Busted!!! Not just once but twice!!!
Peacemaker's Fleece
RR Guns' Peacemaker
At I.A.O. 2010, under a 3 judge panel, Peacemaker was summarily given the gate in the grey class, even though I’m wondering if he’s one of the best alpacas that we’ve produced out of our program. I had the opportunity to discuss his dismissal with the international judges and was informed that “there is no such thing as a grey without a full tuxedo”…
At MOPACA 2011, I was told, by an excellent AOBA judge that the AOBA (arbitrary) show rules specifically now say that a rose grey cannot have a fawn base but the dark fibers need to be brown…
Not too worry. We would have loved to have competed but it doesn’t matter, at least at this time, for our breeding decisions. Peacemaker is not for sale and I suspect will be dating a number of his second cousins in the very near future. We are breeding for grey and believe that there is every reason to believe that it can be bred for in a commercial market ( solid rose gray with minimized tuxedo for maximum fleece utility).
Of course we can only say that because we’re brash, delusional or sufficiently misinformed to dare to proceed into such a venture, but we’re working from a very different operational scheme than most grey breeders.
It appears from everything that I have read over the last few years that there are no shortage of “theories” on greys, but there is very little based on fact or science. There is a promise by some that we are very close to an understanding of the subject because we are going to “crack” the alpaca genome. From my understanding, all that means is that we will have another code to break in trying to assess the functions of the individual nucleic acid sequences and the proteins that they program. It will still take time to decipher and not be a “ready to read” roadmap. More likely we will have an incomplete atlas with some of the roads mapped but a lot of highways and biways “under construction”.
So here’s what I’m thinking…
One of the first thing s that I read when I first got started was Eric Hoffman’s “The Complete Alpaca Book” and was fascinated by a section on page p4-5 (2nd edition) telling us that there was a common ancestral camelid some 35 million years ago, but it’s evolution in North America dates to 9-11 million years.
A wild form, Hemiauschenia, crossed the isthmus of Panama into South America some 3 million years ago. Hemiausechenia eventually evolved into 2 genera Paleolama and Lama some 2 million years ago. Paleolama became extinct 12,000 years ago leaving only Lama (the wild guanaco) and Vicugna (the wild vicuna) in South America
We also know that all 6 known camelid species are able to crossbreed and produce fertile offspring. They include the Bactrian and Dromedary camels, guanacos, vicunas llamas and alpacas. If alpacas formed a separate genetic entity from a distinct llama population , I wonder what the process of natural selection might have looked like and how it might have been influenced through 6 millenia of breeding pressure.
Just “shooting from he hip”, I” imagine” that the earliest domestic alpaca was fawn with vicuna pattern (no surprise here) and there then appeared at least 4 color mutations out of the 2 pigments, phaemelanin and eumelanin i.e fawn/brown as suggested “reds” by Liz Paul, possessing phaemelanin and maroon/ black as eumelanin producers.
I have to agree with Nancy Rehbok that bay blacks are ultradark browns and maroons are a recessive eumelain (black ) allele, at least until proven otherwise. Here’s what Nancy has proposed:
There are the 7 genes and their allelles, the most nt allelle listed first.
A genes : A+ Vicuna pattern pheamelanized animal, A pheamelanized solid color, a+ eumelanin color with tan underbelly, a eumelanized animal.
B genes- instructs for eumelanin form B black, b maroon
C genes- dilutes both pigments but affects phemelanin more than eumelanin, can increase the size of light underbelly to the sides of the animal up mid side, incompletely nt and cummulative. C full color- no dilution, c+ mild dilution, fawn to light fawn, true black to bay black, c moderate dilution, cb maximum dilution, maroons can be pink or beige, blacks can be tan, fawns can become BEWs
D dusty gene- a double recessive pulls out fleece er giving a chalky appearance, combo with dilution genes can make blacks look steely gray. D full er, d chalky, flat coloring to fleece.
E genes- (ok not Mc1 r) but there is a gene that does this. Works in relation with A genes. Ed extra dark eumelanin (black or maroon on B genes), gives either black or maroon overlay to pheamelanized animals, or in eumelanized animals gives the true deep color that do not tip out, E gives dark face and feet (color on feet travels further up on A animals than A+ animals) on pheamelanized animals- but points can also be diluted to gray because of dilution genes. On eumelanized animals the color tips out in blacks and maroons. e a double dose retricts eumelanin production so that eumelanized animals appear white, pheamelanized animals have no significant dark coloring at points
M- disrupts eumelanin somehow turning black to silver, maroon to rose-gray blotchy in it’s effect.Not obvious in Pheamelanized animals but may cause color inconsistency even in these. M disruption of eumelanin, m+ mild disruption of eumelanin, may be the culprit of spotting in black or maroon animals, m has no action on eumelanin.
W- disrupts both eumelanin and pheamelanin. WW may be lethal. Easily modified so that color can come through depending on other factors W will make animals white, pinto, appaloosa, paint, piebald are all W made. w has no action. (Nancy Rehbock)
I also “imagine” a completely different gene locus that causes dark spotting on all of these base colors. It’s dominant, with a very variable penetrance, sometimes skipping a couple of generations. Then there is the “melanoblast distribution gene” which is responsible for “delivering the color”.
I remember learning some 4 decades ago about how the fertilized ovum becomes a blastula, then blastomere, then blastocyst , then trophoblast and embryoblast are differentiated and the embryoblast is like a 3 layered pancake (ectoderm, mesoderm and endoderm) which will bend and fold and with the precision and timing of an olympic gold medal diver mold itself into a cria.
Then…at a very specific time in the embryonic time clock…from a small pore on the top pancake (ectoderm, specifically neurectoderm) called the “neural crest” showers all of the ectoderm with “melanoblasts” which head out like F 15s to settle among other places in the hair follicles;
http://www.ehd.org/slideshow-images.php?slide=34
The melanoblasts, now melanocytes, settle into the population of stem cells in the hair follicle and depending on the genetic message, produce either phaemelanin or eumelanin in the melanosomes of their cytoplasm, which is then deposited into the orthocortex of the hair.
If it produces eumelanin, you get black or maroon, if phaemelanin, you get fawn through bay black. Furthermore, white is a result of no melanin and roan is a result of intermittent, or sputtering of pigment into follicle populations or possibly the individual melanosomes, the cell organelles that store, then release the pigment, creating a stippling effect.
Grey myths (in my mind)…
1) There is a different gene for solid roans and tuxedo roans, the former being recessive, the latter dominant.
2) Roaning does not include a fawn shade of phaemelanin
3) A solid red (rose) grey (no spots) is really a contaminated fawn.
My response to the myths…
1) Our breeding results clearly demonstrate a dominant grey patten using Gun’s ‘n Roses first fifty or so cria, with over ½ being grey, and ½ of those being “modern”, or solid, but after 3 years I can’t give accurate numbers to prove it….here’s why… Firstly, there is no absolute difference between the two…they are a continuum.
I would first submit GnR himself, who is, mistakenly, the poster boy for modern rose grey on the AOBA show website is not a “modern” but a mini-tux, easily proven by just one breeding result, in my opinion: Bred to solid brown (Melani), GnR, has produced Gun’s Next of Kin, an unmistakable “tuxedo grey”:
Aussie Guns n Roses
Melani
RR Guns' Next of Kin
In fact, if you look at the
AOBA website, at pictures for the differences between moderns and solids, almost all of them have evidence of predominantly white fiber in a centripetal distribution (extremities) , many of them with obvious white on their faces, and our own Guns n Roses (modern grey # 3) who is unquestionably a minituxedo grey for the reasons outlined above, not a modern gray! If he were not a “tuxedo”, he would simply not make a dominant “tuxedo” out of a solid !
Moreover, these are all tuxedos from our own herd…
RR Guns of Navarone
Kit Carson and Next of KinGuns n Roses
RR Rose Godiva
- Sakura
- RR Guns ‘ Peacemaker
The best summary that I could find relating to mechanism differentiation of melanocytes was in an article by Parichy et al:
I could find no evidence that the pattern is determined by a gene that affects the melanoblast, but instead suggested that it is in fact chemotactic peripheral dermal factors that attract melanin to the skin, to begin production of melanin by melanocytes some time later. What is the evidence that there is a single gene that controls both pattern and color in alpacas??
Any incomplete centripetal migration of melanoblasts, in my opinion, is a “tuxedo”. Moreover, solid greys, are an extension of the migration of those that have less expression of the “incomplete melanocyte migration gene” so that the pigment does not stop short of the ectodermal disc, in the 3 layered pancake of the embryoblast, discussed above. As a result, all the stem cell populations in the hair follicles are populated and thereby pigmented.
I suspect that the “incomplete (or delayed) melanocyte gene” is simply a result of how late the “embryonic clock” initiates melanoblast migration. Turn on the operator gene early, you fill in all the developing follicles. Start a few hours or days late, and the window of opportunity for melanoblasts to migrate into the hair papillae vanishes and you have “empty follicles” at the extremeties of the ectodermal disc which develop into the head, tail and limb buds; in quantities from very little to a lot, depending on the “lateness”.
This is nothing new. This is how cleft lip and palate develop in the human embryo, when the 2 “half faces” fuse in the midline to form a complete face. It is also why approximately 2% of women have “Mullerian fusion defects”, in which the 2 developing hemiuteri (or uteruses), fail to fuse in the midline, and can causes defects resulting in everything from a simple incomplete uterine septum, to a double uterus, to even a double vagina. The bilateral “mesonephric ducts” that form the kidneys, can do the opposite and actually fuse in the midline, to form a single “horseshoe kidney”. It is impossible to understand patterning genes without understanding embryologic development.
The patterns of migration can sometimes also be very specific, rather than just centripetal, as in appaloosas, and in horses the Overo, Tobiano and Sabino, the latter 3 all being dominant.
It is not clear to me why there is felt to be a single gene in grey that is felt to be responsible for melanin production, roaning effect, dark spotting and incomplete embryonic melanin migration. I wonder if it does not make more sense to have the melanocyte migration gene on a separate but closely linked gene locus and that we might have an explanation for the relatively common vicuna pattern that we see on many of our solids. It would fit our breeding results better to presume that the tuxedo and vicuna pattern are on the same gene locus:
RR Rose la Reina
RR Rose Aliyah
RR Rose Serenade
They are all fawns out of Guns n Roses. They are not “contaminated” with white fibres. Much has been made of the inheritance pattern of solid greys based on ARI cria registration results of a couple of well known “index” solid roan herdsires. I do not know enough about those notable studs’ genotype to reconcile their cited lack of grey transmission, but do believe that any conclusions based on their ARI data, if they are indeed genotypic greys, are likely to be very inaccurate, and here’s why:
RR Rose Delilah is out of Guns n Roses and a medium fawn damn… She had a very successful show career including a color championship at a very competitive CABA show at 22 months in what was unmistakably solid fawn. After her first shear, she is a very obvious solid rose grey.
This all occured after her first yearling shear. We have seen this in a number of our offspring, enough so that even if I wanted to, I would have a hard time making sense of mode of transmission, unless there was a means of “adjusting” color accuracy for the ARI database at 3-4 years of age. We tend to register our cria before 6 months age, as I suspect do most breeders. We tend not to take the trouble to change the registration color data, so pay no attention to it when looking for breeding outcome predictions from Guns n Roses. I can say that we are getting roughly ½ greys with those equally divided between “tuxedos”, mostly mini-tuxes, and solids.
Can I be more specific? Not unless I report data only on offspring over 3 years of age, based on Delilah and other cria, who have emerged as better expressed greys after their first shear. In our breeding scheme, I’ve come to believe that it is far easier to breed for rose greys without spots, than it is solid silver greys without spots. I’m not sure why , but it may be that fawn to brown greys (roans) are more closely related to the original “natural” roan mutation and silver greys are the mutation after it has interacted with the eumelanin (black/maroon) gene.
Ultimately, any science that I would look for however has it’s limitations and the art of breeding kicks in and each of us has to use our God given senses and analytic faculties to decide what we individually, are breeding for.
Musings…
I suspect that in the melange that constituted the earliest breeding stock, all colored alpacas showed evidence of a dominant dark spot gene, but that it may have more effectively been bred out of the lighter solid colors by more intense breeding pressure . It is not a very penetrant gene and even shows up in the best whites, and fawns/browns from time to time and “skips a generation”. In solid colors, it tends to be minor factor in premium lines, because even when present it is usually small and not on the blanket. This is generally not significant and evidence (perhaps) that the extent of spotting, is heritable. I do not believe that a minor dark spot is likely to cause a major problem with pigment distribution in progeny, at least based on my observations, and if it does, it is rare.
It is easy for me to imagine that in a tiered Incan society, the most prosperous breeders were able to select for the scarcer solids and they were at a premium. These breeders, even before the Spanish conquest and widespread llama hybridization, might have been more likely not to have a few bad seasons where they would be forced to breed for huarizos rather than pure alpacas, since hunger is a stronger motivator than cold.
I suspect that less prosperous breeders were more likely to breed the less desirable (for fiber) greys, which might have had more llama genetics and fiber characteristics. I would love to know how many “elite” breeding programs there were in Incan times for grey. Is the improvement in fiber quality all in recent (decades) breeding practices or has it been brewing for centuries?
Is it possible that there is something in how the different pigments (phaemelanin , eumelanin, intermittent melanin i.e. roan and no melanin i.e. whites ) interact with the follicular stem cells. Maybe the characteristics currently being bred into the best fawns and whites will never be manifest in greys and blacks because eumelanin affects embryologic follicle maturation and/or postnatal development of curvature, fineness, density etc so that the best grays or blacks will never have fiber that looks like the best fawns/browns with phaemelanin, or white with no melanin.
2) As to roans not having fawn as a base color:
Where to begin…For one thing I can’t think of any biologic variables, other that don’t have means and standard deviations in form and function. Not only do I believe that there are between fiber variations in pigment, but that there are “within” color variations. If we could measure the “nano” amounts of eumelanin and phaemelanin in each fiber, I suspect that there would be a mean and standard deviation. I suspect that there is a purer white, purer fawn etc…and finding that, barring a revolution in technology, will still be the domain of the artistry of the breeder and the experienced judge.
At this point, a tip of the hat to Paul Vallely, who is measuring “along fiber micron standard deviation”. I’ve seen the results and interpretation and the value of his testing as one more selection tool.
Going one step further, I’ve seen comments on forums that silver greys actually have “true grey fiber”. I even heard that used as an argument that it is that distinction that supports that recognizing fawn greys is “muddy” because it includes too many contaminated fawns.
The “true grey” fiber, would not surprise me, given biologic variability. Somewhere even between the “true white” and the “true black”, despite the roaning effect, there are going to be less white fibers and less black fibers, within the same blanket, so that some are almost in the middle i.e. silver. Perfect…silver grey!
In fact the more of those fibers that are close to the median, the better, I would assume for purposes of uniformity and processing. And that should be true for every color from bright white to ultrablack.
For what it’s worth, I can’t see those fibers, and would have to rely on a microscope, especially in finer animals. I don’t doubt that they are there though, in both rose and silver grey.
So where exactly is the corresponding intermediate color that corresponds in the white/brown blanket to the silver seen in the white/black blanket? What is the “perfect rose”? I’m not sure, but since it isn’t clear from the AOBA color chart, I’m prepared to fail in my breeding plans, if it isn’t very close to Peacemaker. Hey I’m cool with that…risk assessment is something that I dealt with for 36 years professionally and I know that the best that I can do is come prepared.
Incredibly, the same argument for “contaminated fawns” seems to be less of a concern with contaminated whites/silver greys. I have seen a good number of blue ribbon and even banner winning alpacas show in silver grey who appear very close to white, but on opening the blanket can easily be identified as almost certainly having less than 5% black fibers…it seems that there is far less concern with “contamination” in the silver series that rose. I suspect that it is far easier to identify black on white, than it is fawn or brown or white.
To continue rambling…it also makes more sense from anecdotal and personal observation that the original roan mutation was in the fawn brown series and silver grey arose after crossing those roans to blacks…
So here’s our breeding plan…
We believe that there is a possibility of breeding for commercial grey:
We believe that there are obvious advantages in breeding for an alpaca that can produce a solid roan color, with even distribution of pigment across an extensive blanket (minimized tuxedo) where the dark and light fibers are of equal micron, SD, and comfort factor so that there is no need for color blending or synthetic dyes.
Our biopsy results have provided us with a glimpse of the ability to estimate the percentage light and dark fibers, “in skin”, in each of the primary and secondary follicle populations. An explanation of that data can be found for Guns n Roses on this website under his listing. His distribution is very even for light/dark fibers in both primaries and and I wonder if that is a key to his ability to transmit solid roan with remarkable consistency.
In other words, I wonder if some of the index “solid grey” males that have been used to make the case for a separate recessive solid grey gene, have had very uneven light and dark color populations…that is to say that, for example, a male with 99% dark primaries , by biopsy, and 99 % light secondaries, is far less likely to produce solid grey than an alpaca with a 50:50 distribution in the primary/secondary fiber populations.
I also suspect that a good number of “indefinites” are in fact poorly expressed greys, even in those cases where they don’t completely “grey out” after a couple of years. In a case where “one man’s trash is another man’s treasure”, it may be that these animals are ideally suited for a solid grey breeding programs, especially if they have excellent fiber.
I would expect that if these animals were randomly bred in a closed population, there would be a Hardy Weinberg equilibrium that would be reached with a close to 50:50 color distribution of dark and light fibers in these alpacas. Artificial selection decisions could engineer a more even distribution by matching biopsy -established darker light/dark animals with lighter ones, so that much like mixing paints, one could select which males should be bred to which females.
Of course, there needs to be excellent fiber improvement in all other respects as an overriding goal. Color alone is not our paramount fiber concern, and we place brightness, fineness, consistency, uniformity, density and length first.
We believe that breeding greys through the fawn/brown color lines results in much better fleeces than breeding though black or grey to grey. We are now inclined to breed our solid rose greys to each other, or to brown or fawn.
We still breed for solid fawn and brown to maintain candidates to breed back to our solid rose greys.
Our “classic” spotted rose greys, all silver greys and solid blacks are bred back to silver grey. We don’t know on what scale “traditional” tuxedoed and spotted greys will be commercially profitable through smaller mill scale production but believe that there will always be a market for “traditional grey”, and are continuing to breed for better quality. We love our silver greys, spots and all and don’t in any way mean to suggest that there is a better or worse.
If there is a long term commercial production of the beautifully variegated yarns that come off the backs of traditional and improving greys, that will be great. Likewise, if both rose and silver grey fail to achieve success in a commercial setting, but cost more to produce because they being milled on a smaller scale, “we’re still there”…we just want it to be priced as the “champagne of fiber”…I might just have to have one of my grandkids finish the project.
As smaller breeders, we are enthusiastically embracing the model that given that we manage a herd on just 10 acres, that having an option to be “boutique breeders” for a quality rarer product will give us an edge in providing quality end product, but also quality breeding stock for any color.
We are limited by size in retaining only a finite number in our herd and can offer premium breeding stock in all colors. Check out what we have. If what we sell is what you are breeding for, call us. If you are interested in breeding for results and outcomes similar to ours, let us show you what we’ve done and if we can help you do the same.
We are very proud of what we have been able to accomplish in just a few short generations and our successes in competition. We are producing grey fiber that rivals most of the best in any color by assessment of independent judges, evaluation by hand and measurable data such as histograms and skin biopsies.
Not unlike any current theories on transmission of grey, there are undoubtedly “holes” in our breeding plans, but until we see better and more definitive explanations, it remains our breeding paradigm.
One last thought…how many of the very best “contaminated” solids with superb fleece, who don’t fit into commercial solid cremello/fawn/brown might be excellent contributors to a “solid roan” program?
That’s our story and we’re sticking to it…
Ken
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