While you’re here @t_h_wyman, what are your thoughts on feeding transgenic mice to snakes? Do you think it’s safe provided the haven’t been treated/exposed to anything and were breeders only?
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Guessing you may have discovered access to a potential source of free feeders LOL??
No different than GMO crops, so long as they have no exposure to drugs/chemicals/reagents/etc., then it is fine.
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Thanks! Yup! I’ve been doing some mouse work for the past year or so and had to “retire” some old breeders from my project. I’d hate for them to go to waste since they were perfectly healthy and euthanized using C02
I guess part of my worry is that a few of them are the PS19 tauopathy strain, and tau has been shown (in the brain) to propagate via prion-like seeding. While we don’t know that ingestion of tau will lead to tauopathy since no one is eating dementia patients, what if it does (similar to mad cow disease)? I don’t want to accidentally give my snake dementia
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Hmmmm… We know that some prion diseases can transmit by ingestion (kuru, nvCJD, etc.) so that might change the risk factor. That said, do snakes have a tau analog with enough homology/identity that would allow for seeding. You might want to BLAST your tau strain against the scaffolds of the burm reference in Genbank and see if they return a high identity hit. I would do both nt and prot BLAST. If nothing comes back you are probably in the clear (I am assuming burms and balls are close enough evolutionarily to negate any significant divergence in the area of interest)
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I’ve been working on the piebald morph. We still need to do the functional confirmation but I have the candidate gene and mutation. Currently writing up the manuscript. Open to collaboration with others working on the functional work.
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Oh wow, that’s super exciting!! I’m not sure what you had in mind for functional work, but I’d love to help out. Tell us more!
The blastp comes up with multiple microtubule binding proteins in the Burmese python that are a little too close for comfort for me, so I’m a little hesitant to use those ones as feeders for my nice new clown girl. However I may consider trying it on a male normal to see what happens. If tau promotes seeding via oral ingestion it would make for a great paper, although our IACUC may not be too pleased…
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What could the community we have on here do to help out?
I don’t know if samples would be useful or not (scales/ blood/urine…ect) but I’m sure a lot of people on here would be happy to help where we can.
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Thanks! Samples are always useful! All my samples have came from breeders in Canada so having some from other places would be great. I suspect the piebald mutation is the same everywhere, with all piebalds being descended from the original. I read an article that perhaps more than one piebald individual was caught in the early 90s and so more than one mutation may have occurred. More likely I think it’s one mutation that was/is segregating somewhere in Ghana, kept in the gene pool by ‘hiding’ from selection in heterozygotes. I don’t know if it’s possible but it would also be great to have standardized photos of different base morphs to test the hypothesis that recessive morphs in general have a greater effect on colour and pattern (actually on the contrast relative to the wild type since their nocturnal predators mostly have rods in their retina and they’re active at night) relative than incomplete doms because incomplete dominant mutations with high effect will get purged from the gene pool.
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Numerous WC Pied animals were imported in the early days
Assuming you have identified the correct gene, my suspicion is that if you sequence you will find that there are multiple alleles, each arising from a separate spontaneous event, that generate the phenotype. We already see this throughout numerous species/morphologies
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I don’t have any piebalds myself, though I’m happy to send samples of what I do have.
You might find this thread helpful … Next to a Normal for reference
I’ll tag a few breeders I know work with piebalds to see if they can help out in any way.
@stewart_reptiles
@osbornereptiles
@martin_ender
@wreckroomsnakes
I feel like a genie summoned out of his bottle 
@garcia-elfring what kind of sample would you need?
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If you do get the sequence you should share it. It would be a significant boon to the industry if we can successfully map and edit the genome
The results seem to show only one mutation. I think this makes sense based on population genetics (mutation rate per nucleotide per generation * number of possible ‘knockout’ mutations in a gene of a given length). Empirically also, as it’s a general observation that mutant animals (like albinos) are rare in nature.
High DNA containing tissue would be ideal although we’ve been working with shed skin. However, the DNA obtained from shed skin is too degraded to use PCR-free libraries.
I would assume the best way to get that kind of DNA would be something like saliva right? Maybe have people cotten swab the snakes mouth. I dont have any idea about gene research so I dont even know if that’s a viable option so please let me know if I’m just spouting nonsense lol.
They use blood or buccal cells (cheek swap) for most human sequencing, so that would probably be best, but I’ve heard of people using shed skin before
And yet, empirically, there are countless documented cases of numerous mutations to a given locus that result in the same phenotype. Mice have something like seven Albino alleles. Danios have at least three. The black populations of mice that inhabit areas around cinder cones in the desert Southwest all seem to have independent mutations that give the phenotype. Cystic fibrosis in humans has so many alleles that I quit trying to keep track…
Extend the view even further and you see that multiple alleles of genes are dead common: Albino/Siamese/Burmese cats, the BluEL and BlkEL groups in balls, the Albino/Candy/Toffee balls, the Purple/Lav/White retics, the Black group in balls…
I would guess that what you are seeing would more likely be accounted for by closed group sampling. If you were to contact Pete Kahl, who imported countless wild collected Pieds back in the day, and get diverse samples from him I suspect that you may see a different outcome.
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Both Warren Booth and Ben Morrill do extensive work from extracted DNA from sheds.
I’m open to the possibility of compound heterozygosity, but If he imported “countless” pieds and they were from the same area, say in Ghana, I’d be very surprised if there were more than one. More likely I think it would be one mutation. I’ll contact Pete, thanks for the suggestion. Does anyone here know him personally?
You are making some assumptions here that I am not sure apply. We do not know that they were all collected from the same place. Ghana is, roughly speaking, the size of the state of Georgia. What is the likelihood that every collector in Ghana is harvesting wild balls from the same five square kilometer (just assigning an arbitrary number there) area? And if you include Togo and Benin (both areas traditionally know to have been collected in as well) you are now looking at an area equivalent to Georgia and both of the Carolinas. That is a lot of area. And since we have, as I noted above, a significant number of other morphs that are all allelic, there is pretty clear evidence that heterozygosity in mutations is not an uncommon thing in this species
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I do not know him personally and from reports he can be a bit difficult to get a hold of. I have also heard rumour that he is a bit recalcitrant, not sure how valid those rumours are though
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There’s only one way to find out, that’s the fun part. I agree with what you said about the BELs, there are clear candidate genes for the lesser and others. We also don’t need Kahl, we can dertirmne the likely number of alleles with enough samples from the US and even Europe. Mine come from a few breeders in Canada like Mutation Creation. I can ask Billy where the ancestors (in captivity) of those snakes lived but it would be great to get shed skin samples from across the US.