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.
Highlights
Zinc fingers of anthropoid primates[7] and tarsiers, and discussed the possible function of PRDM9 as driving force behind the anthropoid-tarsiiform split and the divergence of the tarsiiform lineage
The examined exon of Western, Philippine and Sulawesi tarsiers was homologous to exon 11 of the human PRDM9 gene and was about 1037–1793 bp long depending on the number of zinc finger repeats
It could be divided into two parts, the 5′sequence and the 3′C2H2 zinc finger array
Summary
Zinc fingers of anthropoid primates[7] and tarsiers, and discussed the possible function of PRDM9 as driving force behind the anthropoid-tarsiiform split and the divergence of the tarsiiform lineage. Alleles 4, 5 and 6 have each ten zinc fingers with minor changes in the amino acid sequence (Fig. 3). Alleles of T. bancanus and T. syrichta are species-specific encoding zinc finger motifs not present in Sulawesi tarsiers.
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