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.
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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