Turtles, birds and crocodylians have genetic remnants of a ‘third eye’

Many lizards have a so-called ‘third eye’, more formerly known as a parietal or pineal eye, which is located smack dab in the middle of their heads.


If you dissect a parietal eye, you’ll see that it very much resembles a normal eye, with structures similar to a cornea, lens and retina, as well as a nerve projecting from the light-sensitive retinal cells.


Just like our normal (‘lateral’) eyes, these structures absorb light and translate it into electrical signals, which are then sent to the brain, communicating information about the abundance and composition of light in the environment. Though the function of the parietal eye is not fully agreed upon, it appears that it at least helps lizards to know how long they need to stay in the sun to warm up, since removing it or blocking it from sunlight leads to lizards staying out the sun longer than normal.

Basking monitor lizard

While this third eye is only found in lizards and the closely-related tuatara, there is evidence in the fossil record that it was formerly much more widespread. If you look at the skulls of many types of fossil reptiles, you’ll find a little hole at the top of their skulls, just like in modern day lizards that have a parietal eye. What’s also interesting is that some fossil species that show similarities to birds, crocodylians and turtles also have this hole in their skulls, despite the fact that these modern birds, crocs and turtles do not have a parietal eye.

Sequence of fossils from primitive reptiles to the earliest turtles

For example, the image above is a phylogenetic hypothesis showing a sequence of early reptiles that all have a hole at the top of their skulls (parietal foramen) until the appearance of some of the earliest turtles (Proganochelys).

Recent research has isolated a couple of proteins that are expressed in the parietal eyes of lizards. These proteins, parietopsin and parapinopsin, function as pigments that absorb light in the parietal eye [1].

Screen Shot 2017-06-16 at 3.47.37 PM
Iguana parietal eye with parapinopsin (magenta) and parietopsin (green) staining [1]
In a recent study [2], I found both the parapinopsin and parietopsin genes in birds, crocodylians and turtles, but they are full of mutations that prevent the formation of functional proteins. This is consistent with the idea that the ancestors of birds, crocodylians and turtles had parietal eyes with functional parietopsin and parapinopsin, but ultimately lost the need for them. The reasons for the loss of this organ are a bit mysterious, but the consistent story told by both genetics and the fossil record makes a convincing argument for these birds, crocs and turtles having evolved from animals with a third eye.

Questions for Creationists

Why did the Creator create birds, crocodylians, and turtles with remnants of genes that are found in the ‘third eyes’ of lizards? Is it just a coincidence that fossils of animals that look similar to these species had holes in their skulls that correspond with the parietal eye of lizards?


1. Wada, S., Kawano-Yamashita, E., Koyanagi, M., & Terakita, A. (2012). Expression of UV-sensitive parapinopsin in the iguana parietal eyes and its implication in UV-sensitivity in vertebrate pineal-related organs. PLoS One7(6), e39003.

2. Emerling, C. A. (2017). Archelosaurian Color Vision, Parietal Eye Loss, and the Crocodylian Nocturnal Bottleneck. Molecular biology and evolution34(3), 666-676.

Photo credit

Parietal eye 1, parietal eye 2, parietal eye 3, pre-turtle skullsbasking lizard


Why cats, hyenas and seals don’t love sugar

The molecular basis for taste is relatively straightforward. On your tongue, you have numerous taste buds that harbor cells with little proteins hanging out on the top. These proteins have the capacity to bind a number molecules on your tongue, and thereby transmit information regarding nutritional content.

Mammalian taste receptor proteins and molecules that activate them.

One of these proteins is TAS1R2, which, along with the protein TAS1R3, binds sweet tasting molecules. This sweet receptor is what allows you to savor the delicious sucrose (table sugar), fructose (fruit sugar) and even artificial sweeteners such as saccharin and aspartame. If you love cake, ice cream, and cookies, be grateful that you have a functional sweet receptor!

Not all animals are fortunate enough to enjoy these treats, however, and evolution is likely to be blamed. Many species are particularly adapted to eating foods that are nearly devoid of sugars, and therefore are not expected to benefit from maintenance of the gene encoding TAS1R2. Indeed, scientists [1] have found that a number of carnivorous mammals, including cats, hyenas, seals, the banded linsang, fossa and Asian small-clawed otter have a pseudogenized (nonfunctional) version of the TAS1R2 gene.

Examples of TAS1R2 pseudogenes in various carnivores

This helps explain why cats behaviorally seem uninterested in sugar. The scientists also confirmed that the Asian small-clawed otter also is not drawn to sweets, consistent with its TAS1R2 pseudogene. By contrast, they found that the spectacled bear, which has an intact TAS1R2 gene and is a known devourer of sweet things like fruits and honey, prefers sugary solutions over water.


These data suggest that the ancestral carnivores did eat sweets on occasion, but certain species avoided sugary foods for so long that sweet receptors were no longer necessary. Eventually mutations rendered the TAS1R2 gene nonfunctional in different carnivore lineages, rendering these species impervious to the effects of sweets.

Questions for Creationists

Why did God create some carnivores with a nonfunctional version of the sweet taste receptor gene? Would it not have made more sense for Him to create them without the gene altogether? Is it just a coincidence that He also created other animals with specialized feeding strategies, such as giant pandas and whales, to lack certain taste receptors?


1. Jiang, P., Josue, J., Li, X., Glaser, D., Li, W., Brand, J. G., … & Beauchamp, G. K. (2012). Major taste loss in carnivorous mammals. Proceedings of the National Academy of Sciences109(13), 4956-4961.

Photo Credit

Taste receptors, hyena, harbor seal, banded linsang,  fossa, otter, pseudogene figure, spectacled bear

Egg yolk gene remnants point to mammals’ egg-laying past

When children learn about different animals and how to classify them, they are often taught that three features unite mammals: hair, milk, and live birth. This last trait is likely taught to contrast mammals with the many other vertebrates that lay eggs.

But this last point is not correct. Nearly all mammals give birth to live young, but a handful do lay eggs. These are known as the monotremes, which encompass the platypus and several species of echidnas or spiny anteaters, all of which live in Australia, Tasmania and New Guinea.

The fact that a few mammals lay eggs, plus that most other land-dwelling vertebrates do as well, points to the idea that the rest of mammals descended from egg-layers. So how might one test this hypothesis? David Brawand and his colleagues [1] had the idea of looking at the genomes of mammals to see if they have any remnants of egg yolk genes.

Besides monotremes, the remaining mammals can be divided into two general groups: (1) marsupials, whose offspring are born early in development and then finish developing in a pouch (marsupium), and (2) placental mammals, which develop with the help of a placenta connecting the mother to the fetus. When Brawand and his colleagues looked at the genomes of three placental mammals (human, dog, armadillo), they found remnants of two egg-yolk genes (VIT1, VIT3), both of which possessed loss-of-function mutations. These mammals share some loss-of-function mutations in the genes, suggesting that the genes were inactivated in a common ancestor. Similarly, the researchers found remnants of three egg-yolk genes (VIT1, VIT2, VIT3) in the marsupials they studied (opossum, wallabies), with shared loss-of-function mutations in each (Figure 1), which, again, imply loss in a common ancestor.


Figure 1. DNA sequence alignment of egg-yolk genes [1]. Highlighted portions indicate loss-of-function mutations. Gallus gallus = chicken; Monodelphis domestica = opossum; Macropus eugenii and Wallabia bicolor = wallabies.

By contrast, at least one egg yolk gene is intact in the egg-laying platypus. Together, these data suggest that the inactivation of egg yolk genes in placental and marsupial mammals is connected with the loss of their egg-laying ability through evolutionary time.

Questions for Creationists

Why do mammals that do not lay eggs have non-functional egg yolk genes in their genomes? If these species do not lay eggs and didn’t evolve from ancestors that lay eggs, why would God have put these in their genomes? Why do some mammals share some identical loss-of-function mutations in their egg yolk genes genes?


1. Brawand, D., Wahli, W., & Kaessmann, H. (2008). Loss of egg yolk genes in mammals and the origin of lactation and placentation. PLoS Biol6(3), e63.

Photo credit

Platypus, platypus eggs, long-beaked echidna, echidna egg,

Why pandas can’t taste meat

Many animals are omnivorous, having a variegated diet ranging from vegetation to fruit, meat to insects, and a host of other items. Consequently, being able to taste and distinguish these foods likely aids in acquiring items that satisfy particular dietary needs.

Having a specialized diet, on the other hand, eliminates the need to taste everything. For example, if an animal is adapted to exclusively eating plant material, it probably would not need to be able to taste meat. But what happens when an herbivorous animal descends from ancestors that ate meat? Can we find evidence that it used to be able to taste meat, but subsequently lost it?


The giant panda (Ailuropoda melanoleuca) is an animal that eats bamboo almost exclusively, but this contrasts with other bears, which are generally omnivorous. It also contrasts with the evolutionary family that bears belong to, known as the carnivorans. Carnivorans, which encompass dogs, cats, weasels, mongooses, hyenas, and others, appear to have adapted to eating meat some 60+ million years ago. Consequently, giant pandas are oddballs in this group.

So how did this shift in dietary preference affect the giant panda’s ability to taste certain kinds of food? Taste in mammals depends on the function of taste receptor proteins encoded by different genes. There is a gene for sweet, two for sour, one for salty, many for bitter and one for savory/umami, the flavor you associate with eating meats and cheeses.

Predictably, carnivorans typically have a umami taste receptor gene, but the giant panda’s copy has become a nonfunctional pseudogene [1,2]. This was discovered by Li et al. [1], who reasonably infer that this is due to the history of giant pandas specializing on eating bamboo. As giant pandas transitioned from eating meat to plants, they probably no longer needed to retain the ability to taste meat. Natural selection wouldn’t have weeded out any mutations that would lead the loss of function in the savory taste gene, and that would subsequently become the norm for giant pandas.

Questions for Creationists

It’s understandable why God might have created giant pandas without the ability to taste meat, but why would He create them with a nonfunctional version of the savory taste gene? Would it not have made more sense to create them without the gene altogether? Why do we see a pattern of taste receptor loss in both the giant panda and whales? Why did God create just one bear that specializes on eating plants?


1. Li, R., Fan, W., Tian, G., Zhu, H., He, L., Cai, J., … & Zhang, Z. (2010). The sequence and de novo assembly of the giant panda genome. Nature463(7279), 311-317.

2. Zhao, H., Yang, J. R., Xu, H., & Zhang, J. (2010). Pseudogenization of the umami taste receptor gene Tas1r1 in the giant panda coincided with its dietary switch to bamboo. Molecular biology and evolution27(12), 2669-2673.

Photo credit

giant panda, clouded leopard, malagasy ring-tailed mongoose, raccoon dog, brown hyena

Sloth and armadillo vision pseudogenes suggest history of underground lifestyle

“The eyes [of the nine-banded armadillo] are rudimentary and practically useless. If disturbed an armadillo will charge off in a straight line and is as apt to run into a tree trunk as to avoid it.” [1]

“If an infant sloth is placed five feet away from its mother on a horizontal branch at the same level, at once the young sloth begins to cry, the mother shows that she heard it calling and turns her head in all directions. Many times she looks straight in the direction of her offspring but neither sight, hearing nor smell apparently avail anything.” [2]

“Infuriated male [sloths] try to hit each other when they are still distant by more than a metre and a half.” [2]

It doesn’t take an expert to read these quotes and recognize that sloths and armadillos have terrible vision! Taking advantage of this knowledge, I recently published a paper [3] where I examined the genes required for cone-based (i.e., bright light) vision in the nine-banded armadillo (Dasypus novemcinctus), Hoffmann’s two-toed sloth (Choloepus hoffmanni) and an extinct ground sloth (Mylodon darwinii).

What I discovered is that all three species have deleterious mutations in several cone-based genes, rendering them rod monochromats. Rod monochromats are predicted to have zero capacity for color vision and an inability to see in bright light conditions.

We had access to DNA for some more sloths and armadillos, so I sequenced fragments of a gene crucial for cone function (PDE6C). I confirmed that Linnaeus’ two-toed sloth (Choloepus didactylus), the pale-throated three-toed sloth (Bradypus tridactylus), big hairy armadillo (Chaetophractus villosus), six-banded armadillo (Euphrates sexcinctus), southern three-banded armadillo (Tolypeutes matacus), and giant armadillo (Priodontes maximus) are also rod monochromats.


Additionally, several armadillos and all four sloths share deleterious mutations, respectively, suggesting that this gene (PDE6C) was inactivated in common ancestors of these lineages.


Examples of deleterious mutations in various cone genes.

Why would sloths and armadillos lose their cone-based vision? Rod monochromacy has been found in animals that dive or live deep in the ocean or underground. The prevailing hypothesis is that natural selection wouldn’t maintain the ability to perceive bright light in animals that have lived in dark conditions for millions of years. If you live in complete darkness, what good to you is color vision?

In my last post I described how armadillos, sloths and anteaters, collectively known as xenarthrans, are more genetically similar to each other than to other mammals. An anatomical feature that unites them are extra articulations in their spine (“xenarthrous articulations). This extra bracing of the spine is useful for digging. Additionally, xenarthrans have a pelvis fused to their spine


long curved claws


and a second spine (=ridge) on their shoulder blade which allows for extra muscle attachment for digging


The retention of these traits in modern and extinct xenarthrans suggests that their last common ancestor was a digging animal. Further evidence of this is that the earliest known xenarthran had limb bones that were proportioned for digging.

Add all of this up: I proposed that the earliest xenarthrans were subterranean, and most remerged to the surface later and adapted to new environments. This would explain the absence of cone-based vision and is corroborated by shared anatomy and the fossil record.

Questions for Creationists

Why would God create sloths and armadillos with such terribly poor daytime vision, especially when so many of them are active during the day? Why would He create them with cone pseudogenes when it would have been simpler to create them with no cone genes at all? Why do two-toed, three-toed and extinct sloths share the same deleterious mutations in a cone gene (PDE6C)? Why would God create sloths with features related to digging when they live in trees?


1. Newman HH. 1913 The natural history of the nine banded armadillo of Texas. Am. Nat. 47, 513–539. 

2. Goffart M. 1971 Function and form in the sloth, vol. 34. Oxford, UK: Pergamon.

3. Emerling CA, & Springer MS. 2015 Genomic evidence for rod monochromacy in sloths and armadillos suggests early subterranean history for Xenarthra. Proc. R. Soc. B282(1800), 20142192.

National geographic reporting on my paper: http://phenomena.nationalgeographic.com/2014/12/24/sloths-and-armadillos-see-the-world-in-black-and-white/

Birds, turtles and other toothless vertebrates have remnants of tooth genes

As stated in a previous post, the toothless baleen whales and the enamelless pygmy sperm whales retain remnants of genes that encode proteins important for developing the enamel crowns of teeth. However, these have become inactivated through deleterious mutations. There are other vertebrate species that lack teeth or enamel, and theory suggests that they descended from ancestors with enamel-crowned teeth. This predicts that these species may also have enamel pseudogenes.

Some examples of toothless/enamelless species include the toothless anteaters, pangolins, turtles, and birds

and the enamelless armadillos, sloths and aardvarks.

Several studies have demonstrated that several enamel genes in these species have become pseudogenes. For example, Meredith et al. [1] showed that the enamelin (ENAM) gene was repeatedly deactivated in the mammalian species listed above:


This figure shows comparisons of toothless/enamelless species with their toothed relatives. Colored regions indicated deleterious mutations. A shows the inactivation of ENAM in the aardvark (Orycteropus); B displays a shared mutation in pangolins (Manis); C in baleen whales and pygmy sperm whales; D indicates shared mutations in sloths (Bradypus, Choloepus) and anteaters (Myrmecophaga, Tamandua, Cyclopes), and separately in armadillos (Dasypus, Tolypeutes, Chaetophractus, Euphractus).

Springer’s lab later demonstrated that two enamel genes in addition to ENAM, ameloblastin (AMBN) and amelogenin (AMEL) were lost in several of these mammals, as well as two turtles and five birds. Of particular interest, all three genes have shared mutations in the birds, indicating enamel genes were lost in the last avian ancestor.


Phylogeny showing distribution of shared and unique mutations in enamel genes across various vertebrates. B = AMBN; E = ENAM; A = AMEL.

This work provides further evidence that all of these species descended from ancestors with enamel-capped teeth, which they subsequently lost during their evolution.

Questions for Creationists

Why would God create toothless and enamelless animals with nonfunctional remnants of enamel genes? Birds and turtles have beaks without teeth, so why would they have these nonfunctional pseudogenes? Why would God create anteaters, sloths, pangolins, armadillos and birds to have shared inactivating mutations, respectively, in these genes? Do you think it’s possible that these animals could have descended from toothed ancestors? What sort of evidence might you expect in support of this hypothesis?


1. Meredith, R. W., Gatesy, J., Murphy, W. J., Ryder, O. A., & Springer, M. S. (2009). Molecular decay of the tooth gene enamelin (ENAM) mirrors the loss of enamel in the fossil record of placental mammals. PLoS genetics5(9), e1000634.

2. Meredith, R. W., Gatesy, J., & Springer, M. S. (2013). Molecular decay of enamel matrix protein genes in turtles and other edentulous amniotes. BMC evolutionary biology13(1), 20.

Nearly blind mammals retain vision gene remnants

Animals that live underground inhabit a lightless environment. Some aspects of vision in this context might not be useful, particularly those that facilitate vision in bright light. If a species has lived underground for millions of years, we would expect that many genes tied to vision have become pseudogenes, just like in animals that live in the dim-light conditions of the deep ocean.

I conducted a study [1] in which I investigated 65 vision genes across three different species of subterranean mammals, including the Cape golden mole (Chrysochloris asiatica), a member of the African golden moles (Chrysochloridae)


the naked mole-rat (Heterocephalus glaber), an African mole-rat (Bathyergidae)


and the star-nosed mole (Condylura cristata), a true mole (Talpidae).


You’ll notice that the naked mole-rat has tiny eyes, and you’ll see the same thing if you examine other pictures of the star-nosed mole. The golden mole has no external eyes; they’re completely covered with skin and fur! You can imagine that vision is not terribly important for these three mammals, especially golden moles.

What I discovered is that the golden mole has 17 vision pseudogenes uniquely derived in its lineage, the naked mole-rat has 12 and the star-nosed mole has 6. Interestingly, this corresponds with the amount of light each species likely experiences. Star-nosed moles frequently foray above ground and often swim; naked mole-rats are entirely subterranean but have an exposed eye; and golden moles are entirely subterranean but have eyes underneath their skin. By contrast, in the above-ground mammals that I used for comparison (e.g., elephants, cows, mice), nearly all of the vision genes were functional.

I then used a method to estimate when these genes might have been inactivated, and compared that to estimations of when these species might have invaded a subterranean habitat. The fossil record and molecular phylogenetics suggests that subterranean mammals descended from above-ground species, suggesting that these vision genes might have become pseudogenes as a result of this transition underground.

As described in my first post, the earliest golden mole, a transitional fossil, dates to 33.9-28.4 million years ago. However, we only have jaw fragments of this species, so we are unable to discern if it was subterranean. The next oldest species, Prochrysochloris miocaenicus (23-16 million years ago), has modifications to its skull to suggest that it lived underground. Of the 16 genes I was able to date, I estimated 13 were inactivated after the earliest date for Prochrysochloris.

African mole-rats are all subterranean, so their last common ancestor is inferred to have lived underground as well. Molecular clock methods estimate that this ancestor dates to approximately 28 million years ago. The earliest fossils don’t appear until 23 million years ago. Regardless, all 10 of the genes I was able to estimate inactivation times for post-dated both of these dates.

True moles vary in their mode of locomotion. Some are diggers, some live above ground, some spend a lot of time in the water, and star-nosed moles both dig and swim. Nonetheless, the oldest fossils of true mole limb bones show modifications for digging, and these date to 33.9-28.4 million years ago. I estimated that 4 of the 5 pseudogenes I found were inactivated after these fossils appeared.

I also examined two published vision pseudogenes in the Mediterranean blind mole-rat


and a single vision pseudogene in the marsupial mole.


These represent two more subterranean lineages, and both happen to have eyes beneath their skin.

The earliest digging blind mole-rat fossils date to 11.6-5.3 million years ago, and I estimated that both gene inactivation events took place after blind mole-rats invaded the underground habitat.

Finally, the only marsupial mole fossil dates to 23-16 million years ago and shows modifications for living underground. The pseudogenization event post-dates the fossil.

Put together, I estimated that 30 of the 35 vision genes across these five underground mammal lineages became inactivated after they became subterranean.


Questions for Creationists

Why would God create mammals with eyes covered by skin and fur? Why would He also give them nonfunctional vision genes? Is it a coincidence that these genes were estimated to have been inactivated after their fossils appear? Do you think these results are consistent with mammals evolving from above-ground ancestors to underground species?


1. Emerling, C. A., & Springer, M. S. (2014). Eyes underground: Regression of visual protein networks in subterranean mammals. Molecular phylogenetics and evolution.

Evolution may explain why whales can’t taste

The sense of taste is largely dependent upon groups of cells on the tongue called taste buds. In mammals, each taste bud cell confers one of five particular tastes: sweet, umami/savory, bitter, sour or salty. Since our tongues are one of the first parts of our bodies to interact with the food we eat, being able to convey information about the nutritional content of your snacks can be crucial for your survival.

Taste bud
Taste bud

Sweet is associated with, you guessed it, sugars: foods high in calories and therefore precious to consume. As such, your body tells you “eat more, eat more!” since it doesn’t know the next time you’re going to come across a candy bar. On the other side of the spectrum, bitter is often associated with toxic compounds, such as those in plants used to defend against herbivores, so for many animals it triggers an aversive response.

So how do these taste cells confer different tastes? Each cell expresses a different set of proteins that binds the molecules we associated with taste. So, for example, your sweet proteins bind things like glucose and sucrose, as well as artificial sweeteners, whereas there are bitter proteins that bind things like strychnine.

Mammalian taste receptor proteins and molecules that activate them.

But while humans and many other mammals chew their food, in the process getting a good taste of what they’re eating, some animals, like whales, pretty much just swallow their food whole. In fact, whales do not appear to have any taste buds at all, consistent with their grab-and-gulp method of eating.

Yet DNA and fossil evidence suggests that whales descended from terrestrial hoofed mammals that were largely plant eaters, and as such would have chewed their food and would have had a lot of use for taste buds. Is there any evidence to support this?

Indeed, when researchers looked for the genes encoding taste receptor proteins in whales, they discovered that the genomes of whales have remnants genes involved in sweet, umami, bitter and sour taste [1]. What’s more is that several of the genes have identical inactivating mutations shared by multiple whale species, suggesting that the genes were knocked out in a common ancestor.

PKD2L1 pseudogenes in whales.
PKD2L1 pseudogenes in whales, encodes a protein involved in sour taste. Inactivating mutations highlighted by boxes.

This suggests that while Shamu here wouldn’t particularly enjoy an ice cream cone, his land-dwelling ancestors just might have.

Orca tongue

Questions for Creationists

Why would the Creator design whales with taste genes that are nonfunctional, especially when whales don’t have taste buds? Why did It create multiple whale species that share identical inactivating mutations? Is it just a coincidence that DNA and fossil evidence suggests that whales descended from plant eaters that walked on land, and plant eaters have all of these taste genes intact?


1. Feng, P., Zheng, J., Rossiter, S. J., Wang, D., & Zhao, H. (2014). Massive losses of taste receptor genes in toothed and baleen whales. Genome biology and evolution6(6), 1254-1265.

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?


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.

Whale color vision gene remnants point to ancestral terrestrial life

Humans are extremely visual creatures. We ask, “How do I look?” before we go on a date. We don’t usually ask, “How do I sound?” or  “How do I taste?”

If a loved one goes blind, most people would consider it a tragedy. If a loved one loses their sense of smell, we may think it unfortunate, but we’re less likely to worry about their quality of life.

Not all animals are as visually oriented as humans are, though, and many see the world in very different ways than we do. One way that our vision is different from many other animals is through the number of colors we can perceive.

Our eyes have two kinds of cells that allow us to see: rods are used in dim light and only allow for black and white vision, whereas cones are used in bright light and allow for color discrimination.

Rods and cones
Rods (beige) and cones (green)

At the most fundamental level, the reason cones allows us to perceive colors is that different cones have different kinds of pigments, known as opsins, that absorb different wavelengths of light. Human cones can have a ‘red’, ‘green’ or a ‘blue’ opsin, and as these pigments absorb different wavelengths (colors) of light, our brains compare and contrast the relative intensities of these signals to discern color. Rods, on the other hand, only have a single pigment, so no compare and contrast is possible.

Opsin absorbances
Relative absorbances of different opsin pigments

Most mammals, such as dogs and cats, only have two kinds of cone opsins. As such, though your pets are ‘colorblind’, they do see colors; just not as much as you. If you have ever known somebody to be red-green colorblind (e.g., Protanopia), this is similar to how most mammals see the world, as shown in the image below.


Finally, some mammals, such as most whales, only have one kind of cone opsin, a ‘red’ opsin, which leads their vision to be completely black and white. Others lack cones altogether, relying completely on their rods for vision.

So what does this have to do with evolution? As discussed previously, the fossil record and genetic evidence suggest that whales are descended from hoofed mammals, and are therefore related to camels, pigs and deers. Notably, all of these mammals have two cone opsins: a ‘red’ opsin and a ‘blue’ opsin. What’s interesting is that whales have genetic remnants of a ‘blue’ opsin [1], suggesting that they lost it as they adapted to an aquatic lifestyle.

Additionally, the whales that lack cones and only use their rods for vision have genetic remnants of both cone opsins as well as various genes involved in translating the light signal absorbed by the pigments into an electrical neural signal (phototransduction genes) [2].

Whale cone pseudogenes
SWS1 and LWS are cone opsin genes. Others are cone phototransduction genes. Red, blue and green indicate inactivating mutations. Choeropsis and Bos represent functional hippo and cow genes for comparison.

Whereas whales’ ancestors likely lived on land and benefitted from perceiving distinct colors, most whales live in a relatively colorless environments in oceans and rivers. Scientists think that perceiving colors was no longer important in these situations, so these genes decayed to the point of becoming functionless pseudogenes.

As such, the genetic remnants of a former life, full of color, further point to the evolution of whales from terrestrial ancestors.

Questions for Creationists

Why would the Creator create whales with nonfunctional cone genes? Would it not have been simpler Create whales without these genes entirely? Is it just a coincidence that the fossil record and genetic analyses suggest that whales descended from land-dwelling ancestors that would have benefited from color vision?


1. Meredith, R. W., Gatesy, J., Emerling, C. A., York, V. M., & Springer, M. S. (2013). Rod monochromacy and the coevolution of cetacean retinal opsins.PLoS genetics9(4), e1003432.

2. Springer, M. S., Emerling, C. A., Fugate, N., Patel, R., Starrett, J., Morin, P. A., … & Gatesy, J. (2016). Inactivation of cone-specific phototransduction genes in rod monochromatic cetaceans. Frontiers in Ecology and Evolution, 4, 61.