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Comparative Study
. 2003 Jul 8;100(14):8337-41.
doi: 10.1073/pnas.1331721100. Epub 2003 Jun 25.

Evolutionary deterioration of the vomeronasal pheromone transduction pathway in catarrhine primates

Jianzhi Zhang  1 , David M Webb
Affiliations
Comparative Study

Evolutionary deterioration of the vomeronasal pheromone transduction pathway in catarrhine primates

Jianzhi Zhang et al. Proc Natl Acad Sci U S A. .

Abstract

Pheromones are water-soluble chemicals released and sensed by individuals of the same species to elicit social and reproductive behaviors or physiological changes; they are perceived primarily by the vomeronasal organ (VNO) in terrestrial vertebrates. Humans and some related primates possess only vestigial VNOs and have no or significantly reduced ability to detect pheromones, a phenomenon not well understood at the molecular level. Here we show that genes encoding the TRP2 ion channel and V1R pheromone receptors, two components of the vomeronasal pheromone signal transduction pathway, have been impaired and removed from functional constraints since shortly before the separation of hominoids and Old World monkeys approximately 23 million years ago, and that the random inactivation of pheromone receptor genes is an ongoing process even in present-day humans. The phylogenetic distribution of vomeronasal pheromone insensitivity is concordant with those of conspicuous female sexual swelling and male trichromatic color vision, suggesting that a vision-based signaling-sensory mechanism may have in part replaced the VNO-mediated chemical-based system in the social/reproductive activities of hominoids and Old World monkeys (catarrhines).

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Figures

Fig. 1.
Fig. 1.
Structure of the TRP2 gene in 12 higher primates. The tree represents the current consensus on the phylogeny of these species. The branch lengths are not drawn to scale except for the timing of the two nodes with black dots. For each exon, “+” stands for the presence of an ORF, whereas “S” stands for the interruption of the reading frame by a premature stop codon, which may have resulted from either indels or point mutations. Shared premature stop codons among species within an exon are shown by “S,” whereas unshared ones are shown by “S*.” Exons with no signs are not sequenced. All primate TRP2 gene structures were determined by comparisons of the genomic DNA sequences with the mouse cDNA sequence.
Fig. 2.
Fig. 2.
Alignment of the first 120 nucleotides of the TRP2 exon 13 sequences from higher primates, rat, and mouse. Dots show identical nucleotides as in the human sequence. Premature stop codons are boxed. The entire exon has 393 nucleotides in the mouse. The sequences from the human, rat, and mouse are retrieved from GenBank (accession nos. X89067, NM_022638, and NM_011644).
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