In anyone’s experience does incubating at lower temperature have any benefit to problematic genes in allowing them to have better odds of development. I see a lot of things that just says incubate lower it helps them, but nothing really that proves it. If allowing these eggs more time has any benefit, Why would I want to incubate any of my eggs hotter/faster.
Also have any genes been actually proven to counter act another genes physical or neurological disorder?
Has a lot of work been put into anything like this?
Is it even worth the effort, is anything proven to help or have any affect what so ever?
Adding another gene is not gonna correct an issue which has been seen in Spider Combos, there has been enough year and enough combos made to know that stacking up the genes has no effect.
Same with other mutations that have issues.
Ah, so this is actually exactly what I study in real life (outside of pythons). @stewart_reptiles isn’t quite correct here because there most definitely are mutations in genes that will make the spider neurological phenotype either better or worse, as pretty much every disease has “modifiers” which alter disease progression for better or for worse. The catch is that they likely aren’t genes that cause a change in coloration or pattern (what we call morphs), but rather likely mutations/SNPs/genetic rearrangements in other genes that we don’t have a visual readout for. So crossing in other “morphs” isn’t going to alter the spider neurological problem, but there are definitely spiders ball pythons out there that are doing better or worse based on the effect of modifier genes.
We’ve found thousands upon thousands of genes that alter disease progression in neurological disease by either enhancing (making it worse) or suppressing (making it better). Many of these genes are transporters, involved in the cytoskeleton or involved in synapse maintenance. However, short of sequencing thousands of spider ball pythons and pairing that with a phenotypic readout of impairment, you aren’t going to know what these genes are.
Something that will make this easier to understand is differentiating “gene” and “morph”.
In @chesterhf explanation, gene is the “code”.
“Morph” is merely the visual reaction of certain “codes”.
In humans, a big nose would be a visual morph.
Cystic fibrosis would be a non-visual morph.
I hope I’ve not made that worse.
I have heard from several people who I trust say that lower temps is the key to super cinny and super black pastel. Me personally I have given up on trying , tried one season with a lot of pairings. I had a total of 9 and only one was viable. Some pairings in my opinion are just not worth it. So many nice combos out there that I stay away from ones that have serious know issues.
Blackhead totally takes away the spider wobble. And is a als.
Can you tell us which ones those are? As far as i know there has only been “speculation” that certain morphs have “taken away” the spider wobble. But as we all know spiders can have a varing degree of wobble which can increase with age, so just because it didn’t show a wobble as a baby does not mean it does not or won’t as a sub-adult or adult with stress.
Unless it has been done time and time again and shown to have the same result, one pairing or incubation does not make it true.
Blackhead takes it away. There is no speculation it has been proven for years. Ralph Davis is the one who proved this to be true I believe.
Intresting cause i have heard of blackhead spiders that do show a slight wobble.
From who? The blackhead spider combo has been known for over 10 years at least. I’ve seen a bunch of them and never any wobble at all. But it’s literally Doesnt look like a spider or a blackhead. But it has been proven allelic.
I don’t believe chester was saying that there are known morphs out there made up of the genes needed to counter the wobble.
I think it was more along the lines of, them genes are likely out there but it could be in a non-visual mutation, which would make it next to impossible to prove out.
Like the blackhead spider lol. It pretty much looks like a normal ball python but is proven allelic.
This seems like it might be useful here
seriously??? i am not going to list of names of people that i have talked to over 10 years and heard this from.
oh no i get that, and i was actually in the middle of writing when you wrote yours. Some people refer to genes as morphs and vs versa.
Wasn’t being mean just curious. Ralph Davis discovered the blackhead morph and proved it out a long time ago. And I’m not claiming to be the foremost expert on all things snake. But I have been breeding snakes since 2001 so been doing it for a minute. And the blackhead spider combo has always intrigued me lol.
So crossing in other “morphs” isn’t going to alter the spider neurological problem, but there are definitely spiders ball pythons out there that are doing better or worse based on the effect of modifier genes
So you agree
What affect spider the most are environmental conditions not stacking up genes.
At the end of the day spider combos wobble and yes there are those claiming that blackhead spider do not and there are even those that claim their spider don’t, ultimately if you look long enough hard enough you can tell.
I wasn’t referring to morphs, but as @eaglereptiles pointed out, I was referring to genes. Given that you can find genetic modifiers of pretty much any genetic disease, it’s almost guaranteed that there are multiple genes in the ball python genome that when altered will either suppress or enhance the neurological defects seen in spiders.
A perfect human example of this is Huntington’s disease. An expansion of the CAG repeats in the gene Huntingtin leads to an autosomal dominant neurodegenerative condition. If you have over 40 CAG repeats in this gene, you will get Huntington’s disease. Period. Usually the more CAG repeats you have, the earlier/worse case of the disease you will get. HOWEVER, if you look at a chart correlating the age of onset and the number of repeats, there’s a pretty big variation. Certainly some of it is environmental influence, but we’ve found thousands of genes that alter disease progression and severity . While Huntington’s disease is a monogenic disease (caused by one gene), the effect of thousands of other genes determine severity.
In much the same way, while undoubtedly environmental influence and husbandry affect the severity of the spider ball python’s neurological problems, other genes are going to influence it as well. If you systematically went through and either unregulated or knocked down each gene in the spider ball python genome you would find some that made the phenotype worse and others that improve. As far as I know, no one as done that.
If someone were to find out exactly what mutation is causing the spider phenotype and consequently the neurological defects, I could plop into into a Drosophila model and some ReN cells and then give you a list of modifiers in 6-12 months. But until then speculations are all we have
@stewart_reptiles No, to say that no morphs affect the severity of the spider ball python’s neurological defects is fair, but to say that no genes do is incorrect. Terminology is important here
We are talking about BALL PYTHONS not humans so let move back to the original discussion before we start talking about everything in between. Thank you.
@chesterhf was using that human example to express a way to understand what she was talking to as in gene play with Spiders.
For people like myself, who aren’t a geneticist, an example as such is a easy way for me to understand and connect the dots related to the discussion.
Nothing wrong with using that as an example since I think all of us can agree human genes and snake genes aren’t the same, and again for people who don’t really understand genetics, examples like that are helpful.
I get what you are saying here, however the original post was in regards to morphs not “possible genetic code” that can alter the animal without altering the way it looks (morphs). This is a totally different topic than what was orginal asked. Was just trying to bring it back to the original topic at hand.
Technically someone with Cystic fibrosis would actual be a visual, because both parents have to carry the genetic defect for cystic. Also a person can be a carrier of cystic (het) and show some of the characteristics of cystic without having the full blown disease process. ( ex: het markers)
But we are getting off topic agaiin