Peafowl Genetics for Dummies (in other words us)

I agree with George. The genetics of those birds are not the same. The first bird is not silver pied. I see a couple of colored eyes. I see some green saddle feathers.

I do agree the first bird is poorly labeled. It is obviously at least split white eye. Given the whole "saddle must be silver to be silver pied" requirement, it cannot be silver pied. If I now understand silver pied correctly it is most likely a split silver pied bird. The single white eye marker is the silver pied white eye allele as opposed to the plain white eye allele.
 
I agree with George. The genetics of those birds are not the same. The first bird is not silver pied. I see a couple of colored eyes. I see some green saddle feathers.

I do agree the first bird is poorly labeled. It is obviously at least split white eye. Given the whole "saddle must be silver to be silver pied" requirement, it cannot be silver pied. If I now understand silver pied correctly it is most likely a split silver pied bird. The single white eye marker is the silver pied white eye allele as opposed to the plain white eye allele.


OK, then look at the two pics I linked. One is the first under the label "pied" despite being obviously also white eyed. Yes, I see some green in the mantle. But also look at the pattern of blue spotting on the back of the head.

http://www.unitedpeafowlassociation.org/IndiaBluePiedPeafowl.html

Now look at the first pic under "silver pied". Once again, you see some green in the mantle. And look closely at the pattern of blue spotting on the back of the head.

http://www.unitedpeafowlassociation.org/IndiaBlueSilverPied.html

It looks as though it could even be the same bird. In the first pic, the train is held together, and it appears that very little is white in the center. In the second pic, the train is spread out, showing more white in the center. BUT...if you look at both pics back and forth, it appears that what looks like the "center" in the first pic is actually both "colored stripes" in the train being held together, with the center folded somewhat underneath. When spread out, the "colored stripes" are further apart, and the white center becomes more apparent as the feathers fan out. Even if they're not actually the same bird, I can't see a specific "silver pied trait" which is in one but not the other. Please point it out to me if you can see it.

:)
 
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Rosa.... The 2nd photo is from Craig Hopkins and is a number of yrs. old. I don't remember how long it has been but this bird probably came from Brad Legg as he was the first to really have them available He has all white eye or white train feathers and if you took the white away you would still have a white eye in them. Please note the hen colors on Craig's bird also as this is how a hen should look, with the darker shade appearing to have depth . some people have stated that they have a S P hens and all I am try to do is help people recognize one when they see it. The photo of the first bird is a good pied but has some feathers that are not W Y. From some of my experience, The W Y gets better with age to a point but I think it is only a good pied W Y..
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connerhills
 
On my screen, the first pic on the "pied" page shows a male with some white in all the ocelli visible in the pic. The ocelli aren't all ALL-WHITE, but there's at least a dot in the center of each (again, as I'm looking at it on my screen). I was comparing ONLY the first pic on the "pied" page with the first pic on the "silverpied" page. In both pics, I see some ocelli with color on the outside, but white on the inside. I see other ocelli that are totally white. I see green on the mantles of both. I don't see any "diagnostic difference" between those two pics which would result in one (but not both) being called "silverpied". In any case, it's confusing to illustrate "pied" phenotype with a peacock who also has white ocelli (which are due to a different mutation, and are not necessary for a bird to be called "pied") and not make notice of that in the caption.

I mean no disrespect, but I understand if it is taken with some -- regardless, I'll ask. Take it as an opportunity for improvement rather than a rant.

Is this intended to cause confusion, or is it just sloppiness on the website? I mean, this is supposed to be the "United Peafowl Association", the unified body of knowledge on these birds.

:-/
 
Good morning all. I am setting here drinking my coffee and see that I should have not offered any info to start with, but I always get to some point that I want to say something.. Brad says "see why I don't go there" I take no offence at anything said as I been down this road many times. in my 75 yrs. .That is the way it is in life now days, but if you don't have some kind of guidelines every one just goes which ever way they think makes them feel happy. Yes , I know Carol and she has good birds and works hard at it If you and her call it a white eyed, that is fine . I won't confirm or reject every bird on the net. In regard to the content and presentation on the UPA web site I been there also , there have been a number of people in charge of the UPA site and started to redo it so that we had what everyone thinks it should be like. Due to egos that too folded. We lost the web master and was in limbo for a while. The current web master I think is trying. HIs guidance will be from Jay Louden At a BOD meeting once I stated the very same thing that the UPA should be the authority for a source of info on peafowl as at that time The UPA had the people that wrote the book . But there has not been an unified body in the UPA for as long as I was active and still not. . Thank you for letting me be a part of this thread . George
 
Christopher
Presence of codominant genes can give birds with different phenotypes ?
Codominant = war of dominance? .... the result is not known!
 
In reality, unless a mutation results in a gene not being transcribed/translated (ie. "silenced"), they are expressed even when an individual is split to a recessive mutation. It's just that we don't see an effect with our eyes that differs from an individual homozygous for the "normal" version of the gene. But that's a limitation of our eyes -- if you measured things differently, there is an effect. For example, let's say you have two black cats. One is black split for the Siamese/ColorPoint mutation, the other is homozygous (or "pure") black. Just looking at them with our eyes, we can't tell them apart. HOWEVER, if you were to measure the actual amount of melanin deposited in the hairs, there would be a difference. The "pure" black cat will have more pigment in its hairs than the black split to siamese cat. It's not enough of a difference to be noticeable with our eyes, but it is enough of a difference to be able to be measured in a lab.

So, we classify a mutation as recessive when being heterozygous for it shows no apparent difference. But within the body, there is a difference -- individuals with two copies of the "normal" version of the gene will produce more of that protein than individuals with only one "normal" copy. When the mutation is considered recessive, the less-than-"normal" amount of that protein is still enough to give the "normal" appearance. The mutated protein doesn't work the same way, but at the same time, it doesn't interfere with the "normal" version working the "normal" way. Only when there's no "normal" version of that gene present (i.e. the bird is homozygous for the recessive mutation) do we notice the difference -- because there's no "normal" version of that protein being produced which is required for "normal" appearance.

Now look at co-dominance, incomplete-dominance, etc. This time, the mutated version "does something" that either interferes with the "normal" version, or blends with the "normal" version to give a "blended" phenotype. Co-dominance is classically illustrated when there's a gene with one allele for red petals, and one allele for white petals, in a particular flowering plant (I think it was petunias, but I'd have to go back and check). Have two copies of "red"? The flowers are red. Have two copies of "white"? The flowers are white. Have one of each? The flowers are pink -- not red splashed with white, but an even pink. In this case, it's as though the White gene reduces the overall amount of pigment produced evenly. "Pink" flowers are thus "red" flowers with an even decrease in amount of pigment. But in appearance, we interpret it as both genes being visible at the same time, resulting in a blended phenotype that is neither one nor the other.

Incomplete- or partial-dominance is slightly different, but again, it's based on how we interpret the appearance of the phenotype. An example in peafowl would be any of the white-spotting mutations (White, Pied, and White Eyed). Have no copies of either? The pea has "normal" pigmentation. Have one copy of either? The pea has some "disruption" of pigment, but not as much as having two copies of either. Why the spotting rather than an even dilution? Possibly because the white-spotting genes affect pigments produced on-site to not "fit" into the feather tubes, leaving filaments without pigment. Since pigment is produced for feathers basically right where they'd get deposited (as opposed to somewhere like the liver, and then floating through the bloodstream to be evenly dispersed), if one cluster of melanocytes (pigment-producing cells) makes the "too big to fit in the feathers" pigments, that cluster will result in a section of unpigmented feather (not necessarily an entire feather). So one copy of the gene will make the faulty pigment, but the "normal" copy will make the "normal" pigment that CAN fit into the feather to be deposited.

In peas, look at the White Eye gene, which we call Incompletely- or Partially-Dominant. Why? Because when there's one copy of White Eye, we see an effect. Why is it not Co-Dominant? Because we don't see a blended phenotype -- we see a patchwork phenotype -- in birds which have only one copy of White Eye. Some ocelli are white, some are "normal". We don't see "gray" ocelli all over -- we see some of each. When a pea has two copies of White Eye, then all (or virtually all) ocelli are affected.

OK, then what goes on with recessive mutations that "dilute" pigment? Well, it's hard to be specific since I haven't studied them specifically, but I can say that there is no one gene for melanin. The pigment is produced through a series of reactions, involving proteins that are either directly synthesized from genes or are the result of other reactions. Let's think of making melanin like making a cake, and the separate ingredients and tools are the proteins involved in its production. Some come from genes (things like, for example, eggs...or milk..or other ingredients that are "harvested" as-is) while other ingredients come from previous processes (things like white flour, which had to be refined from wheat seeds). Then you have the tools -- mixing bowl, egg beater, etc.

If you delete one of the necessary tools, like a mixing bowl or baking pan, you can't make the cake at all, and you end up with no cake (like an albino, which has no melanin). If you change an ingredient, you'll get cake, but perhaps not the same cake. Let's say you use whole-wheat flour instead. You'll have cake, but it won't be as fluffy -- it'll be a little more "bran-y". Or perhaps you switch out the four chicken eggs in the recipe for four goose eggs. Goose eggs are larger, so you'll have an "eggier" cake. With mutations that modify (but don't delete) the pigment, you're changing one of the ingredients, resulting in a modified cake. Perhaps the cake won't rise as much, so it'll be smaller in volume. Perhaps the mutation "reduces" sugar -- having one copy results in 3/4 of the "normal" amount of sugar, and having two copies results in 1/2 of the "normal" amount of sugar. You can still get a cake that's "sweet" with 3/4 the sugar, and you probably won't notice it much. But delete half, and there's a noticeable difference. That's like a recessive mutation.

The white-spotting mutations clearly don't result in the peafowl being unable to make pigment -- they have pigment in their eyes -- just that the pigment doesn't "fit" into the feathers. That's like making a cake in a pan too large to fit in your friend's fridge -- you made cake, for sure, but you can't put it where you thought it should go (It might be the other way around -- the white-spotting genes might make the feather tubes too small to allow the pigment to get through, which would be like your friend not leaving you enough room in the fridge for your cake -- I don't know, but you get the point).

ETA -- one often hears that a white mutation "isn't albino" and it seems odd that someone would just insert that. What's the difference? Well, albinos can't make melanin, whereas white non-albino animals CAN make melanin, but it just can't "fit" where it "normally" goes. So? Well, making melanin involves steps that are important for making other VERY IMPORTANT substances needed for other things, like certain neurotransmitters. If the "mistake" that prevents melanin ALSO prevents (or severely interferes with) production of those neurotransmitters, then you have the "unhealthy" effects sometimes seen in albinos. But that's a whole other topic....

At the DNA level, unless a mutation results in a "silenced" gene, there's not much difference between a recessive, co-dominant or incompletely-dominant mutation. We assign those labels based on what effects we see in the individuals. The genes aren't "battling for dominance." If there's any dominance, it simply means that we can see an effect when there is only one copy of that version of the gene. Recessive simply means the effect is "hidden" from our vision, even if we can detect an effect using other tools (such as with the cat example I mentioned in the beginning). For example, if someone had the blood type of A+, but his mother was O- (meaning no A and no Rh proteins) you'll know that he's split for O and for Rh-, even though he "types" at A+. But if you were to measure the actual amount of the A and Rh proteins produced, it would be less than that produced by a person "pure" for A+. When we blood type someone, we just check for presence -- not quantities -- of specific blood proteins. If you have the A and Rh proteins, you are A+.

:)
 
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I wanted to add that this is why it is certainly genetically possible for a pea to express two color mutations at the same time. In my cake analogy, it is like modifying two ingredients in one cake. Take, for example, the first known combination, Peach, which results from a pea expressing both the Purple and Cameo mutations. Separately, each has a sort of "dilution" effect on the "normal" IB color -- but each has a DIFFERENT dilution effect. Peach peafowl thus exhibit TWO dilution effects. In the cake analogy, let's say I was going to bake a cake for two people. One can't have dairy, and the other can't have gluten. I can make a cake that satisfies both -- in other words, a cake with two modifications. The result is a gluten-free, dairy-free cake (and yes, I've made recipes like this -- I like the challenge of modifying recipes after understanding how each ingredient functions, and making appropriate substitutions which satisfy those functions). The result is NOT a cake with some gluten-free but dairy-inclusive parts, and some gluten-inclusive but dairy-free parts. And the pea is not colored with some Purple and some Cameo parts. Perhaps that is where the confusion about "colors can't be combined" originated. Each mutation affects "normal" IB appearance in different ways. A pea can thus certainly display both effects together, and the result is a "blend" of both rather than a "patchwork" of each. How that result will appear may not be easily predicted, being as we don't fully understand exactly what each mutation "does", but it would certainly be interesting to discover by trying.

A parallel in chickens would be the two diluting mutations Lavender (aka Self Blue) and Andalusian Blue. Both result in a "diluted black" but not the same way. While it is frowned upon, because the result of combining them is a chicken which fits neither color standard, it IS possible to have a Lavender-Blue or Lavender-Splash chicken. I was curious to see how they looked, and obtained a few pics of Lavender-Blue chickens from BYC a while back. In the roos, you can see the Blue pattern of dark hackles and sickles and a lighter breast, but the darkest shade is Lavender, and the lighter shade is paler still -- the effect of two copies of Lavender and one copy of Andalusian Blue working together. I haven't seen pics of Lavender-Splash (two copies of Lavender and two copies of Andalusian Blue), but I don't doubt they exist, or are at least possible.









:)
 

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