English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Natural variation in the zinc-finger-encoding exon of Prdm9 affects hybrid sterility phenotypes in mice

MPS-Authors
/persons/resource/persons227010

Abualia,  Khawla       
Research Group Meiotic Recombination and Genome Instability, Department Evolutionary Genetics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

/persons/resource/persons227020

Damm,  Elena       
Research Group Meiotic Recombination and Genome Instability, Department Evolutionary Genetics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

/persons/resource/persons201528

Ullrich,  Kristian K.       
Department Evolutionary Genetics (Tautz), Max Planck Institute for Evolutionary Biology, Max Planck Society;

/persons/resource/persons182643

Odenthal-Hesse,  Linda       
Research Group Meiotic Recombination and Genome Instability (Odenthal-Hesse), Max Planck Institute for Evolutionary Biology, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Abualia, K., Damm, E., Ullrich, K. K., Mukaj, A., Parvanov, E., Forejt, J., et al. (2024). Natural variation in the zinc-finger-encoding exon of Prdm9 affects hybrid sterility phenotypes in mice. Genetics, iyae004. doi:10.1093/genetics/iyae004.


Cite as: https://hdl.handle.net/21.11116/0000-000E-6424-9
Abstract
PRDM9-mediated reproductive isolation was first described in the progeny of Mus musculus musculus (MUS) PWD/Ph and Mus musculus domesticus (DOM) C57BL/6J inbred strains. These male F1-hybrids fail to complete chromosome synapsis and arrest meiosis at prophase I, due to incompatibilities between the Prdm9 gene and hybrid sterility locus Hstx2. We identified fourteen alleles of Prdm9 in exon 12, encoding the DNA-binding domain of the PRDM9 protein in outcrossed wild mouse populations from Europe, Asia, and the Middle East, eight of which are novel. The same allele was found in all mice bearing introgressed t-haplotypes encompassing Prdm9. We asked whether seven novel Prdm9 alleles in MUS populations and the t-haplotype allele in one MUS and three DOM populations induce Prdm9-mediated reproductive isolation. The results show that only combinations of the dom2 allele of DOM origin and the MUS msc1 allele ensure complete infertility of intersubspecific hybrids in outcrossed wild populations and inbred mouse strains examined so far. The results further indicate that MUS mice may share the erasure of PRDM9msc1 binding motifs in populations with different Prdm9 alleles, which implies that erased PRDM9 binding motifs may be uncoupled from their corresponding Prdm9 alleles at the population level. Our data corroborate the model of Prdm9-mediated hybrid sterility beyond inbred strains of mice and suggest that sterility alleles of Prdm9 may be rare.