ArticleScientific reports2016
The pioneering role of PRDM9 indel mutations in tarsier evolution.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Behavior of femaleOpen veterinary journal · 2025Article
- Multiple losses of aKRAB from PRDM9 coincide with a teleost-specific intron size distribution.BMC biology · 2024Article
- Evolution of the recombination regulator PRDM9 in minke whales.BMC genomics · 2022Article
- Pinpointing theFrontiers in genetics · 2021Article
- PRDM9, a driver of the genetic map.PLoS genetics · 2018Review
- PRDM9 and Its Role in Genetic Recombination.Trends in genetics : TIG · 2018Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PRDM9 is currently the sole speciation gene found in vertebrates causing hybrid sterility probably due to incompatible alleles. Its role in defining the double strand break loci during the meiotic prophase I is crucial for proper chromosome segregation. Therefore, the rapid turnover of the loci determining zinc finger array seems to be causative for incompatibilities. We here investigated the zinc finger domain-containing exon of PRDM9 in 23 tarsiers. Tarsiers, the most basal extant haplorhine primates, exhibit two frameshifting indels at the 5'-end of the array. The first mutation event interrupts the reading frame and function while the second compensates both. The fixation of this allele variant in tarsiers led to hypothesize that de- and reactivation of the zinc finger domain drove the speciation in early haplorhine or tarsiiform primates. Moreover, the high allelic diversity within Tarsius points to multiple effects of genetic drift reflecting their phylogeographic history since the Miocene.
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