Antaresia stimsoni mutation

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Saying that any animal with less melanin can be considered T+ is way off the mark bro. As mentioned T+ is a recessive mutation that has been proved out over a few generations now.
Also the Latta line T+ originated in Mount Isa locality childreni. Someone who knows a lot more about their distribution than me told me that a lot of childreni in that area could be considered stimsons intergrades.
 
" Yeah that stimmo is most likely a t+ albino. But that term is really ambigious, basically any animal with less melanin than what is 'normal' (and what is a 'normal' stimmo?!?) can be considered a t+ albino. So by saying that it is most definitely a t+ albino is correct but its about as meaningful as saying its 'hey thats a pale looking animal'. "

Not really... T+ refers to a quite specific form of albinism, where the fault is located at the pigment cells themselves, rather than the more traditional albino ( such as darwins) lacking pre-cursor enzymes. T+ specimens in herp hobby terms, are generally easily identified, as the failure in the melanophores isnt normally a cessation of pigment production altogether, more a faulty version of darker pigment is produced.

Anyway, who knows what this animal is, or if it is even inheritable in a mode that is easily reproduced. It is very early to draw any conclusions, or to allude that it could be an intergrade or a hybrid. I have been keeping an eye on this thing for a while, and we really know sweet FA about it, lines or locale, so making assumptions is premature.... For all we know the parents may not have to be carriers of the genetics. Keepers all too often overlook the possibility of spontaneous mutations, which in this case, a single hatchling displaying the trait sounds a very likely scenario. Time will tell, first hurdle is to breed it, and work out the mode of inheritance, if there is one.

Dotty, I wish your mate good luck with this project, love my stimsons, and if he ever cracks them be sure to drop me a line.
 
Hi everyone, I thought as the owner of this snake its probably best that I sign-up and explain a few of the comments Dottyback posted earlier on my behalf given the interest shown in this little stimmo. By the way, thanks everyone for your nice (really nice!) comments and input.

Here's an explanation of what I was talking about: Tyrosinase positive albinism (T+) is caused by the presence of tyrosinase but for some reason this enzyme is prevented from entering melanophores (pigment cells) or (in some definitions) tyrosinase can enter the cell but melanin production is inhibited at a later stage by faulty proteins/enzymes or various other reasons. Generally, some amount of melanin is still produced when tyrosinase 'leaks' through the cell membrane or when a pigment cell ruptures. In some cases, faulty pigment compounds may be produced with altered light absorbing properties as mentioned by ihaveherps. Notably, in one way or another this is also the same definition applied to hypomelanistic morphs.

So why does this even matter? The problem is there can be many different genetic causes of t+ albinism with potentially different modes of inheritance and depending on how they affect melanin production each could result in a different morph. For example, how much tyrosinase can 'leak' into the cell or the light absorbing properties of the faulty pigment will depend on exactly how melanin production is affected and bunch of environmental factors. So basically any morph that results in an animal with slightly less melanin than the 'norm' right through to something that closely resembles a 'classic' albino fits the description of t+ albinism so long as tyrosinase is present in the body. Therefore, the term 't+ albino' doesn't tell you what's causing albinism or its mode of inheritance, it just tells you that it's not caused by a complete lack of or defective tyrosinase. This is one of the major reasons why both the medical and scientific communities have abandoned the term and it's really only us herpers that are hanging on to it (actually, it's going out of fashion in overseas herp circles because each genotype that causes a reduced melanin morph generally has a separate name such as 'dilute, caramel, sunkissed' etc and isn't lumped into the t+ albinism category even though they fit).

So what is this little guy? Well, we may never know the exact root cause of this potential morph unless someone decides to study it in detail, and it doesn't really matter so long as the health of the animal isn't affected. I don't feel that it's the same morph as the latta line childreni's just because they don't look very similar in real life at this age (I've seen both) and as I've discussed there are a lot of other possibilities.

I hope this clears up where I'm coming from and sorry to be so long-winded. If it does turn out to be a simple genetic trait I'll let someone name the morph, but until then its just a cool looking snake in my collection.

Cheers!
 
Yes, very well said Geared! From my understanding, what you have said is spot-on. It is nice for someone to reinforce their statements with actual scientific fact for a change.
 
updated photo's from me mate!


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that is stunning i really hope it is heritable and your friend can get them out and about in the comng years.
 
That is the most amazing stimmie... wow wow wow!!! Hope it can pass on this trait!
 
Gorgeous snake. This question might have been answered somewhere in the thread already, but what locality is it from?
 
:shock: !! Oh my goodness! That stimmie is gorgeous!! Very lucky guy to get that out of the clutch. I hope he can get more of them down the line.
I wonder what sort of genetics made it come out like that ....
very nice, and thanks for sharing. :D
 
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