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.

Baleen whales have remnants of tooth genes

One of the major components of teeth is enamel. Enamel caps teeth and is the hardest known substance in the human body, an understandable feature considering the amount of grinding that teeth are used for.


Several genes are crucial for enamel development, including some that encode proteins that build a scaffold for the deposition of mineralized enamel and others that breakdown these proteins.

Baleen whales, which lack teeth entirely, are thought to be derived from ancestors that possessed enamel-capped teeth, as demonstrated by evidence from the fossil record and their genetic relationships to other toothed mammals. This leads to the prediction that genes important for enamel formation have become nonfunctional in baleen whales and preserved as pseudogenes.

Sure enough, Demere et al. [1] discovered that the enamel genes ENAM (enamelin) and AMBN (ameloblastin) are inactivated in baleen whales while remaining functional in other toothed mammals, including toothed whales. Meredith et al. [2] also demonstrated that the pygmy and dwarf sperm whales, two toothed whale species that lack enamel, have shared mutations in ENAM. Another paper by Meredith et al. [3] discovered that the enamel gene MMP20 (enamelysin) has been disrupted by an inactivating retrotransposon (“jumping gene”) shared in all baleen whales, suggesting that enamel formation was likely inactivated in the last common ancestor of baleen whales.


A figure from Meredith et al. [3] showing a summary of enamel gene mutations across a whale phylogeny and transitions from toothed to toothless species incorporating the fossil record. Nodes that are black denote toothed species, gray are enamelless but toothed species, and white are toothless.

Questions for Creationists

Why would God create nonfunctional enamel genes in whales that completely lack teeth? Is it a coincidence that all baleen whales and pygmy and dwarf sperm whales have shared inactivating mutations, respectively? Is it a coincidence that the presence of tooth pseudogenes was predicted by molecular phylogenetics and the fossil record?


1. Deméré, T. A., McGowen, M. R., Berta, A., & Gatesy, J. (2008). Morphological and molecular evidence for a stepwise evolutionary transition from teeth to baleen in mysticete whales. Systematic Biology57(1), 15-37.

2. 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.

3. Meredith, R. W., Gatesy, J., Cheng, J., & Springer, M. S. (2010). Pseudogenization of the tooth gene enamelysin (MMP20) in the common ancestor of extant baleen whales. Proceedings of the Royal Society B: Biological Sciences, rspb20101280.

Why whales can only taste salt

Taste, as people are generally familiar, is dependent upon taste buds located on the tongue. These taste buds consist of cells with taste proteins embedded on them to directly interact with chemicals that the tongue encounters. These proteins detect at least five basic tastes in mammals: sweet, umami/savory, bitter, sour and salty.

We’d generally expect that the taste receptors present in a particular animal would correspond to things in an animal’s diet. Humans are omnivorous (i.e., we eat plants and animals) and therefore benefit from experiencing all of these types of tastes. But what if an animal adapted to an extreme diet does not require the ability to detect all sorts of tastes? An evolutionary biologist would expect that they would lose at least some of their taste capabilities, and this change in taste would be reflected by the presence of taste receptor pseudogenes.

Whales potentially fit this criterion, as they live in a marine or freshwater environment and feed on fishes, krill and related animals exclusively. When was the last time you saw a whale eat a sweet apple or a sour citrus? Another thing to consider: if you’ve ever been in the ocean, do you think if you tried eating fish with your bare teeth you could taste anything but salt? Perhaps this extreme diet and salty medium have induced whale tastes to change through time.

McGowen et al. [1] highlight the fact that taste buds in whales are rare or completely absent, and a recent paper by Feng et al. [2] demonstrated that this taste bud reduction/loss is mirrored in the genes that code for taste proteins. Specifically what they discovered is that most whales appear to have lost the ability to taste anything but salt.


This means Shamu here could at least appreciate some french fries.

The genes T1R1 and T1R3 encode the umami/savory receptor, whereas T1R2 and T1R3 encode the sweet receptor. This means that the protein encoded by T1R3 is crucial for both of these tastes. Feng et al. [2] acquired DNA sequences for the T1R3 gene in two baleen and five toothed whales and discovered that they all have the same shared inactivating mutation (pseudogene), suggesting that the ancestor to modern whales had lost both umami and sweet tastes. Additionally, the T1R1 gene has a mutation shared by three baleen and six toothed whales, suggesting this too became a pseudogene in the ancestor to modern whales, while T1R2 appears to have been lost independently in the ancestor to baleen whales and toothed whales respectively.

The bitter taste is encoded by many genes (T2Rs), with at least 10 discovered in whales. Eight of these had inactivating mutations shared by all baleen and toothed whales looked at in the study, while the other two genes were apparently inactivated in different groups of whales independently. The exception is that the T2R16 gene, while inactivated in two baleen whales, appears to be intact in three others, which would seem to indicate that these whales (fin, minke and bowhead) still have some bitter taste capacity.

The sour taste is encoded by the genes Pkd1l3 and Pkd2l1. While the authors could not find the former gene, they did find pseudogenic versions of Pkd2l1 in one baleen and two toothed whales.

The salty taste receptor, encoded by Scnn1a, Scnn1b and Scnn1g is, however, intact in the one baleen and two toothed whales that were examined. Whether or not these are actually used for taste however is unclear. These genes are also associated with other aspects of physiology, such as blood pressure, meaning that these genes may be maintained strictly for other purposes. Nonetheless, it does suggest that there is a possibility that whales can still taste salt.

Questions for Creationists

Why would God create whales with taste genes that are nonfunctional? Additionally, why would He create them so that both baleen and toothed whales share the same mutations? Would it not have been more straightforward to create whales that completely lack the genes entirely rather than having nonfunctional remnants?


1. McGowen, M. R., Gatesy, J., & Wildman, D. E. (2014). Molecular evolution tracks macroevolutionary transitions in Cetacea. Trends in ecology & evolution29(6), 336-346.

2. 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.

Genetic evidence that whales lost a complete organ in their evolutionary past

The vomeronasal organ is used for chemical detection in many vertebrates. It is similar to smell, but it usually functions in pheromone reception. Pheromones are chemicals produced by animals that are used to communicate with each other, for example in their urine.


Snakes flick their tongues to gather chemicals in the air to pass over the entrance to their vomeronasal organ.


Horses and cats exhibit the flehmen response to gather airborne molecules for their vomeronasal organ

McGowen et al. [1] highlight the fact that extant whales completely lack a vomeronasal organ. As I described in a previous post, early fossil whales showed evidence of a vomeronasal organ (i.e., the presence of incisive foramina), which is consistent with its presence in other hoofed mammals, but this was lost by the time Remingtoncetus appeared approximately 48.6-40.4 million years ago. This makes sense because the vomeronasal organ, as well as smell, generally work best with airborne molecules rather than molecules dissolved in water.

If the vomeronasal organ was lost during whale evolution, it would suggest that the genes crucial for vomeronasal organ function have been rendered pseudogenes in whales. In fact, the bottlenose dolphin possess 36 V1R pseudogenes, genes that formerly would have ‘captured’ odors to induce electrical signals to the brain. Another vomeronasal gene, TRPC2, is exclusively expressed in vomeronasal neurons. This is not only a pseudogene in the bottlenose dolphin (toothed whale) and the fin whale (baleen whale), but the pseudogenes of these two species share the same inactivating mutation. This implies that this gene was inactivated prior to the last common ancestor of modern whales, a feature that is consistent with the fossil record.

Questions for Creationists

Why might God have created whales with vomeronasal pseudogenes? If the vomeronasal organ is entirely absent, would it not have made more sense to create whales without remnants of these genes? Is it a coincidence that a baleen whale and toothed whale share the same inactivating mutation in a vomeronasal gene? Is it also a coincidence that this shared inactivated mutation is consistent with the fossil evidence for vomeronasal organ loss in whales?


1. McGowen, M. R., Gatesy, J., & Wildman, D. E. (2014). Molecular evolution tracks macroevolutionary transitions in Cetacea. Trends in ecology & evolution29(6), 336-346.