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How Did the Cat Evolve to Become Tame?

Paper Type: Free Essay Subject: Biology
Wordcount: 3318 words Published: 23rd Sep 2019

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How did moggy become so tame?


In Cyprus 9.5 kya, and later Asia, as humans shifted towards more agricultural lifestyles, we see the first evidence of the domestic cat (Felis silvestirs catus) 1, 2. This may have been a result of the benefit cats provide farmers through vermin control. Today, the domestic cat is one of the world’s most popular pets, with up to 600 million individuals globally 3. However, despite this, the genetic basis behind their domestication has remained a mystery, until recently. In 2014, the comparative sequencing of the domesticated and wild cat genomes identified key genes that were responsible for different features of domestication 4. Solving the mystery of the domestication of cats while important in its own right also has a wider biological importance by helping us understand how domestication has evolved across the animals, where there are alternative hypotheses.

Figure. 1

Phylogenetic relationships among F. silvestris groups as defined by mtDNA. Tree is rooted at sand cat. All known domestic cats cluster into domestic-Asia, domestic-Europe, or Near Eastern wildcats, regardless of provenance, and these groups also cluster together.2



Tameness is a feature of the “domestication syndrome”, a set of phenotypic traits including for example coat colour changes, reduction in tooth size and changes in craniofacial morphology, which Darwin observed seem to be similar across taxonomically distant domesticated species 5, 6. The observation that many domesticated animals share the same phenotypic traits suggests that domestication may be evolving the same way in many animals, maybe involving similar genes; and indeed, two hypotheses have been proposed to explain this 7. The first is the thyroid hormone hypothesis (THH) proposed by Susan Crockford, and is based on the idea that domestication might be a form of neoteny (the retention of juvenile features) since many aspects of the domestication syndrome, including tameness are more apparent in young animals 8. Thyroid hormone concentrations affect both embryonic and post-natal development; being much higher in the juvenile stages7. Therefore, domestication could have evolved via a small number of changes in thyroid metabolism resulting in pro-longed high levels of thyroid hormones resulting in a more juvenile phenotype. There is evidence for this, the self-domesticated species of chimpanzee Pan panscus has increased high levels of high thyroid hormones compared to its related non neotenous species Pan troglodytes9. The second hypothesis is the neural crest cell hypothesis (NCCH). Neural crest cells are an intermediate structure during the development of vertebrates and give rise to a diverse range of cell lineages, including cardiovascular cells, pigment cells and connective tissue. This supposes that deficits in neural crest cells in their final locations can give rise to a diverse range of phenotypes associated with domestication syndrome. For instance, neural crest cells are involved in the development of adrenal glands. Deficits in neural crest cells here result in smaller glands and less adrenocorticotropic hormones (fight or flight hormones), resulting in more docile and tame animals. This has been seen in domesticated foxes and rats 5. However, these hypotheses seem to conflict each other. While in the THH hypothesis where only a small number of mutations in the thyroid metabolism system would be sufficient to produce a domesticated phenotype, NCCH suggests additive variation with many more mutations since there is not one known mutation in these set of genes that could give range to all of the phenotypes observed under the domestication syndrome. It is more likely that a combination of mild loss of function mutations in neural crest cell genes give rise to the variety of phenotypes observed in domestication. That said, it is possible that both could be acting simultaneously since inhibiting thyroid hormone expression (possibly due to a mild loss of function mutation in the receptor) during embryonic development significantly impairs neural crest cell function 10.

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These two hypotheses provide a useful starting point, even before the sequencing of the cat genome as we have an idea of what genes to look for; expecting differences in thyroid hormone metabolism, or neural crest cell development, or maybe both between domestic cats and there wild counterparts. Moreover, since cats are a semi-domesticated species as populations do mix with wildcats, and we not completely control their food intake 11 the effect of domestication on the genome should not be as great as what we see in dogs for example 4 .

Analysing the genome

Since the domestication of cats, they have diverged into many breeds, each with their own unique genetic features. If we just compared the genome of one cat breed with one wild cat it would be hard to distinguish between features selected for during domestication and features that has evolved by random fixation during the selection of breeds. Therefore to account for this sequence data was combined from 6 different domestic cat breeds, which were compared to European ( F. silvestris silvestris) and Near Eastern (F. silvestris lybica) wildcats 4. Comparing the sequences and looking for regions with both low Hp (Pooled heterozygosity – a low value identifying regions for the genome that have been selected for) 12 high Fst (genetic variance statistic – where a high value implies the populations are separate and not mixing genetics) 13. From this analysis they found 13 genes across 5 chromosomal regions that were different between the wild and domestic cats. Interestingly, 5 of these genes had significant effects in neural development. Notably this is less than what we see in the domestication of dogs 14, which is as we expecting since cats are considered to only be semi domesticated species, with some populations mixing with wildcats 4.


One chromosomal region identified contained two proto-cadherin genes which are involved in several neuronal functions, such as maintaining neuronal connections and specifying synapses 4. However, it is clear they have a function in tameness since they are also involved in fear conditioning. Previous research in mice has found that individuals with mutant proto-cadherin genes expressing the protein at 20% of the wild-type level show more anxious and fearful responses when undergoing a fear-conditioning test 15. In addition to this, PCDHA1 and PCDHB4 have been implicated in serotonergic innervation. Research into the self-domestication of the bonobo has shown that the socially tolerant species Pan paniscus has an altered serotonergic innervation compared to it’s more aggressive sister species Pan trogloyte9. This pattern has also been seen in rats and foxes 16, 17. Since serotonin is generally higher in juveniles, and higher serotonin levels correlate with decreased aggression, paedomorphism in the serotonergic system may be an adaptation for tameness.


A different region of a chromosome was also highlighted in their findings, containing the gene DCC , highly expressed in the dopamine neurons; encoding the netrin receptor. It is essential for synaptogenesis in the developing brain, but has since been found to regulate synaptic plasticity in the adult brain. More importantly, it has also been implicated in domestication since mice deficient in DCC show altered behaviour and reward responses18. Interestingly, DCC is also linked to axon development and neural crest cell migration via interactions with the Myosin Tail Homology 4 (MyTH4) domain of MYO10, which has also been seen in mice and frogs19, 20.


On another chromosomal region, B3, AT-rich interaction domain molecule 3B was identified. This gene, like DCC is again involved in the development and survival of neural crest cells. During neural crest cell development, MYCN promotes increased neural crest cell proliferation, and ARID3B promotes neural crest cell survival by preventing apoptosis. ARID3 knock out mice are lethal in addition to being associated in tumour formation. The gene has also a role in the development of synaptic ganglia in the mouse embryo 21, 22.


This gene, via interacts with MyTH4 (like DCC) also affects neural crest cell regulation, and transcription factors related to growth and development. In addition to causing psychiatric disorders in humans when modified. 23

What does this show?

It is clear from sequencing the domestic cat genome and comparing it’s with the wild counterpart, key genes behind domestication can be identified. Moreover, it is also evident that these genes are involved in domestication in other species too, supporting the idea of a “domestication syndrome” where many phenotypic aspects of domestication are shared across distant taxa. This research also has wider impacts on how domestication evolves in species in general. As mentioned 5 of the 13 genes identified are implicated in neural crest cell development and migration, supporting the neural crest hypothesis of domestication as oppose to the thyroid hormone hypothesis where only one locus was identified 4. This locus, identified by high Fst, included the gene TSHR which encodes a thyroid stimulating hormone receptor, however they did not find evidence that this gene was under selection for domestication. However, that said the same gene has been found to have a significant effect in the domestication of chickens when mutated, causing more frequent egg production which has gone to fixation in the domestic breed. The mutation is also associated with tameness and lower aggression when compared to the wild ancestor Red Jungle Fowl 7

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It may not be surprising that THH and NCCH hypothesis don’t appear to be acting together. Although it was mentioned previously that both could be acting simultaneously since inhibiting thyroid hormone expression (possibly due to a mild loss of function mutation in the receptor) during embryonic development significantly impairs neural crest cell function 10; this is not concurrent with the idea that juvenile characteristics in neoteny arise from pro-longed exposure to thyroid hormones 7.

Moreover, it may also not be a surprise that the cat genome sequencing supports the neural crest cell hypothesis. A review conducted in 2017 looked at recent comparative genome sequences of domesticated animals including the cat, horse, dog and rabbit. They found that although there is evidence for the THH, for example the CRYM gene in dogs, overwhelmingly there is more evidence for the NCH hypothesis (for example with 11 genes shown to support this in dogs)7, 14, summarised in figure 2.

Figure 2.

Table summarising signatures of domestication in horses, cats, rabbits and dogs associated with the Thyroid Hormone Hypothesis (THH) or the Neural Crest Cell Hypothesis (NCCH).

In addition, KIT , another gene involved in neural crest cell development and white spotting (another symptom of domestication syndrome) in both pigs and horses 7, has been found to be associated with pigmentation of white paws (gloving) in a specific breed of cat, the Birman4, with all Birman cats with gloving being homozygous for two recessive mutations in the Ig domain of the gene.

However, interestingly the Ragdoll breed which also has gloving only shares the KIT recessive mutations in 12.3% of the sampled population. This may be because of endogenous retroelements inserting into the KIT intron which can produce the same phenotypic effect 4. While the neural crest cell hypothesis and thyroid hormone hypothesis explain the basis of domestication they fail to explain variation within domesticated species, hence the role of mobile elements, such as those in the Ragdoll have been studied further. The idea here is that the variation within domesticated species is a consequence of their ability to acquire retroelements affecting the gene expression which has shown to be a possible factor in silk worm domestication20. Moreover, in cattle this idea has been combined with that of pleiotropy, suggesting that there are clusters of genes containing mobile retroelements which surround a core of pleiotropic genes favouring domestication; providing the high level of variation we see in some domesticated species7. Thus not only has the sequencing of the cat genome highlighted the genes behind their domestication and provided evidence for the neural crest cell hypothesis, it has also supported the role of mobile genetic elements in domestication.

In conclusion, it is apparent that the genes behind the domestication syndrome in cats, especially tameness may be similar across various other domesticated species, and as we expected the effect of domestication of the cat genome is more modest than that of the dog genome due to their mixing with wild populations. Moreover, when the genes are not similar they often have a similar function, which is usually to do with modifying neural crest cell development, but occasionally is also involved in the regulation of the thyroid hormone. Finally, the role of mobile elements in development as seen in the Ragdoll, is also seen in other species and which via pleiotropy may explain plasticity among domesticated species.


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