Reptile & Amphibian Forums

okay, right to the point. if i have lets say a salmon and a normal and i bred them together would i get salmon,and normal, het for salmon, or what?
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1.2 leopard geckos1.0 jungle carpet python
1.1 columbian BCI

Salmon is the same gene as hypomelanism, which is a co-dominant gene. The pair you mentioned when bred together would produce salmons(hypomelanistic) and normals, there would be no hets.

while the first post was correct this can be further explaned.

assuming the salmon you have is not a super salmon (homozygous salmon), technically it is heterozygous for hypomelanism.
when bred to a normal, half of the offspring should also be heterozygous for hypomelanism. as mentioned in the other post hypomelanism is co-dominant, which means that a heterozygous animal will look visually different from a normal type animal.

just trying to make sure you are aware that there is a homozygous and a heterozygous form of hypomelanism. although i may have been to technical for you to understand and if so i appologize.
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- Jason F.

Hypomelanistic (Salmon) boas are the result of a DOMINANT mutation.
The Homozygous (Super) and Heterozygous (non-Super) forms look identical. If there was a phenotypical difference between the Homozygous and Heterozygous forms it would be CO-dominant.

Salmon (non-Super, the Heterozygous version) bred to a normal will yield:
50% Hypomelanistic (Heterozygous form)
50% Wild-type.
This will look like Half Salmon half normal.

If the Salmon is a Homozygous Salmon, also called SUPER.
When bred to a Wild-type you will get 100% Salmons (heterozygous form).

REMEMBER; Heterozygous means it carries ONE allele for the mutation, homozygous carries a matching pair (2).
An animal that has a dominant or co-dominant mutation will NOT LOOK NORMAL in the Heterozygous state.

DO NOT GO BY ADS. Often ads are posted saying an animal is possible dominant. This is WRONG. An Animal is either Homozygous or Heterozygous for a mutation. The mutation is either Co-dominant, dominant, recessive, or sex-linked recessive.

Jason, I saw you other post below, good information. I just wanted to make this one a little clearer for the original poster, I know you understand this stuff. If you could use capital letters at the start of sentences it would make your posts easier to read though

First, I appologize for not using capitol letters, it is a bad habbit from using word and outlook.

Second, you are correct about hypomelanism being DOMINANT not co-dominant. I have been talking about genetics a lot today and made a mistake.
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- Jason F.

for those who realize it, lol.

Too bad so many people actually think it is co-dominant, and not from a lack of being told otherwise.

Although I know that genetically the trait is dominant, I feel homozygous animals tend to have less black pigment around the tail blotches AFTER the vent when compared to heterozygous hypomelanistic animals. I think this is the cause for confusion in the case of its genetic inheritance.
I would like to see pictures of proven homozygous animals that do not have a reduction in black pigment surrounding the tail blotches after the vent.
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- Jason F.

by chance could you point out some good sights that show me pictures of heterozygous and homologous hypomelonistics? i know you said that they look the same but i'm curious of the price difference and finding a verifiable breeder. as of the info everyone gave me, thanks, it cleared everything up. i'm encluding some pics of my female. she was labeled a normal but she looks a little funky. can anyone clear up her pattern? i put my male boa in there too for comparison. he's the pic with the arm in there.

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1.2 leopard geckos1.0 jungle carpet python
1.1 columbian BCI

None of those animals you posted are hypos, but rather are nice looking normals. I would suggest maybe going to salmonboa.com to see lots of pictures of hypomelanistic boas as well as to read more about the genetic trait.

Just for reference here is a picture of a 05' hypo (heterozygous) ... when looking at hypos note the lack of black pigment around the tail blotches.

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- Jason F.

Hello Chris,

First let me say...I am by no means a genetics guy...but I do find it interesting....

I did not know where to put this post but hoped you would see it here.....

I have been thinking about Celia's Hypo/Motley litter....

Everyone says that the Hypo trait plays games with other traits causing great confusion....
I have seen hypo Arabesques...that I really did not think were Arabesques.....but they were...I guess....

My Theory for what is going on is that when the two co-dom traits come together...one tries to dominate the other and in my opinion the hypo trait is the Victor in most cases.

This makes sense to me...except that in Celia's litter...the normals were affected as well. But I found some reading that seems to make it sound like a new form is created...please read below....

My theory:

If this genetic crossover plays havoc with the melanin....and the Motley being mainly a form high in melanin...that if the melanin was shut off genetically would not the hypos take on a super hypo form? Now would this animal still reproduce both forms??

The following is just pasted in from something I found....

Gene Function and mutant alleles

It is important to realise that almost all colour morphs are produced by defective alleles for a locus pre-existing and functional in the normal bird. All these new colours are not being produced by the new mutant allele, they are being revealed by the dysfunction caused by the allele. Once this fact is realised, we can start to view colour morphs in a new light and begin to understand the true action of each locus that they help us identify. It is what is missing from the wildtype phenotype that is the true product of the locus being investigated.

If the mutant alleles for a locus are recessive to wildtype, then that tells us that a single functional wildtype allele is all that is needed to produce the gene product. If mutant alleles are co-dominant or dominant, then we know that the gene product requires two functional alleles coding for it, to produce its full effect. This generally indicates that the gene product is a protein with at least two base units (a dimer).

Co-dominant interactions can produce the third phenotype in three different ways. The most common is a blended type. In this case the heterozygous phenotype is midway between the two homozygous phenotypes. The best example is the dark factor locus where one mutant allele results in half the function of the homozygous wildtype genotype and two mutant alleles result in virtually no function. Alternatively, in cases where alleles have differential expression in different parts of the plumage, the heterozygous form is a sum of the greater effects. This is seen with the dilute locus in Budgerigars, where different alleles differentially deposit melanin within either the cortex or the medulla and the heterozygous phenotype represents a combination of the greater effects of each allele.

The third type of co-dominant interaction is known to occur only with alleles of the blue locus. It involves the process of complementation. In these cases the gene products of certain heterozygous genotypes are more functional than either mutant allele normally would be alone. The most likely theory is that the defect from different alleles act in a complementary interaction with one another, resulting in a greater than expected enzyme function for the end product.

As more colour morphs are discovered in each species, multiple allelic series are becoming increasingly identified. This is to be expected because there is a limited number of loci involved with pigment control and therefore limited places where a mutation can occur. So far no allelic series is known for loci with dominant or co-dominant mutant alleles, only those with recessive mutant alleles. And in all known cases a dominance hierarchy is formed within the allelic series. Mutant alleles with greater function (closer to wildtype) are either dominant or co-dominant with alleles with less function. I know of no situation where less functional alleles are dominant to other alleles in a series.

Andy
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Chris...do you know anything about the pearl boa that ..I think jeremy stone produced?? I was wondering what type of litter breeding that came out of? Thanks Andy
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to Jeremy about not only the Hypo Motley breedings he did, but about his Pearl as well.

The breedings Jeremy did were with the Salmon line. The Salmon Motleys DID NOT have classic Motley pattern, but it was obvious they were Motleys. They had the striping on their sides, the belly characteristics, the tail stripe, and connected saddles. The saddles just were not where they should be or shaped like they should be. It was more of a stretched out pattern (best descriptor in words without pictures I can think of).

I DO NOT think that Celia's litter was the result of the Motley male, if it was, it was only partial. There are no babies that are Motley in that litter.

I am not sure exactly what you were looking for in your first post. I assume you were looking for my opinion on the Motley X hypo litter of Celia's.

I posted below, this is taken from that post:
is that the babies were the result of old sperm from the Jungle last season. The Y chromosome sperm may have been weaker, and not have done its job. This account for the slugs. The X chromosome sperm is stronger and resulted in all female offspring.

There is one problem I could see. Are slugs JUST OVA, or were they improperly fertilized and died EARLY? If they were at one point fertilized ova (even if the sperm was bad) then my theory might work. If they are only bad OVA then this will not work, as they do not have the chromosome pairs from the sperm

On the Pearl. I do not know much. I do know it died of an (at the time) unknown cause. I believe it was a RANDOM mutation.
Jeremy had given me a little information, but I don't recall it. If you give him a call I am sure he will help you out with what you are looking for. Also, email him for some pictures of his Salmon Motleys.

Sorry, if I didn't give you the answer you were looking for.

>If this genetic crossover plays havoc with the melanin....and the Motley being mainly a form high in melanin...that if the melanin was shut off genetically would not the hypos take on a super hypo form? Now would this animal still reproduce both forms??

As far as I know, we have no reason to believe that motley and salmon are located on the same chromosome. Even if they are on the same chromosome, crossover is not necessary to explain things.

Albino shuts off melanin production. Combining albino and salmon produces sunglow, which is lighter than super salmon. It would be interesting to see what an albino, salmon, motley combination produces.

For what it's worth, every genetic combination I've worked with could be taken apart.

>The following is just pasted in from something I found....
>
>Gene Function and mutant alleles

If this piece was a bridge, it would be like one of the bridges that Indiana Jones keeps finding, the type thrown together from rotting planks and ropes frayed to a thread. Let's examine the last paragraph. By the way, the piece is about Budgerigars, which are not among the genetically best-known organisms.

>As more colour morphs are discovered in each species, multiple allelic series are becoming increasingly identified.

Pretty generally true, as far as I know.

>This is to be expected because there is a limited number of loci involved with pigment control and therefore limited places where a mutation can occur.

Again true, though "limited number" was 50 in mice around 20 years ago. It's probably higher, now.

>So far no allelic series is known for loci with dominant or co-dominant mutant alleles, only those with recessive mutant alleles.

I don't know about budgerigars. It's not true in mice or pigeons, to name only two species.

>And in all known cases a dominance hierarchy is formed within the allelic series.

Again true, as far as I know, even in the series containing dominant and codominant mutants.

>Mutant alleles with greater function (closer to wildtype) are either dominant or co-dominant with alleles with less function. I know of no situation where less functional alleles are dominant to other alleles in a series.

What is the definition of "greater function"? Whetever it means, I don't think it agrees with my experience with the dominant yellow mutant in mice.

Dominant yellow in mice is codominant to the other alleles at the a locus. A mouse with two dominant yellow mutant genes dies before it is a day old. A mouse with a dominant yellow mutant paired with one of the other alleles gets fatter and has fewer babies than normal mice. Whatever the dominant yellow mutation actually does, it clearly produces a mouse with a survival disadvantage.

Paul Hollander

We recently added a page to our site outlining Salmon genetics listing genotypes and phenotypes of several breeding scenario's. Shoot us an email and let us know if this helps out.

Thank you,
John
Salmonboa.com
Salmon Genetics

I think that page is helpful to refer to people in question about hypo and albino genetics.

I think a page should be created similar to the outdated/un-updated boa morphs page one kingsnake. A page that would include both a glossary of genetics terms as well as the known genetics and history behind the boa morphs.
I have been compiling a list (posted it in another post) for this reason, but I am not able to create a website.

Sorry to take things a bit off topic ... I think that page couldnt be anything but helpful.
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- Jason F.

From what I read on this forum, even experienced breeders often can't tell the difference between a salmon (Ss) and a super salmon (SS). Breedings 2, 4, and 7 on that page produce both SS and Ss snakes and show idealized expectations. How are these matings going to help anyone, particularly newbies, unless SS and Ss snakes can be distinguished?

Paul Hollander

a very good point you raised
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1.2 leopard geckos1.0 jungle carpet python
1.1 columbian BCI