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Colour Genetics UK

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  • Colour Genetics UK

    I'm wondering if someone can explain the base colours and dilutions, also telling me the phenotypes of each. I'm not clued up on any of this, hense asking.
    Are certain colours only certified in certain countries? Or at least for specific breeds as I am aware that say a Shire, can not be accepted in Chestnut colours in the UK.

  • #2
    There are two base colors: red and black. Everything else is a modification layered on top of those.

    There are different dilution genes (for example, one copy of cream on a red base produces a palomino, two copies on a red base produce a cremello).

    There's a lot of information on this on the internet; and breed standards on their individual websites.

    Start Here:
    https://www.animalgenetics.us/Equine...olor/Index.asp
    Veni vidi vici. With a paint pony, nonetheless.

    Comment


    • #3
      The link Arelle posted above is a great place to start.

      The problem is that "color genetics, ready set go!" is such a broad topic that it's really hard to figure out where to begin and what direction to take things in.

      Another component to this you actually vaguely touch on, I think - certain colors aren't acceptable in certain breeds (or simply aren't represented). Depending on where the mutation was first introduced and what breeds/registries you are looking at, there is a limited (or no) chance for those genetics to get introduced to other breeds of horses. Old closed registries can be some of the most limited color-wise due to the lack of accessibility to introduce those "new" colors (the mutations) into the genetic pool.

      Comment


      • #4
        Various registries block various colors. Sometimes this is because that color gene really does not exist in the breed (no creme dilutes in purebred Arabians) and sometimes it is a mistaken idea that it doesn't (Quarter Horse excluding pintos) and sometimes it's an effort to shape the breed. Most registries predate modern genetic knowledge and can be based on false assumptions about color genetics.

        A registry where all the horses are the same color and very phenotypically similar like Haflinger or Friesian must have a very small genetic pool.

        For whatever reason, stock type horses and feral horses in the Western USA have a high percentage of "modifier" genes like creme and dun, as well as several different pinto patterns and appaloosa (which is a breed) and also roan. And silver bay in Rocky Mountain gaited horses!

        So palomino, buckskin, red dun, grulla, perlino and cremello, dunalino, and blue roans and red roans, plus pintos and Appaloosas in all these colors. These modifications might not all be that common in the UK.

        There is also a pinto pattern, Frame Overo, that mutated in NA in horses of Spanish descent. It doesn't historically exist in the UK. All the piebalds and skewbalds in the UK would be considered Tobiano pinto in NA.

        Comment


        • #5
          Ah. Color. While I was at the WEG, my friend who lives in SC received a text from a local friend that her 11 year old Friesian had been found dead in the field. It was then my friend said something along the lines of well.....there are so often genetic problems with Friesians. I was all, what?? Then I looked it up. Heart problems, intestinal problems, all presumably linked to the very small gene pool. Is it small because of selectively breeding for the black color?* The "average" age listed for most horses is 16-26. For Friesians, it is 11-16. Apparently, if they have the heart defect, they rarely live beyond 4. Shocked the heck outa me. I'm an Appy person (talk about color LOL), but have always thought Friesians were quite lovely, even though "lotsa hair" isn't my thing.

          (*Years ago, friends and I mocked an exhibition by a woman who had mostly Friesians, and then presented a "rarer than the mythical unicorn" chestnut Friesian. We joked that it had probably been exported under cover of darkness, before the breed society found out that someone's horses had produced a chestnut. Now, it seems like that might have been a horse that needed to be kept in the gene pool.)

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          • #6
            That's interesting, Belowthesalt because the black base is actually easier to express -- red is the recessive gene. The problem is the agouti gene as you'll need a double recessive (no agouti) to express black. I assume they've been breeding the agouti out as I can't recall ever seeing a bay Fresian. (Though, admittedly, in Texas it's not like I see them on every corner - ha!)

            I was at an APHA seminar a couple years ago talking to the UF color guru regarding paint breeding, since obviously that's a big deal in getting a solid or not. We don't get the performance permits appys do. Anyway, she was explaining an interesting phenomenon that the chromosome that controls gut motility also contains the lethal white gene and they figured that out since a lethal white (homozygous LWO) is... well, lethal due to the fact that their intestines are underdeveloped and contracted and they cannot move material through their intestines. It's interesting to think that various genes on chromosomes can control something like color AND development of tissue.
            Veni vidi vici. With a paint pony, nonetheless.

            Comment


            • #7
              Originally posted by Arelle View Post
              That's interesting, Belowthesalt because the black base is actually easier to express -- red is the recessive gene. The problem is the agouti gene as you'll need a double recessive (no agouti) to express black. I assume they've been breeding the agouti out as I can't recall ever seeing a bay Fresian. (Though, admittedly, in Texas it's not like I see them on every corner - ha!)

              I was at an APHA seminar a couple years ago talking to the UF color guru regarding paint breeding, since obviously that's a big deal in getting a solid or not. We don't get the performance permits appys do. Anyway, she was explaining an interesting phenomenon that the chromosome that controls gut motility also contains the lethal white gene and they figured that out since a lethal white (homozygous LWO) is... well, lethal due to the fact that their intestines are underdeveloped and contracted and they cannot move material through their intestines. It's interesting to think that various genes on chromosomes can control something like color AND development of tissue.
              Yes, all Frame Overo are heterozygous for Lethal white which is why you don't breed two Frame Overo (even ones with minimal expression). 25% chance of a LW foal. Not the most functional color mutation out there, though I love my Frame Overo mare! They seem to have no issues other than that far as I can tell.

              Comment


              • #8
                The Friesian horse had a population bottleneck around 1900 with only 3 studs left, according to Wikipedia, so definitely concentrated genes.

                Comment


                • #9
                  Originally posted by Scribbler View Post

                  Yes, all Frame Overo are heterozygous for Lethal white which is why you don't breed two Frame Overo (even ones with minimal expression). 25% chance of a LW foal. Not the most functional color mutation out there, though I love my Frame Overo mare! They seem to have no issues other than that far as I can tell.
                  Yes; I own five currently. (As well as two W20/n, and two To/n)

                  Unfortunately, I've seen two lethals this year posted to Facebook. Stallion management wasn't posting genetic testing and in one case, sold a bred SPB who wasn't tested but was LWO/n. (Yes - solids can be positive for frame overo!) Very sad and very preventable.

                  I could also use the example that HERDA/n horses have anecdotally shown "fancier" movement - which many say is attributed to hyper extendable joints. My point was not LWO horses but how breeding for specific attributes affects other genes on the chromosomes and I find it fascinating.
                  Veni vidi vici. With a paint pony, nonetheless.

                  Comment


                  • #10
                    Originally posted by Arelle View Post
                    Anyway, she was explaining an interesting phenomenon that the chromosome that controls gut motility also contains the lethal white gene and they figured that out since a lethal white (homozygous LWO) is... well, lethal due to the fact that their intestines are underdeveloped and contracted and they cannot move material through their intestines. It's interesting to think that various genes on chromosomes can control something like color AND development of tissue.
                    That expiation isn't quite right. The gut of a lethal white foal isn't under-developed per se, but it lacks nerve cells called ganglion cells which trigger and control gut movement (peristalsis). The gut basically has a "nervous system" of its own, which doesn't form in lethal white foals. So what does this have to do with coat color? Both the primitive neural cells which give rise to the gut's network of ganglion cells and the melanocytes which produce skin and hair pigment originate from an early embryonic structure called the neural crest. Some of the embryonic cells in the neural crest migrate out from the neural crest to the gut and to the skin where they go on to become ganglion cells and melanocytes, respectively, (The ones that stay behind go on to form the brain and spinal cord.) In lethal white syndrome, that crucial cellular migration never happens. So the foal is born with no pigment cells in its hair follicles (so it's completely white) and a gut that can't move food because it lacks the nerve cells that cause the peristalsis motion (so the foal dies of colic).

                    So lethal white syndrome is a defect in only one thing: a critical cellular migration event in the early embryo. But it's a defect that leads to two seemingly separate observable abnormalities, one of which just happens to be fatal.

                    Comment


                    • #11
                      Originally posted by aredhel View Post

                      That expiation isn't quite right. The gut of a lethal white foal isn't under-developed per se, but it lacks nerve cells called ganglion cells which trigger and control gut movement (peristalsis). The gut basically has a "nervous system" of its own, which doesn't form in lethal white foals. So what does this have to do with coat color? Both the primitive neural cells which give rise to the gut's network of ganglion cells and the melanocytes which produce skin and hair pigment originate from an early embryonic structure called the neural crest. Some of the embryonic cells in the neural crest migrate out from the neural crest to the gut and to the skin where they go on to become ganglion cells and melanocytes, respectively, (The ones that stay behind go on to form the brain and spinal cord.) In lethal white syndrome, that crucial cellular migration never happens. So the foal is born with no pigment cells in its hair follicles (so it's completely white) and a gut that can't move food because it lacks the nerve cells that cause the peristalsis motion (so the foal dies of colic).

                      So lethal white syndrome is a defect in only one thing: a critical cellular migration event in the early embryo. But it's a defect that leads to two seemingly separate observable abnormalities, one of which just happens to be fatal.
                      LOVE the scientific explanation - thank you!! I'm definitely not a scientist, nor do I play one on TV. I just breed paints.
                      Veni vidi vici. With a paint pony, nonetheless.

                      Comment


                      • #12
                        Originally posted by Arelle View Post

                        LOVE the scientific explanation - thank you!! I'm definitely not a scientist, nor do I play one on TV. I just breed paints.
                        Happy to oblige!

                        I don't know if it's ever been tested (because they die so young), but I wouldn't be surprised if lethal white foals are also born deaf. Guess where the embryonic cells that become the hair cells of the inner ear originate? (This is also why some horses with the Splash gene that end up with completely white ears are also deaf - they have no inner ear hair cells, for the same reason they have no melanocytes in the ear hair. It's the same problem - no neural crest cells got there - but it's confined to a small area of the horse's body, and therefore not usually problematic.)

                        Comment


                        • #13
                          Originally posted by Arelle View Post
                          was at an APHA seminar a couple years ago talking to the UF color guru regarding paint breeding, since obviously that's a big deal in getting a solid or not. We don't get the performance permits appys do.
                          Well, learn something new every day. I had thought that the reason APHA had "breeding stock" paints was so they were permitted to show, like CPO Appies ('cause in the old days, non-color Appies couldn't show.) There was a lovely breeding stock paint gelding at my old barn - blood bay, four white socks, full blaze - but it was irrelevant since they were trail/hunt seat riders who rarely showed and never at breed shows. A really solid (pun) citizen type horse who would go anywhere, do anything from age 3.

                          For myself, meh. CPO. The horse I owned before the present one was one of three that the breeder had for me to look at. One was black & white, but only 15.2 and TB build, the other - the one I bought - was a blanketed chestnut a little over 16 hands at 4 and finished at 16.2 - and the third was solid - looked like a WB. But I while I acknowledge that even Foundation bred horses occasionally come out solid, I was more of the mind that if I'm buying an Appy, I want the color.

                          I showed almost exclusively open - eventing, hunter/jumper, dressage and have had only Appies since 1977. I always laughed that when I retired my last eventer from eventing and thought I'd try out the Appy circuit, he was Circuit Champion Jumper at his very first double-point show - at age 19. Never even had to jump off. I realized the breed circuit wasn't for me, and stuck to open from then on.

                          Comment

                          • Original Poster

                            #14
                            Originally posted by aredhel View Post

                            That expiation isn't quite right. The gut of a lethal white foal isn't under-developed per se, but it lacks nerve cells called ganglion cells which trigger and control gut movement (peristalsis). The gut basically has a "nervous system" of its own, which doesn't form in lethal white foals. So what does this have to do with coat color? Both the primitive neural cells which give rise to the gut's network of ganglion cells and the melanocytes which produce skin and hair pigment originate from an early embryonic structure called the neural crest. Some of the embryonic cells in the neural crest migrate out from the neural crest to the gut and to the skin where they go on to become ganglion cells and melanocytes, respectively, (The ones that stay behind go on to form the brain and spinal cord.) In lethal white syndrome, that crucial cellular migration never happens. So the foal is born with no pigment cells in its hair follicles (so it's completely white) and a gut that can't move food because it lacks the nerve cells that cause the peristalsis motion (so the foal dies of colic).

                            So lethal white syndrome is a defect in only one thing: a critical cellular migration event in the early embryo. But it's a defect that leads to two seemingly separate observable abnormalities, one of which just happens to be fatal.
                            I really appreciate the details in this! It is a lot easier to understand highly detailed descriptions of things that quick comments. Thank you

                            Comment


                            • #15
                              Reading about all these wonderful colors with no photos is worse than reading the dessert menu when on a diet!
                              "When a true genius appears in the world, you may know him by this sign, that the dunces are all in a confederacy against him."

                              Comment


                              • #16
                                I am in the UK and while I like knowing the names for the genes, I think that it is important that we also keep our traditional names for colours. It is perfectly reasonable and easy enough to learn both and I think that it would be a shame if terms such as 'skewbald' were lost to history. Also there are situations where a shorter or longer answer is appropriate depending on the context of the conversation and who you are talking to.

                                There is one very confusing one though and that is buckskin/dun. In the UK everything that is biscuit coloured with black points is called 'dun' even if it doesn't have the Dun gene and is actually bay + cream (buckskin). Yes, every single 'dun' Conny is actually Buckskin.

                                Shetlands and Highlands have Dun.
                                Welshies and Connemaras have Cream.
                                Gypsy Cobs and Highlands have Silver Dapple (pic of Silver dapple Highland below).
                                What is often called 'sabino' is known as Blagdon in the UK (pic of Blagdon Gypsy Cob below).

                                In regards to broken coloured horses (pintos) we do mostly have Tobiano. There is also a form of Splash White that causes white legs and apron faces, often with belly spots too but that doesn't technically count as a coloured horse due to lack of white above the elbow to gaskin line. There is also the aforementioned Blagdon (sabino type white markings).

                                There is also the true Roan gene (dark headed roan) in the UK, eg New forests and Welshies have it.

                                ETA - the Gypsy Cob is EE, nSb1, negative grey gene gg, for those interested
                                Attached Files

                                Comment


                                • #17
                                  Originally posted by itiscourtney View Post
                                  I'm wondering if someone can explain the base colours and dilutions, also telling me the phenotypes of each. I'm not clued up on any of this, hense asking.
                                  Are certain colours only certified in certain countries? Or at least for specific breeds as I am aware that say a Shire, can not be accepted in Chestnut colours in the UK.
                                  There is a strong element of fashion in horse colours. Right in the beginning of the TB breed Oliver Cromwell had a good grey stallion but it has gone down in history as 'Place's White Turk' because once king Charles II regained the throne, no-one wanted to admit they used Cromwells horse (his stud groom was called Place) and the colour became deeply unfashionable in race horses. All the grey TBs today go back to Adcock's Arabian and the ones in the UK herd via a French horse, Roi Herode.

                                  The Suffolk Punch is only ever chesnut - and notice the missing 'T' because that is how the colour was spelt in the 18th century. No other colour permitted. Curiously enough, Suffolk cattle are also a lovely rich red.

                                  The Pura Rasa Espanol (PRE), loosely called Andalusian, until recently could only be registered as grey, black and bay. This was because chestnut Breton horses were used in the 19th century to improve Spanish horses for pulling things - so, by default, a 'pure' Spanish horse could not be chestnut. Grey is still the preferred colour in Spain but market pressure from around the world, and the number of pedigree animals that turned up red, means a chesnut PRE is now permitted. The Lusitano horse in Portugal, which shares the Iberian gene pool, retained a far more diverse range of colours, including dilutes, which the Spanish bred out. In Portugal bay is the status colour: the royal stud only breeds bays. If you look at Renaissance equestrian portraits the Iberian horses are all kinds of fancy colours but they all became unfashionable.

                                  Another problem with colours is that different cultures and different people use the same words to describe different things. To me, as Brit, 'spotted' means a dotted coat, like a leopard spot appy, but apparently spotted can refer to any broken colour in the USA.

                                  As Kaspercat said above, most UK skewbalds are tobiano and we simply do not have the genetic variation and diversity found in the US herd (presumably via the Iberian and Barb horses of the Spanish Conquistadors) but the kool, hip dudes like to say their bay skewbald is a tri-colour tobiano and fail to understand it refers to a colour pattern.

                                  Colour names change with time. When I was a child "sorrel" was a specific shade of deep rusty red chestnut. It is word vanished from modern UK terminology, unless it is still used regionally, but is obviously alive and well in the QH.
                                  "Good young horses are bred, but good advanced horses are trained" Sam Griffiths

                                  Comment


                                  • #18
                                    I'm adding a photo because I found one of an unusually loudly marked splash white Welsh Cob. I don't think that there are many out there like this, I've certainly not seen one IRL.
                                    Attached Files

                                    Comment


                                    • #19
                                      some clydesdales express Splash almost as loud as that cob!

                                      I've heard speculation that the wide range of colors in the SW US mustang feral population and the QH/Paint population was from the Spanish sending over the loud colored horses that had gone out of fashion so the SW horses got a larger than normal concentration of creme dilutes, duns, and the various pinto patterns. And Appaloosa!

                                      On the other hand the silver dapple, silver bay, colors tend to show up in some of the rarer gaited breeds but are in general rare in North America.

                                      I'm all for keeping regional terms, as long as we realize how they compare. In North America there is a basic East/west English/ Spanish divide on some horse terms.

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