Are chestnut horses really "hot bloodied"?

Research project coming up soon!

Some people believe that chestnut horses are particularly sensitive and with a tendency to be “hot blooded” – in much the same way that redheads are sometimes said to be fiery. It’s not impossible that some association exists, if the gene for chestnut is linked to other genes that affect temperament. However it hasn’t – to my knowledge – been scientifically tested. Furthermore one can always think of quiet chestnut horses that don’t live up to the reputation, suggesting that – if there is a link at all - perhaps it isn’t a complete one. Possibly a link may exist that is stronger in some breeds than others.

I'm designing a project to see if there are any identifiable links between color and pattern genes and temperament traits. Watch out for this in a few months time since I’ll need lots of you to complete questionnaires about your horses if we’re to be successful in advancing knowledge in this area. Thankyou!

For now I hope the research summarised below will interest some of you. Happy reading...

Color, pattern and behaviour

Animal domestication, including horse domestication, has inevitably been associated with selecting for docility and tameness. It has been shown in foxes that selection for tameness leads to foxes with areas of depigmentation (Belyaev, 1979, Trut, 1999). In other animals, although extreme depigmentation can lead to neurological impairment (Grandin, 1998), piebaldness is thought to be associated with docility, including in cats, dogs, hamsters, rats, cows, birds and horses. It is possible that some other colors and patterns are also associated with particular behavioural characteristics. To think about this further we’ll look at some of the known connections between color, pattern and other characteristics of the horse, and of other animals.

Most forms of piebaldness (colored and white, as in paints) in horses are caused by pigment cells not being found in the white areas. Pigment cells (melanocytes) occur at the base of hair follicles, where they synthesise pigments that are secreted into the hair. They also color the skin and eyes.

Melanocytes are formed during embryo development and migrate throughout the body. A fold develops down the back of the embryo called the neural tube, with melanocytes forming in an active region called the neural crest. They migrate from here to several specific sites along the back, sides, head and tail, where they proliferate. The new cells migrate outwards forming patches that spread down the legs, over the head and over the rest of the body. Eventually the patches join up under the chin, neck and belly.

Other cells also originate in the neural crest, including nerve cells (ganglia) of the intestine. In foals homozygous for the overo gene both pigmentation and nerve cells are lacking (aganglionosis) due to abnormalities during foetal development. Such foals are all-white with blue eyes and die of complications from intestinal tract abnormalities. The overo gene is for the endotheline-B receptor (Metalinos et al), which is involved with both the migration of pigment and nerve cells. Mutations that affect the migration of cells from the neural crest are known to be associated with white coats, pink and blue eyes, deafness and intestinal abnormalities, not only in horses but also in other animals, including humans.

Pigment cells also migrate to the brain. They occur in various (and possibly all) parts of the brain, including the substantia nigra, the locus ceruleus, the dorsal root ganglia and the cranial ganglia. They also occur in the membranes surrounding the brain (the leptomeninges). The substantia nigra, for example, is a part of the midbrain that regulates mood, produces dopamine (which is also produced in pigment metabolism) and controls voluntary movement. Mutations that prevent melanocytes from reaching the brain are known in various animals and can have a range of affects on behaviour, including stress response. They can also affect other characteristics, for example causing movement disorders.

Disorders of the pigment cells themselves (rather than disorders caused by their absence) can cause a range of affects on non-color traits. For example, hooded rats homozygous for a red-eyed dilution gene have numerous associated disorders including hypertension leading to kidney damage and altered behaviours, such as high anxiety, low aggression and a predisposition to alcoholism! They are used as models for human psychiatric disorders, including depression, anxiety, obsessive compulsive disorder and eating disorders. Because the red-eyed dilution gene affects different cell components in different types of cells there are several (i.e. pleiotropic) effects of the mutation. The things that go wrong may not be directly associated with pigment production. Nevertheless they are associated with a particular color and pattern phenotype and are selected for by breeding for this color and pattern. This is rather a dramatic example of how selecting for color and pattern can cause selection for particular behavioural traits at the same time. I believe that some colors and patterns in horses may well be associated with behavioural characteristics, though perhaps not usually in such an extreme way as in this example. There might even be some truth in the old tale about red horses being more fiery than others!

The relative amount of eumelanin (black) and phaeomelanin (red) is regulated by the interaction of the MC1R with alpha-melanocyte stimulating hormone (alpha-MSH) and the agouti signalling protein (encoded by the agouti locus). Binding of alpha-MSH to the receptor stimulates eumelanin production (Zalfa et al, 2001, Jung et al, 2001). The agouti signalling protein (produced by the agouti gene) competes with alpha-MSH for the melanocortin receptor. Binding of the agouti signalling protein blocks the signalling process that leads to eumelanin production (Zalfa et al, 2001). This is similar to what happens for chestnut color, only in chestnuts the receptor is itself altered so that eumelanin production is stopped altogether (see the melanin research page for more information). The agouti locus reduces eumelanin production to some degree (depending on the allele) and only in some areas of the body. The recessive black allele A^a has been found to have an 11 base pair deletion causing its loss of function, so that the signalling process isn’t blocked and eumelanin is produced throughout the body (Rieder et al, 2001).

In other mammals, including rats and humans, the agouti signalling protein also binds to the melanocortin receptors in the brain (Lu et al, 1994, Willard et al, 1995) and possibly also in fat tissue (where it may affect energy metabolism, Voisey and Daal, 2002). It has long been realised that non agouti rats are calmer and tamer than agouti rats (Keeler, 1942, Cottle and Price, 1987). More recently it has been realised that this is probably to do with the effect of the agouti signalling protein on neural melanocortin receptors, and the consequent effects on the brain. This is another example of how color is associated with behaviour: selection for docile laboratory rats has led to over 80% of them being non agouti.

From the above evidence it is possible to see that there may be an association between color and docility in horses. Perhaps black horses – which don’t produce agouti signalling protein - are more docile than bays. Maybe there’s a gradient with browns being more docile than bays and red bays being friskier than dark bays with lots of black hair! (Actually there are bound to be complicating factors so that a simple relationship might be hard to detect). In lab rats there are no mutant forms of the extension locus known. However in horses the chestnut mutation occurs and perhaps this also has an effect on the biochemistry of brain, and ultimately on behaviour. Interestingly the chestnut mutation occurs in the same gene that causes red hair in humans. It is well known that both chestnuts and “red heads” are associated with “old wives tales” about them being more fiery!

References and further reading

Jung, Gi-Dong, Yang, Jeong-Yeh, Song, Eun-Sup and Park, Jin-Woo. 2001. Stimulation of melanogenesis by glycyrrhizin in B16 melanoma cells. Experimental and Molecular Medicine 33 (3), 131-135.

Metalinos, D.L., Bowling, A.T. and Rine, J. 1998. A misense mutation in the endotheline-B receptor gene is associated with Lethal White Foal syndrome: an equine version of Hirshsprung Disease. Mammalian Genetics 9, 426-431.

Rieder, Stefan Taourit, Sead Mariat, Denis, Langlois, Bertrand and Guérin, Gérard. 2001. Mutations in the agouti (ASIP), the extension (MC1R), and the brown (TYRP1) loci and their association to coat color phenotypes in horses (Equus caballus). Mammalian Genome 12 (6), 450 – 455.

Zalfa, A. Abdel-Malek, M. Cathy Scott, Minao Furumura, M. Lynn Lamoreux, Michael Ollmann, Greg S. Barsh and Vincent J. Hearing. 2001. The melanocortin 1 receptor is the principal mediator of the effects of agouti signalling protein on mammalian melanocytes. Journal of Cell Science 114, 1019-1024.

Where do rat colors come from? http://www.ratbehaviour.org/CoatColorMutations.htm. This is really interesting and has lots of links to other sites.