology, Texas A&M University, College Station, United States

Abstract

Studies of highly diverged species have revealed two mechanisms by which meiotic recombination is directed to the genome—through PRDM9 binding or by targeting promoter-like features—that lead to dramatically different evolutionary dynamics of hotspots. Here, we identify PRDM9 orthologs from genome and transcriptome data in 225 species. We find the complete PRDM9 ortholog across distantly related vertebrates but, despite this broad conservation, infer a minimum of six partial and three complete losses. Strikingly, taxa carrying the complete ortholog of PRDM9 are precisely those with rapid evolution of its predicted binding affinity, suggesting that all domains are necessary for directing recombination. Indeed, as we show, swordtail fish carrying only a partial but conserved ortholog share recombination properties with PRDM9 knock-outs.

Funder

National Institutes of Health

National Science Foundation

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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