Whales, seals and others retain genetic remnants of a ‘second-nose’

When an animal moves from land to water, their senses don’t work the same in both media. Water affects light, sound and chemical cues, often to a dramatic degree, so if an organism transitioned from being a land-dweller to a water specialist, like scientists believe about whales, then they presumably had to undergo major changes to their sensory systems.

One sensory organ that seems to have changed during the evolution of aquatic mammals pertains to the vomeronasal organ. This organ is used for chemical detection in many mammals, in a way very similar to smell, so it is sometimes called a ‘second nose’. It often functions in detecting chemical signals (pheromones) used for communication, such as in horses or cats, or hunting prey, as can be seen in the tongue flicking of snakes and Komodo dragons.

So where is this vomeronasal organ? It’s a tiny structure located above the roof of the mouth, connected via small ducts coming from the mouth or the nose. When a snake flicks its tongue in and out, its putting chemicals it has collected on its tongue up into this organ to get an idea of where their prey has run off to.

So what’s so special about the vomeronasal organs of whales? Well, they don’t have one! But while modern whales do not have a vomeronasal organ, interestingly some of the earliest, land-dwelling whale fossils appear to have had it. However, as whales became increasingly aquatic, they appear to have lost it entirely.

But it’s one thing to show that some fossils that look like land-dwelling whales had an organ and that the aquatic ones didn’t, it’s another to show evidence of such an evolutionary event in modern whales.

One prediction of losing the vomeronasal organ during evolution is that any genes crucial for vomeronasal organ function would have been rendered nonfunctional genes (pseudogenes). One such gene, TRPC2 [1], is notably present as a pseudogene in the bottlenose dolphin and the fin whale [2], representing both major lineages of whales. Perhaps even more significantly, the pseudogenes of these two species share some of the same inactivating mutations, implying that the gene was knocked-out in their common ancestor.

What’s more is that other aquatic mammals also retain TRPC2 as a nonfunctional pseudogene, such as the harbor seal and river otter [2]. Manatees, representing an another aquatic lineage, also lack a vomeronasal organ, and after a quick analysis of a manatee genome, I found evidence that TRPC2 is also retained as a pseudogene in this mammal.

TRPC2 protein alignment aquatic mammals
TRPC2 protein alignment in aquatic mammals [2]. Upward-pointing arrows indicate inactivating mutations.
Vomeronasal organs aren’t just gone or reduced in aquatic mammals, however. The same is true for apes, Old World monkeys and some bats. As expected, these mammals not only don’t have a functional TRPC2, but you can find remnants of this gene in their genomes [3–5]. Furthermore, apes, including humans, share inactivating mutations with Old World monkeys, suggesting the organ was lost in our common ancestor with other apes and Afro-Asian monkeys.

So while you and I may wonder what it would be like to have a ‘second nose’ (how would food taste? How much worse would body odor be?), we’ll simply have to be content that our genomes provide a record of this organ in our distant ancestors.

Questions for Creationists

Why would the Creator create whales, seals, otters, apes, monkeys and bats with remnants of a defunct gene associated with an organ that these animals don’t have? If the TRPC2 pseudogene has a function imbued by the Creator, why don’t other mammals have a TRPC2 pseudogene? Why is it that only the mammals that lack a vomeronasal organ have this genetic trait? Is it a coincidence that there is fossil evidence that early whales had this organ before being lost, and this vomeronasal gene shows evidence of having been pseudogenized in the common ancestor of modern whales? Why do we share the same inactivating mutations as other apes and monkeys if we were created separately from them?

References

1. Stowers, L., Holy, T. E., Meister, M., Dulac, C., & Koentges, G. (2002). Loss of sex discrimination and male-male aggression in mice deficient for TRP2. Science, 295(5559), 1493-1500.

2. Yu, L., Jin, W., Wang, J. X., Zhang, X., Chen, M. M., Zhu, Z. H., … & Zhang, Y. P. (2010). Characterization of TRPC2, an essential genetic component of VNS chemoreception, provides insights into the evolution of pheromonal olfaction in secondary-adapted marine mammals. Molecular biology and evolution, 27(7), 1467-1477.

3. Liman, E. R., & Innan, H. (2003). Relaxed selective pressure on an essential component of pheromone transduction in primate evolution. Proceedings of the National Academy of Sciences, 100(6), 3328-3332.

4. Zhao, H., Xu, D., Zhang, S., & Zhang, J. (2010). Widespread losses of vomeronasal signal transduction in bats. Molecular biology and evolution, 28(1), 7-12.

5. Yohe, L. R., Abubakar, R., Giordano, C., Dumont, E., Sears, K. E., Rossiter, S. J., & Dávalos, L. M. (2017). Trpc2 pseudogenization dynamics in bats reveal ancestral vomeronasal signaling, then pervasive loss. Evolution, 71(4), 923-935.

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