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Thursday, 1 January 2015

Dedomestication series Pt. I: From wild to domestic

About eight months ago, I intended to do a dedomestication series on how domestication works per se, what happens when domestic animals run wild, and how this is relevant for “breeding-back”. But I never got to it, and actually I am happy about that because I gathered much more information in the meantime. Also, the drafts for the articles were unnecessarily long, so I am going to do more succinct versions here, which are easier to read for you and quicker to write for me.

So the subject of the first part is going to be how a wild animal becomes a domestic animal with all its morphologic and behavioural changes. My post from April 2014 covered this question already (http://breedingback.blogspot.co.at/2014/04/breeding-back-and-dedomestication-pt-i.html), but IMO not sufficiently, so I decided to write another, more inclusive and handier one.
Domestication has a strong developmental background. I am an amateur on developmental biology as much as I am not a geneticist, so feel free to point me to conceptual errors in this text if you spot some.

Per definition, domestication is the process that occurs when man shapes wild animals for his purpose by artificial selection. This process always results in similar morphologic and behavioural traits, regardless of which species or domestication event, suggesting that there are universal underling mechanisms that are always the same. These mechanisms are very likely part of these factors:

Genetic drift: This is the very first effect of domestication. Man snatches out a small population out of a larger wild population and and starts breeding with it. But that factor is of minor importance here.  
 
A normal and a hypothyroidic mouse. The latter shows
floppy ears, smaller body size and shorter limbs and
snout. Taken from [2].  
Developmental delay: This is way more important. The famous Farm fox experiment which selected captive silver foxes for tameness over decades, the results are human-friendly foxes with juvenile behavioural and morphological characters, as well as novel traits. The retention of juvenile characters, known as neoteny or paedomorphy, is common to all domestic mammals and is the result of a developmental cascade due to the selection on tameness [1,2]. The reason for that is that behaviour is regulated by hormones, and selection on certain behavioural traits changes the endocrinology. And selection on tameness, or in other words, a reduction of the so-called fight/flight reaction, seemingly has a dramatic effect. Main hormone groups involved are corticosteroids and those produced by the thyroid gland [1,2]. The former play a role in the animals reaction to stress, and indeed the level of corticosteroids in the domestic foxes dropped to a quarter compared to the control group [1]. Also, the surge of this hormone group during postnatal development got delayed, suggesting that the hormonal change that causes the behavioural change also results in neoteny.
The thyroid hormones have an even greater impact. They play a crucial role in postnatal growth, pigmentation, brain development, adrenal gland function and development of the gonads [2]. Hypothyroid rats are smaller than the average, have a shorter snout and floppy ears, which are typical domestic traits [2]. Neoteny in amphibians is the result of hypothyroidism as well, and so is the so-called cretinism in humans. Symptoms of cretinism are shortened extremities, reduced body size and lowered cognitive abilities. I don’t know if we can connect the reduced brain volume we see in domestic animals with these reduced cognitive abilities, but the parallels between typical traits of domestic animals and the effects these hormones have in humans and rats are obvious.
The reduced sexual dimorphism has to have a hormonal cause as well. Probably – and this is now my presumption – the selection for tameness and the change in the endocrinological activity also affected the production of steroids that are responsible for the development of secondary sex characteristics, androgens and oestrogens. Distorted production of these hormones in humans results in syndromes such as virilism. Indeed the farm foxes show reduced sexual dimorphism in cranial morphology.
Another result of the Farm fox experiment and of domestication in general is earlier maturity. The domesticated foxes mature one year earlier and give rise to one more pup. This was achieved by selecting for tameness only, while the efforts by fur breeders by selecting on earlier maturity directly for decades remained fruitless [1].

Pleiotropy: (forgive me that I just recycle this paragraph from my earlier post) Pleiotropy
takes place when genes do not affect one single trait but have a number of functions. This can also be the case in genes for discrete, monofactorial traits like coat colours – these “colour genes” actually have more than one function. A prime example is the KITLG locus that produces the ligand for tyrosine-kinase (coded by the KIT-locus), which has a function in germ cell, neural cell and blood cell development. Mutations on these two loci are either hyperpigmentation or leucisms [3], responsible for many of the spotted patterns we see in domestic animals [4].  KIT mutations are the cause of the typical white streak along or the “star” on the face of many domestic animals, and is also displayed by humans having similar mutations (“piebaldism”). The spots are the result of a disordered migration of the melanoblasts from the neural crest where they are produced. White-faced cattle like Hereford have a greater susceptibility to Cancer Eye or Bovine Squamous Cell Carcinoma [4], and depigmentation in general increases the risk of cancer because melanin is an important barrier for mutagenic UV radiation, which is evident in basically every animal. The Agouti-locus has a role in pigmentation (responsible for colour dilutions in many mammal species), but also in regulating lipid metabolism in adipocytes [5]. The Dun-locus, a dilution locus as well, has functions in the nervous system and metabolism. Mutations on this locus cause neuromuscular disorders which can result f.e. in arched tails (see dogs and pigs) because of myelin degeneration [6]. The phenylalanine metabolism might be disturbed as well [6]. Not all mutations on these loci are necessarily disastrous, otherwise all domestic animals with deviant colours would regularly be born with serious disorders. Pleiotropy certainly is the cause of some other traits displayed in domestic animals as well, perhaps such as over- and under-bite in dogs.

Relaxed Selection: This refers to the loss or reduction of adaptions that are otherwise required by living in nature in its ecological niche. For example resistance to diseases, seasonal mating, climatic adaptions, certain behavioural or morphological traits. 

Phenotypic plasticity: The genotype alone does not determine what an organism will be like. Rather, the actual phenotype is the outcome of the products of the genotype interacting with the environment. Phenotypes of the same genotype can differ under different environmental conditions. This is called phenotypic plasticity. Limited food for example restricts individual growth, or that of horns and antlers. Muscles grow or shrink by being trained or not trained – if an animal is able to live and move freely, it should be well-muscled. If it has to live in a small confined place, it will have a rather hypotrophic musculature. The impact that the environment can have on the phenotype depends on how much is permitted by the genotype. This is called the reaction norm. Muscle size depends on training, yes, but there is a genetic basis for what is possible and what is not (influenced by hormones such as steroids or the protein myostatin and its antagonist follistatin). In the same way, you can’t make a Chianina grow horns as big as in Watussi by supplying them with extra-calcium-rich food, and vice versa. Phenotypic plasticity is not inheritable and therefore not really a part of domestication mechanisms, but determines what these animals look like in the end, and so it is relevant for the subject too, as you will see in the subsequent posts.

To sum it up: artificial selection for behaviour alone alters the hormonal cocktail responsible for development and behaviour, what not only results in tameness but also paedomorphism, shorter limbs and snouts, smaller size, reduced sexual dimorphism and affects brain development and pigmentation. Other domestic traits arise through pleiotropy, when genes that play a role in the nervous system (and therefore also behaviour) are altered, what also affects pigmentation or causes curled tails. Relaxed selection dilutes adaptions of the wildtype to required by living in the wild. Other traits seen in domestic animals might be the result of pleiotropy as well. Phenotypic plasticity influences the phenotype as well, but depends on environment and is not inheritable.

The next part is going to be on what happens when domestic animals run wild. 

Literature

[1] Trut, 1999: Early Canid Domestication: The Farm fox experiment.
[2] Dobney & Larson, 2005: Genetics and animal domestication: new windows on an elusive process. Zoological Society of London. 
[3] http://ghr.nlm.nih.gov/gene/KITLG
[5] https://en.wikipedia.org/wiki/Agouti_signalling_peptide
[6] http://www.informatics.jax.org/wksilvers/frames/frameRST.shtml


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