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Super Tessera's

So, I don't have any supers, but some of the things you noticed are also present in my "het tesseras". I'll post pictures below to provide perspective:

Anery tessera (het stripe phet amel) I hatched in 2014. Has a break in the neck, but a fairly regular cheek pattern:

12122483_10208175814452414_1760811367809186872_n.jpg


And its belly:

12066064_10208175832212858_6954383885557759028_n.jpg


Next, one of this year's anery tesseras (het stripe, phet amel). Has the break in the neck, a regular cheek pattern, but the belly pattern matches your suspected super tessera pattern:

12118891_10208175852693370_5243580985570657841_n.jpg


Cheek:

12112075_10208175842453114_1349574881681734228_n.jpg


Belly:

12122934_10208175937455489_4761819776074240649_n.jpg


Normal tessera (het stripe phet amel) that I hatched this year. Has the break in the neck, the typical belly pattern, but the cheeks are regular:

12140703_10208175962096105_6515520651199278674_n.jpg


And the belly:

12096184_10208175962656119_101278864965226942_n.jpg


Anery tessera (het stripe phet amel) with the neck break, the belly pattern, but not the cheeks:

12115953_10208175969816298_2797210565200975030_n.jpg


12074806_10208175971336336_4263043615506824615_n.jpg


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I hope that helps in telling apart what may or may not be a super marker. Personally I haven't really seen anything that jumps out at me as a het marker, but who knows :)
 
I think that what Nick Mutton discovered about the Super Caramels (in Carpet Pythons) likely holds true with the Super Tessera's, in the fact that some non Supers will have some markers, but all Supers will have all the markers.

Coincidentally, a Super Caramel marker is in the cheeks as well.
 
Here is a thread on Super Tessera's posted by Rich Hume in 2013.

These are the photos he emailed to me.
 

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Just thought I'd give this thread a little bump to update it with pictures of my babies from a Tessera to Tessera pairing. Statistically each of the tessera babies has a 25% chance of being a super tessera, so it is possible that they all missed the odds, but I find it unlikely. I'm not really seeing any strong indications of the potential markers personally, but have a look and see what you think. Here are pictures of all of their neck and cheek patterns.

Arroyo:

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Bougainvillea, such a sweet snake:

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Cholla:

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Creosote. This one to me seems more likely to be a super than the others, if these patterns turn out to be actual markers. He cheek pattern seems more broken up (a little bit) and his neck stripe is detached.

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Hibiscus. Patterning is very hard to see with him because of his morph. I think I might be seeing a broken cheek pattern and partially detached neck stripe (although that could be influenced by his diffused gene).

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More babies in the next post!
 
Lantana. Very clean cheek stripe and very regular looking neck pattern.

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Monsoon. Maybe seeing the markers here.

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Ruellia, snow tessera. Nearly impossible to photograph, so it's hard to see his pattern.

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Saguaro:

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Sahara:

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More to come...
 
I think you could be on to something with the cheek pattern, but should also be prepared for the chance that there are no markers for super tesseras.

The reason for this relates to mechanisms of dominance. One mechanism is called "dominant-negative." Dominant negative is when a dominant mutation is dominant because the gene product of the mutant allele is not only nonfunctional, but basically poisons the product of the wt allele. This can happen when the protein product of a gene functions as a "dimer" or "multimer," meaning that the protein product of the gene has to bind to other copies of itself to carry out its function. If a member of the complex is the product of the mutant dominant-negative allele, the complex no longer functions, and the phenotype is similar to what you would get if the animal were homozygous for two non functional alleles at that locus, hence the term dominant (since the allele is dominant)-negative (since the phenotype is similar to homozygous for a null allele). With dominant-negative mutations, the phenotype is usually not exacerbated when the animal is homozygous for the dominant-negative allele.

But hopefully you do find reliable markers!

I was just reading through this thread for the first time and was basically going to say this, until I saw that it had already been said!

Many dominant traits do not have heterozygous markers (indeed, strictly, if a trait does have heterozygous traits it isn't dominant, but co-dominant). For example, wild type colouration is a dominant trait over amelanism, but to my knowledge there are no 'het markers' that can be observed in a normal that suggest it's het amel.
 
(indeed, strictly, if a trait does have heterozygous traits it isn't dominant, but co-dominant)

As far as I understand it, "codominant" is misused frequently in herpetoculture; most genes labeled as codom are in fact incomplete dominant. I'm not sure of any true codom genes existing in corns or ball pythons.

I've always seen the example of a red flower with a gene that, when homozygous, renders it pure white. If the white allele is incomplete dominant to wild type, it has a reduced effect over the wild allele, turning a heterozygous flower pink. If it is codominant with wild type, you end up with a white and red splotched flower in the het form, with one allele or the other expressing in any given part of the flower.

I imagine this is vastly oversimplified, but this is how I've always understood the difference between the two terms.
 
As far as I understand it, "codominant" is misused frequently in herpetoculture; most genes labeled as codom are in fact incomplete dominant. I'm not sure of any true codom genes existing in corns or ball pythons.

I've always seen the example of a red flower with a gene that, when homozygous, renders it pure white. If the white allele is incomplete dominant to wild type, it has a reduced effect over the wild allele, turning a heterozygous flower pink. If it is codominant with wild type, you end up with a white and red splotched flower in the het form, with one allele or the other expressing in any given part of the flower.

I imagine this is vastly oversimplified, but this is how I've always understood the difference between the two terms.

I believe the difference between incomplete dominance and co-dominance is one that remains muddy to this day, with even those at the forefront of research having rather different opinions (or no opinions at all) on the definition of the two terms.

However, the convention at the moment, as I understand it (and I'm very happy to be told otherwise if I'm wrong) is based not on the effect of the gene visible to the naked eye but on how it works on a molecular level. To try and explain it simply

  • Co-dominance describes the situation when two alleles at a locus have different functions, and in the heterozygote these functions are therefore both carried out such that it is distinguishable from either homozygote. For a fictional example, imagine a snake with a locus that determines scale colour. At this locus are two alleles, one of which encodes a yellow pigment, another a blue pigment. A snake with either two yellow or two blue alleles will be yellow or blue respectively, but a heterozygote will produce both yellow and blue pigment in the skin and therefore appear green.
  • Incomplete dominance[/b] describes the situation where one allele at a locus possesses an activity (such as pigment production) that the other does not, but there is a dosage dependent effect such that having two of the 'active' alleles results in twice as much as the relevant activity and this is visible to an observer[/b]. To use a fictional example similar to the previous one, imagine a snake that always produces yellow pigment from one locus, and has another locus that controls the production of blue pigment. At the blue locus, one allele encodes blue pigment, while another does not. A snake with two inactive blue alleles is yellow, because the yellow pigment locus is still working normally. One with one active and one inactive blue allele produces some blue pigment, which when overlaid with the yellow pigment appears green. One with two active blue alleles produces so much blue pigment that the yellow is swamped and the snake appears blue.


So, based on the fictional examples above, it can be impossible to distinguish co-dominance with incomplete dominance (aka haploinsufficiency) until you know exactly what the allele products involved are doing.

To give a real-world example - royal pythons have a locus that controls scale formation during development (they probably have multiple, but we only need to focus on one). One homozygote is completely covered in scales, the other is more or less completely scaleless, and the heterozygote has scales everywhere apart from its head.

So is this co-dominance or incomplete dominance?

  • If it were co-dominance, the following explanation could be given - the 'scaled' allele encodes a product that promotes the formation of scales, the 'scaleless' allele encodes a product that actively prevents scales forming. So we have two alleles with different functions; one that promotes scale formation, and one that hinders scale formation. When these come together in the heterozygote, their different activities result a reduction of scales, with some missing on the head.
  • If it were incomplete dominance, the following could be said - the 'scaled' allele encodes a product that actively promotes the formation of scales, while the 'scaleless' allele has no/little activity at all. So one allele possesses an activity the other does not - the ability to promote scale formation. However, one scaled allele is not enough to completely cover the snake in scales - two copies are needed for that, so in the heterozygote, there are scales but not to the extent that we'd seen in a homozygote for the scaled allele.

In the particular case of scaleless royals, it is almost certainly incomplete dominance - it usually is when some trait is 'missing', but formally we don't know this for certain.

So what's going on with tessera corns (I know it would get back on topic eventually)?

Well...

If there ARE differences between homo and heterozygotes that we just haven't found yet...
  • They could be co-dominant - the 'normal' allele tells pigmented cells to do 'a thing' (it could instruct them to produce pigment, or instruct already pigmented cells to migrate - we'd need to know more about the development of corn snake patterns in the wild type to know), while the 'tessera' allele tells them to do 'another thing'. In the heterozygote, the mixed messages result in a pattern that is different to either homozygote (though only slightly, or we'd have noticed by now).
  • There could be incomplete dominance - the 'tessera' allele tells the cells to do 'a thing' that the normal allele does not, however one tessera allele is not sufficient for the full potential effect of the activity. In the homozygous tessera, there is more of the tessera activity telling the cells how to behave, leading to a different/stronger pattern than that of the homozygote.

If there ARE NOT differences between homo and heterozygotes and it is a truly dominant trait (far more likely imo)...
  • Tessera could be a gain-of-function dominant mutation - this means that the 'normal' allele was mutated in such a way that it gained a new ability, and one copy of this mutated allele was sufficient to get the full range of effect. This is essentially the same as incomplete dominance except that here one allele is strong enough that the activity is already maxed out and adding another makes no difference.
  • Tessera could be a dominant negative mutation - this means that the normal allele has an activity the tessera allele does not, but the non-functional product of the tessera allele interferes in some way with the function of the normal allele. For example it may bind to it and prevent it from carrying out its normal function. The result is therefore the same as if there were no normal alleles at all, which is the case in the 'super tessera'. I personally believe this is the most likely explanation and that therefore no 'super markers' will ever be found, but I could well be wrong.

    In any case, because it's often impossible to distinguish between co-dominance and incomplete dominance, I think the herping hobby as a whole might as well pick one and use that to use them both. Since incomplete dominance is probably more common than co-dominance (it's easier to lose a function than gain one), that might have been a better one to choose, but over all it doesn't really matter.

    On a more personal note, I will soon be getting a scaleless tessera (from a tess x non-tess pairing), and will post pics of her cheek and head/neck patterns to show how they look without scales 'obscuring' the pattern.
 
Like I said...it was vastly oversimplified, and like early taxonomy, entirely based on the visual effects. If we can't know for sure at the molecular level without extensive (and expensive) testing, I agree it might make sense to just pick one to use. I can understand why so many prefer to use "codom" over the mouthful that is "incomplete dominant."

I find scaleless tesseras fascinating, the side patterns in particular...so smooth compared to scaled, I imagine because of the timing of scale formation during pigment migration?
 
Heh, sorry for the essay, I was bored in work and got a bit carried away =P

But yeah, as soon as I have my li'l scaleless and she's settled in, I'll snap loads of pics. I'm actually not sure how the patterns are gonna' look up-close myself, so looking forward to it.
 
I never mind an essay! I'm actually thinking about enrolling in an online course on bioinformatics now...

I'd love to see hypermacro images of your scaleless if you have the capability. If not but you have an extra $35 or so, I've had decent success with this USB scope.
 
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