I just had an epiphany...

[Foschi Exotic Serpents]

I read that entire thing. I'm not into the science of it like you are but its all very interesting to me. I too have wondered about the differences between co-dom and incomplete dom. Its interesting you brought up the blood type example. The one that always confused me was 0- verses 0+. For example.. I am 0+. When I got pregnant I was told by the Dr that if it was a girl I would most likely lose it unless they caught it in time for suppliments. The babies dad is 0-. I was told that 0- is not compatible with 0+ if the fetus is male. I do not understand this but because the fetus was male, my son was born being 0- just like his father, grandfather, grandmother and aunt. How does that work?? Ive wondered if it is similer in snakes genes. Like how some mutations do not survive. The pearl for example dies shortly after hatching. In boas the super motley does not live to breeding age. Could it be the same type of genetic incompatibility?

[unspecified42]

Also, not enough is known about the genetics of super mojaves and super lessers to determine if the gene that causes that mutation sits at the same locus or just coincidentally cause a BEL when bred together. We don't know if the mutation is with the actual color or just the level of pigment. It could be that both color mutations are link with a pigment saturation mutation. So if you could turn off the pigment saturation mutation, perhaps a super lesser would look different from a super mojave, which would look different still from a mojave/lesser.

[unspecified42]

I read that entire thing. I'm not into the science of it like you are but its all very interesting to me. I too have wondered about the differences between co-dom and incomplete dom. Its interesting you brought up the blood type example. The one that always confused me was 0- verses 0+. For example.. I am 0+. When I got pregnant I was told by the Dr that if it was a girl I would most likely lose it unless they caught it in time for suppliments. The babies dad is 0-. I was told that 0- is not compatible with 0+ if the fetus is male. I do not understand this but because the fetus was male, my son was born being 0- just like his father, grandfather, grandmother and aunt. How does that work?? Ive wondered if it is similer in snakes genes. Like how some mutations do not survive. The pearl for example dies shortly after hatching. In boas the super motley does not live to breeding age. Could it be the same type of genetic incompatibility?

Are you sure you heard right? That's completely bizarre and I have never heard if that before (I studied genetics on a college level for a while, and I know an abnormal amount of pregnant women). It also makes no sense.

If a person has a negative blood type, they lack an additional marker (independent of the A,B, and O blood typing). A body will attack any blood cells it doesn't recognize as its own, but it won't recognize a cell as foreign if it lacks markers, only if it has additional markers.

A shot called Rhogam (which I suspect is what you are talking about) is given to women who have negative blood types. This is because if their blood mixes with the baby's, their blood could attack the baby's blood cells if the baby is positive

None of that is related to the gender of the fetus. Also, O(-) blood is a universal donor type- it is given to everyone regardless of their blood type because it lacks all major markers, therefore no one's body will recognize it as foreign and attack it regardless of their blood type.

If you are sure that that is what your doctor told you, your doctor was a complete quack.

[Foschi Exotic Serpents]

I have no idea. I never thought it had anything to do with the sex of the fetus either. Oh and I worded that wrong. I meant to say that I was told it wasnt compatible if the fetus was female. I know 0- is a universal blood type but for some reason I was told that if the mother is 0+ and the father is 0- then its more likely that a female fetus would be faught off. I didnt understand it either. Maybe the Dr meant it the other way around? Or that it would depend on the fetus' blood type? They did mention something about the shot being used in those cases too. If what you say is right then that Dr may have been confused about whats compatible and what isnt. I havn't seen that Dr since my son was born 5 years ago and maybe thats a good thing lol.

[Russ Lawson]

The reason that it appears this way is not because it is true, but because of the nature of blood typing.

When we talk about 'A,' 'B,' 'AB,' and 'O,' we are talking about specific markers on the surface of the cell. 'O' is the absence of markers. That is why, phenotypically, 'AA' and 'AO' are the same thing- you gain nothing from the O. Both are being expressed equally, but you just can't see the 'O' being expressed.

Also, a roan cow (or horse or whatever) is not the same as incomplete dominance. You are thinking of the animal as a whole, not the individual hairs. Take a strawberry roan- they have both red and white hairs. Some hairs are red, some are white. If this color trait were incompletely dominant instead of codominant, you would have an animal with hairs that were all one color, and that color would be an intermediate between the two- so a lighter shade of red.

Think of it as flowers. If you take a white flower and crossbreed to a red one, a plant with incomplete dominance for the color gene will produce a pink flower. A plant that has a codominant color gene will produce a flower with some white petals and some red petals.

Regardless, blood type is a result of multiple alleles. There is no other way to describe the A and B type mutations. I also read this at a few different sources online after researching this a bit further. That fact was just left out in the description of co-dominance I had always been given. With that information it would have made sense to me much sooner.

If you're going with the definition of co-dominance from the roan example, if the white or red is the wild-type it is not the same thing as blood type because there are three different alleles, the wild-type O and the mutant A and B. It makes sense to me at least that type O would be the wild type seeing as no antigens are present (I forget the name of the rule, but it's along the lines of the simplest explanation is the most likely one). Additionally, I didn't say the roan was the same thing as incomplete dominance. They are both inherited in the same way, just with a difference in the way the phenotype is expressed, and I think in some instances it would be nearly impossible to tell between true co-dominance and incomplete dominance. Would it be logical to expect real co-dominance in reptiles going something like this: a snake has a red phenotype and a black phenotype, would the heterozygote be expressed as an animal with alternating red and black scales? Also, many reptile mutations don't even seem to fit the bill of incomplete dominance, as some (YB and cinnamon for example) don't appear as phenotypical intermediates (of any level - I know it doesn't have to be roughly halfway between to be incomplete dominant) between the wild-type and their respective homozygotes.

As far as the bit about the antigens being present on the surface of the blood cells, I already knew about that O was the absence of antigens, but I believe it is impossible to say if you're dealing with a partial dominance or full dominance simply due to the fact that the O type is the absence of antigens. Can you really say it is expressed fully if there is no real way to be certain of that? It is at least clear that A and B are some form of dominance, but considering the circumstances, it makes more sense to me as them being fully dominant to the lack of antigens in the O type. (If you haven't noticed by now I have a question everything attitude about life.)

As far as the entire BEL complex goes, I think it makes more sense given the number of combinations that do produce blue-eyed leucistics when bred together that they are different mutant forms of the same allele than that they are just coincidental. The fact that each makes blue-eyed leucistics in its own homozygote would seem to back up the allelic theory in my mind. I would also consider the fact that blue-eyed leucistics have never been produced from a mojave x lesser (or any other combo) blue-eyed leucistic bred to a normal, but if this ever does happen, I will gladly admit I was wrong. Until then, I have no problem saying the mutations are allelic (same with YB/spectre/Amir's granite that made the ebony) because that is how they seem to be working to me.

[Russ Lawson]

I have another argument for my theory that blood type is dominance and not co-dominance: Dominant until proven otherwise. This is the way I treat any mutation. For my example, assume for a moment that the O allele is actually telling the cell not to bond any antigens (I am not saying I believe this, but this is the easiest example I can give to portray my argument). If this were the case, in a type AO individual, the concentration of A antigens would be lower than in a type AA individual due to an equal number of conflicting signals. (However, this may have consequences because it is possible AO wouldn't be compatible with AA in this example if the O allele would be sending signals not to bond antigens, which is not the case in reality - basically why I do not believe this to be true.) This would be the sort of evidence I would need to agree that blood type is co-dominance and not dominance. If any studies have been done that would conclude that there is a lower concentration of antigens present on the surface of blood cells in a heterozygote than a homozygote, I would agree it is co-dominance. However, if the concentration of antigens was roughly equal, it would seem to support my theory of dominance over co-dominance. Again, I am only expressing that I think it is impossible to say for sure if blood type is co-dominance, which is why I disagree with calling it such.

[unspecified42]

Regardless, blood type is a result of multiple alleles. There is no other way to describe the A and B type mutations. I also read this at a few different sources online after researching this a bit further. That fact was just left out in the description of co-dominance I had always been given. With that information it would have made sense to me much sooner.

Sorry, I missed the part where you were confused about the number of alleles. I don't know how anyone could have explained blood typing without telling you that there were three alleles. That's good thinking on your part to have picked up on that if that's not the way it was taught.

If you're going with the definition of co-dominance from the roan example, if the white or red is the wild-type it is not the same thing as blood type because there are three different alleles, the wild-type O and the mutant A and B. It makes sense to me at least that type O would be the wild type seeing as no antigens are present (I forget the name of the rule, but it's along the lines of the simplest explanation is the most likely one).

Whether O is a wild-type or not really doesn't have bearing on what type of dominance occurs, though. Also, the number of possible alleles isn't really relevant to whether something is incompletely dominant or codominant, either. If you have a black cow and breed it to a white cow and produce a blue roan, you have produced an animal that is codominant. If you produced a grey animal (each hair is grey- an intermediate between black and white), you have produced an animal that is incompletely dominant.

It really depends on the mutation you are talking about. We accept what the pattern of a normal ball python is. However, there are clearly still different types of dominance that come into play. For example, it's clear that piebaldism is simple recessive, while pastel is incompletely dominant.


(and the theory that you are talking about is called Occam's Razor)

Additionally, I didn't say the roan was the same thing as incomplete dominance. They are both inherited in the same way, just with a difference in the way the phenotype is expressed, and I think in some instances it would be nearly impossible to tell between true co-dominance and incomplete dominance.

That is true. However, it doesn't mean that it doesn't exist, as you previously posited.

Also, don't forget that genetics is far, far more complicated than it appears on the surface. You (or someone else) mentioned before the fact that some mutations don't appear to survive. Or consider the spider wobble, or the high incidence of kinking in caramels. These suggest that these color/pattern mutations are linked with other traits as well that we don't really know about or understand. Have you studied the idea of independent assortment versus genetic linkage during crossover?

The level of understanding that most people (particularly in the BP world) have stops at simple Mendelian principles. Which is fine for the most part- it gets us where we need to go without getting bogged down in ridiculously tedious detail. But don't forget that Mendel was able to figure these things out with a few pea seeds, his eyes, and some simple math. Science has come a long, long way since then, and so has our understanding of genetics. What we've realized is that it's far more complex than we ever imagined!

Would it be logical to expect real co-dominance in reptiles going something like this: a snake has a red phenotype and a black phenotype, would the heterozygote be expressed as an animal with alternating red and black scales?

Yes

Also, many reptile mutations don't even seem to fit the bill of incomplete dominance, as some (YB and cinnamon for example) don't appear as phenotypical intermediates (of any level - I know it doesn't have to be roughly halfway between to be incomplete dominant) between the wild-type and their respective homozygotes.

A homozygous YB is an ivory, a homozygous cinny is a super cinny. YB and cinnamon are the phenotypical intermediates. Both are incompletely dominant genes.

In true codominance, there is no phenotypic intermediate. You have black and you have white, and together they produce black AND white, not grey.

You are correct when you stated earlier that in the BP world the term 'codominant' is often misused.

As far as the bit about the antigens being present on the surface of the blood cells, I already knew about that O was the absence of antigens, but I believe it is impossible to say if you're dealing with a partial dominance or full dominance simply due to the fact that the O type is the absence of antigens. Can you really say it is expressed fully if there is no real way to be certain of that? It is at least clear that A and B are some form of dominance, but considering the circumstances, it makes more sense to me as them being fully dominant to the lack of antigens in the O type. (If you haven't noticed by now I have a question everything attitude about life.)

That's a good attitude to have.

I don't know how one could tell if AA and AO are phentypically different unless you can quantify the number of cell markers and determine that AA has more than AO. I can't find the results of any research that has been done in that area, though, as blood-typing is typically just done qualitatively.

Regardless of whether type O is codominant or recessive, though, we do know that A and B are codominant. When found together, they both retain the same qualities and express them equally. A and B create AB, which carries the same genotypic traits as each separately, only they are equally and simultaneously expressed.

As far as the entire BEL complex goes, I think it makes more sense given the number of combinations that do produce blue-eyed leucistics when bred together that they are different mutant forms of the same allele than that they are just coincidental. The fact that each makes blue-eyed leucistics in its own homozygote would seem to back up the allelic theory in my mind. I would also consider the fact that blue-eyed leucistics have never been produced from a mojave x lesser (or any other combo) blue-eyed leucistic bred to a normal, but if this ever does happen, I will gladly admit I was wrong. Until then, I have no problem saying the mutations are allelic (same with YB/spectre/Amir's granite that made the ebony) because that is how they seem to be working to me.

If I'm understanding, you are saying that mojave and lesser are alleles that are on the same locus, correct? That does seem possible. However, the fact that two fires produce a BlEL and two YBs produce an ivory makes me think that there is just something else there- something that has to do with the fact that mojaves, lessers/butters, and fires all seem to exhibit a good deal of blushing, fading, and all-over lighter coloration than a normal. Perhaps these color mutations are all linked with a pigment mutation that overrides the color in the super form.





(I know that replying in this format can sometimes come off as hostile online- picking apart someone's post. But please realize that I don't intend to come off that way. I just think that it's more organized to format my reply this way because you've posed so many questions. You've brought up some really interesting points and I'm enjoying the intellectual work-out!)

[unspecified42]

I have another argument for my theory that blood type is dominance and not co-dominance: Dominant until proven otherwise. This is the way I treat any mutation. For my example, assume for a moment that the O allele is actually telling the cell not to bond any antigens (I am not saying I believe this, but this is the easiest example I can give to portray my argument). If this were the case, in a type AO individual, the concentration of A antigens would be lower than in a type AA individual due to an equal number of conflicting signals. (However, this may have consequences because it is possible AO wouldn't be compatible with AA in this example if the O allele would be sending signals not to bond antigens, which is not the case in reality - basically why I do not believe this to be true.) This would be the sort of evidence I would need to agree that blood type is co-dominance and not dominance. If any studies have been done that would conclude that there is a lower concentration of antigens present on the surface of blood cells in a heterozygote than a homozygote, I would agree it is co-dominance. However, if the concentration of antigens was roughly equal, it would seem to support my theory of dominance over co-dominance. Again, I am only expressing that I think it is impossible to say for sure if blood type is co-dominance, which is why I disagree with calling it such.

We were typing at the same time and reached the same conclusion.


I think you are misinterpreting what an absence of cell markers means. Type O doesn't actively do anything. It doesn't say "don't bond with antigens." It simply has no antibodies so it doesn't bond. It doesn't produce incompatibility in any form. Someone with type AB blood has no genotype for O at all, and yet they can still receive a transfusion of type O blood with no reaction. So can someone with type A blood, or type B blood.


Finally, though, the fact that makes all of the above purely academically moot is the fact that we DO know that regardless of whether type O is recessive or codominant, types A and B are codominant in an individual with type AB blood.

[Russ Lawson]

I would quote all of yours in the same fashion you've done mine (no I don't perceive it as a hostile approach), but it started to get fairly convoluted when I tried that way, so I'll just reply. I agree that A and B are co-dominant with respect to each other. When other mutations work in the same manner, I agree they are forms of co-dominance rather than incomplete dominance. I do think that when you are dealing with animals that have any pattern versus a solid colour though, it could potentially get to the point where it might be incredibly difficult to tell whether a mutation is co-dominant or incompletely dominant (though I've never seen an example of any mutation like this that may potentially have been co-dominant and not incompletely dominant).

I don't remember what I was thinking when I said co-dominance didn't exist. It was late, and I have a bias against the term since I always see it being used incorrectly. It exists in exactly the same way I originally perceived it: identical to incomplete dominance apart from the way the phenotype is expressed.

Homozygous fatal mutations, and side affects of other mutations such as kinks and wobbles make perfect sense to me. The resultant mutated proteins have adverse affects besides those on pattern and colouration. That is the only logical explanation due to the fact that these conditions are only passed on to the mutated offspring of these specific pairings. Mutations in DNA are translated to mutations in proteins. Mutated proteins do things they aren't supposed to do, and it's rare they only do one thing wrong.

Have you studied the idea of independent assortment versus genetic linkage during crossover?

It sounds familiar, but it's been a while since I looked at anything like that, so I'd need a refresher. I'm finally going to be taking my college genetics course in the summer semester, so I'm sure I'll hear all about it then. I came up with simple enough explanations for the kinks and wobbles without this information though. (I'm also going to be taking a bioinformatics course this Autumn, which should be pretty exciting).

Also, anyone who ever (maybe that's a bit harsh, I'll go with since people started beginning to understand DNA) thought genetics would always be as simple as Mendel's principles was a fool. Yes, it's a good start, and decent for those who need nothing more than a basic understanding of genetics, but it's easy to see it definitely gets much more complex than that (look at something like human eye colour, or skin colour to see that).

I never disagreed that YB and cinny were incompletely dominant - I was merely stating that neither appeared to be a phenotypical intermediate of the homozygote at first glance (or even after studying them for a while), so the real meaning of the term is somewhat lost on them.

I don't know how one could tell if AA and AO are phentypically different unless you can quantify the number of cell markers and determine that AA has more than AO. I can't find the results of any research that has been done in that area, though, as blood-typing is typically just done qualitatively.

Regardless of whether type O is codominant or recessive, though, we do know that A and B are codominant. When found together, they both retain the same qualities and express them equally. A and B create AB, which carries the same genotypic traits as each separately, only they are equally and simultaneously expressed.

I agree with you on this, except for now I believe A and B are co-dominant with respect to each other and dominant with respect to O. Call me stubborn. Also, I didn't mean to imply I believed that type O was actively doing anything. I was giving a hypothetical example to try to explain my stance.

If I'm understanding, you are saying that mojave and lesser are alleles that are on the same locus, correct? That does seem possible. However, the fact that two fires produce a BlEL and two YBs produce an ivory makes me think that there is just something else there- something that has to do with the fact that mojaves, lessers/butters, and fires all seem to exhibit a good deal of blushing, fading, and all-over lighter coloration than a normal. Perhaps these color mutations are all linked with a pigment mutation that overrides the color in the super form.

Yes, that is exactly what I am saying. Additionally, I believe Russo hets and phantoms/mystics are two different mutant alleles located on the same locus. I agree it is possible that there is something else going on that causes leucism in all of the examples you gave. I wouldn't agree that it is the same mutation all are linked to considering combinations of say lesser x fire or fire x YB do not make leucistic animals as well. Also, judging by the appearance of "paradox" individuals of these mutations (which aren't particularly uncommon), I believe this gets turned off in certain parts of the animals, unlike the typical paradox of say an albino, which I think most people agree is more likely caused by a chimerism. If you pay close attention when you come across a picture of a paradox super mojave, ivory, or super fire, the pattern on these animals looks like a more extreme version of the respective heterozygote.

[WingedWolfPsion]

Rhogam is not given to protect the baby--it is given to the mother to prevent her from developing antibodies against the baby's blood. Exposure is not expected to occur until birth, so Rhogam doesn't do anything in terms of the current child.

Instead, it enables the woman to avoid problems with any FUTURE + blood type children she might have--to prevent her immune system from attacking the fetus. If there aren't going to be any more (for certain), then the shot is unecessary.