I really like something like Super Cinnamons and Super Black Pastel but is the risk of deformity worth it? I know you basically bring the risk of deformity with every breeding for reasons known and unknown . I’ve seen that these are possible line problems and people have had no problem producing either of these? Along with the Spider Complex having known neurological “problems” but also seeing so many acting “normal”. Do you personally take the chance or how do you reduce the chance? I’m still hesitant to mess with Spiders but recently when going to someone’s house and them showing me thier adult Spider, it is one of the best looking snakes I’ve seen in person. I think part of it is the forbidden part about them but she was almost intimidating with her markings. What do you do , avoid all together? Extremely selective? Or just have at it?
I think it really depends on what sort of projects you’re wanting to work with. I personally am going to avoid super cinnamon and super black pastel, and instead work towards a cinnamon suma (super mahogany)… as for spiders, I have several individuals in my collection with the gene that I plan to breed, but they’re not a specific part of the projects.
I just don’t see the issue with them and based on my research and interactions with them, don’t think the wobble is really an issue.
Good husbandry/less stress = happy snake with little to no wobble. Only time mine have had any real wobble show is when they’re being fed or when they’re freaked out.
I am really interested in super cinnamons, from the research I’ve done the issues seem to be more related to certain lines than the inherent in the gene (If I’m wrong I would certainly love to know) so I feel that the risk can likely be managed through breeding selection and practices.
EDIT: Spoiler alert; I’m wrong!
With spiders there doesn’t appear to be any way to control the odds of whether a hatchling will have a wobble, or how severe it will be. While it doesn’t seem to affect function or quality of life for most, there are enough that are seriously affected that it feels like breeding for that gene is too much of a risk for me personally. Partly because my personal philosophy when breeding anything is if I produce an animal with a deformity or disability I need to be prepared and willing to care for that animal for life and my resources are fairly limited. If I can find a knowledgeable pet-only home, that’s great but it’s not something I will count on.
Super cinnamon and super black pastel always have a chance of duckbills and severe kinking. That is why there isn’t many on the market, because many of the babies die. Honestly even if some people try to say only certain lines have it (likely breeders that just want to justify breeding them for profit) it still isn’t worth the risk of getting babies that are likely not going to thrive or even live long and have to be euthanized.
I don’t know of any snakes with wobble that are severely affected by it so long as they are actually kept properly and without stress/lower temperatures (max of 88°F). I have only seen a handful of videos showing a bad wobble, and chances are those animals were extremely stressed just to produce said outcome for shock value and views. Thousands of wobble morphs thrive without issues, and are easy to keep from having issues so long as you are a good keeper. Given there are hundreds of wobble morphs on the market, the babies/adults clearly survive just fine. Unlike super cinny/super black pastels. If you want a dark snake with no risk at all, just get a super mahogany.
I am still also interested in producing some. But finding different lines of cinnamon or any line can be difficult. Might just come down to chooseing what you want to work with. Hoping to find people who’ve had more success or even less success. Interested in odds and outcomes of clutches. They definitely would be hard clutches to watch but rewarding. It seems like dirty work, maybe even other combos could change the odds.
If it’s the look of the super cinnamon or super black pastel you like I feel like the best thing to do to get a similar looking snake without the kinking, duck billing, shark-jaw or cleft palate that’s very common with those animals is to go for a super mahogany and add other dark genes like a single layer of black pastel or cinnamon and other genes like blackhead or chocolate.
Definitely. Mahogany was the first project I bought into.
I went back last night to see if I could support my own claim and this time I found a lot more that seems to indicate the issues with super pastels/super cinnamons are morph linked and more common than I’d previously thought. I assume I’ve gotten better at finding the information since then, the search engines presented me with different results and/or my own biases and faults in what I process. Thank you for prompting me to look into it further and I apologize for stating something I can’t back up.
I’m also about to try and dive down a rabbit hole of research papers to see if I can find somewhere that can provide some structured data on morph defects.
Hey! I’m not sure if you’re still active and I apologize for reviving such an old thread, but I’m currently doing research for this project as I’m hoping to eventually get a research grant as I continue college/uni. I am on the same page as you, and honestly super fascinated about ball python genetics!
If you’ve ever heard about genetically altering the spider gene, you’ve probably heard that they cannot alter it because the gene that expresses the spider pattern is on top of the regulatory gene that also causes that inner ear canal deformation. Since they are on the same gene, it is nearly impossible, if not possible, to completely separate both the wobble and the pattern without losing the pattern entirely.
The reason I bring this up is because I believe that both the cinnamon and black pastel gene are inherently pleiotropic which means that they alter more than one trait genetically. They possibly have a gene that alters their skeletal development in its heterozygous form, and in return in its homozygous form duplicates the issues causing a variety of issues.
Since some super cinnamons hatch fine, I truly believe the issue behind super cinnamons and super black pastels is that they reside too close to a regulatory gene that causes issues in skeletal development when in its homozygous form. I am currently working on this project and breeding ball pythons to fund my research and data collection into Super Cinnamons.
While it is genetic, I personally think that it is not that the babies are already predetermined to have the DNA for a defect once the embryos are established, but that there is a code in their genes that CAUSES them to have deformations during their development instead of being born with them. The homozygous version of gene causes issues in the cells that specifically reside in craneofacial and spinal development which is why they are so prone to those specific issues.
Some Spiders hatch fine too…
The issue with the BlkPastel complex is no different than the issue with Spider - the problem lies with the mutation to the gene, not with some second mystery factor. In the homozygous expression, the altered gene product has just enough functionality to sit on the knife’s edge where stochastic effects can cause an issue, this is why the negative phenotypes are “inconsistent”. In the WT and heterozygotes, these stochastic effects are fully dampened by the presence of WT gene product
Thanks for the detailed explanation, I appreciate how you broke down the idea of stochastic effects and gene dosage, and how the presence of a wild-type gene in heterozygotes can help buffer against instability. That perspective does make sense in terms of why some animals may hatch fine while others show defects, even within the same clutch. However, I have worded it incorrectly when saying the “wobble and pattern” cannot be separated. It was more towards the inner ear canal deformity and the pattern rather than the actual symptoms of the gene. I do agree that some spiders hatch completely fine as well which is where I was incorrect.
That said, I don’t fully agree that Spider and the Black Pastel or Cinnamon complex function the same way. In the case of Spider, we know that even animals without visible symptoms of wobble still tend to have underlying developmental issues. Inner ear malformations have been documented in Spider ball pythons regardless of whether or not they show external signs. To me, this suggests that the Spider mutation causes a consistent defect that is present in all carriers, even if the severity of expression varies. So I don’t think it’s just a matter of random developmental chance, I think the gene itself disrupts more than one process. That would make Spider a pleiotropic mutation that causes both pigmentation changes and structural issues in the nervous system.
This differs from Cinnamon and Black Pastel. In their heterozygous form, they don’t seem to cause any issues. Animals with one copy of either gene are generally normal in both behavior and development. It’s only when the animal inherits two copies that problems start to appear, which usually involve craniofacial or spinal defects. That’s why I lean toward the idea that these are also pleiotropic genes, but their effects are only triggered in the homozygous state. It may be that the gene dosage interferes with developmental signaling during a specific stage of embryogenesis, which doesn’t happen with just one copy. That’s why they are not part of the Spider complex and rather part of their own complex. Just to add to my earlier point, I understand that it is possible to argue that the wild-type gene might buffer or suppress instability in heterozygous animals. But if that were truly the case, we would expect to see at least some Cinnamon or Black Pastel heterozygotes show partial or inconsistent signs of those same defects, even if only rarely. Yet that is not what breeders typically report. Heterozygous animals are generally stable and show no developmental issues, even in large numbers. This is very different from Spider, where every heterozygous animal shows at least some degree of neurological abnormality, even if it is not always externally visible. That difference suggests that the mechanism behind these mutations may not be the same. In Spider, the mutation appears to directly affect development even in the heterozygous form. In contrast, Cinnamon and Black Pastel seem to function normally unless two copies are inherited. That points more toward a pleiotropic effect that is triggered only when gene dosage is doubled, rather than a mutation that is unstable in all forms…
There are examples in other animals that mirror this pattern. In certain dog breeds, mutations in the MITF gene control coat pigmentation, but also affect the development of the inner ear. This leads to deafness in dogs with extreme white patterning, showing how a pigment gene can also impact neurological development through shared embryonic origins. Another example is the double merle gene in dogs. A single copy of the merle gene causes a marbled coat, but when two copies are inherited, many dogs are born deaf, blind, or with underdeveloped eyes. Not all double merles are affected, but the risk is very high, and it shows how pigment-related genes can influence structural development depending on how many copies are inherited.
That’s the parallel I see with Cinnamon and Black Pastel. In single-gene form they cause pigmentation changes, but in double form they may also begin interfering with skeletal or cranial development, not necessarily through random chance alone, but as a secondary effect of what the gene does during development which is why I believe it resides close to a regulatory gene and during development alters it, not that there is a secondary gene or mystery factor at play. That’s why I feel it’s not accurate to say the Spider gene behaves the same as the 8-ball complex. Spider shows consistent neurological issues in heterozygous animals, while the 8-ball genes only begin causing problems when homozygous, and only then in some cases they will hatch will they hatch with no issues.
I really appreciate the conversation and your input. This is helping me think through how to approach this more precisely in the research I’m working on for uni, thank you so much to responding to my comment! It is nice to see different point of views on these issues. 
They are not part of the Spider complex because the genes are totally different genes. They are as unrelated to one another as apples are to oranges
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I do not think you do understand what I am saying. The WT gene is not “suppressing instability” of the mutant Blk-complex gene anymore than the WT tyr allele “suppresses the instability” of the Albino allele. The presence of only a single copy of the WT gene, in both cases, is sufficient to prevent the phenotype. However, in the case of the Blk-complex, it is only the secondary phenotypes that are prevented
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No, we would not. For exactly the same reason we do not see “partial or inconsistent signs” of albinism in het Albino animals. The deleterious effects are only seen in the homozygous state because that is the only state where the precarious balance of gene product function impacting these secondary phenotypes exists
You keep making the comparison to Spider but you seem to have missed that you are ignoring two very large factors here. First, Spiders are the het expression whereas SuperBlk and SuperCinny are the homozygous expression. So a more accurate analogy of comparison would be how we have an inconsistent rate of kinks in SuperBlks in the same way we only have an inconsistent rate of live SuperSpiders hatching out - we do not see the kinking in single gene BlkPastels for the same reason we do not see single gene Spiders just dying in egg. The second factor you are not considering is the reason my analogy is more accurate - The gene that is mutated in Blk-complex is not an essential gene while the gene mutated in Spider is
The pleiotropic effects are likely explained by the shared developmental origin of the affected cells in the neural crest, which migrate and differentiate into pigment cells, peripheral neurons and glial cells, as well as craniofacial and vestibular structures. Therefore, when a mutation alters the behavior of neural crest cells, it can impact both pigmentation and nervous system function. You are right, and this is why the phenotype can’t be separated from its effects, although they can present at varying levels of severity.
Edit to add: I think it’s interesting what happens when Black Head is introduced to Spider, as a side note.