Reptile & Amphibian Forums

Jeff, I've just read your last post from last week. I'm pasting it here so others don't have to try and find it.
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"Posted by: Jeff Favelle at Fri Jul 11 18:36:16 2003 [ Report Abuse ] [ Email Message ]
Precisely when you started to talk about dogs.

Genetics is one thing. I'll full discuss and debate Ball Python inbreeding if you want to use tools like Hardy-Weinberg Theorem, genetic drift, bottlenecks, founder effects, gene flow, etc etc etc. But as soon as you "try" to use examples from an animal that isn't even in the same Class and infer that the same things are going to happen, I lose interest. Real fast. "
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Before I even get started, I have to lay out a few things to make sure we're on the same page.

1) You are against the further importation of any ball pythons.
2) You believe that the captive population will remain unchanged and therefore unaffected by any defective genes for all of eternity.
3) You didn't like my example/comparisions of defects that have been displayed in dogs and horses because they are in a different taxonomic class.
4) Yet you give genetic laws and theories that were based on studies done in other classes. I don't have a problem with that, because genes are genes. That and the fact that those theories have applied to every single other species they were set against, and I have no reason to doubt that they would apply to ball pythons.
5) For our discussion here, we will assume (as per your assertations) that today all importation of wild stock was halted and for the rest of eternity, we will breed ball pythons based on today's captive population.

Anyhow, the specific examples you listed leave me wondering if you just did a Google search on "popluation genetics" and listed a few phrases that sounded good. I'm very interested in how you plan to illustrate that the "Hardy-Weinberg Theorem, genetic drift, bottlenecks, founder effects, gene flow" will affect the captive ball python population in such a manner as to protect them from "bad genes" like we see in the dog and horse examples I gave before.

THE HARDY-WEINBERG EQUATION

A wonderful concept that would not even apply to your captive population. First, it requires an infinitely large, or at least big population, which we would not have. Second, it requires totally random mating which CANNOT occur in a captive population. Third, it requires that NO MUTATION occur within the population, of which we already have evidence (a convenient example being the two blue eyed leucistics that were hatched from two normal parents).

POPULATION BOTTLENECKS:

In our closed captive population, you could say that "today" was the the beginning of a bottleneck (a crash in poplulation size) since the wild population from which they came is many, many times larger.

FOUNDER EFFECTS:

As a consequence of the bottleneck, the remaining animals (our captives) would be the founders for all the future generations of ball pythons to come. This means that a certain proportion of the variance found in the original population has been lost. From here on out, only the variation in the captive founding animals will be available to future generations.

GENETIC DRIFT:

Due to the decrease in population size, genetic drift would dictate that even more variance would be lost from the population over time. The less variance, the greater the chance of two "bad genes" coming together to create a homozygous animal.

GENE FLOW:

Gene flow only exists when there is an influx of new genes from another seperate poplation. Since we are not importing an more ball pythons, there would be a very small amount of gene flow only when animals are shipped back and forth from other captive popualtions (like Europe). However, they are not completely seperate gene pools, having originated from the same place and already having "traded" some genes.

INBREEDING:

Due to the small popluation size and the exaggerated selection of mutated traits, the probability that two "bad genes" will come together in one snake increases, and over time, the overall quality (fitness) of the population decreases. Then we get to a point where, in the wild, natural selection would lead to a purging of the bad gene, but in captivity, natural selection is muted.

Purging could happen on an artificial basis, assuming we were able to identify and test for bad genes as they cropped up and cull our breeding stock as a result, which was the point Randy and I were trying to make. However, that technology, while it does exist, is not readily available yet.

Kassandra Royer

Thank you for a fascinating post! I do not care to read flame wars and forum arguments, nor do I care to participate in them - but regardless of the argument that prompted this post, I feel that it was worth reading, and should be read by everyone who discussses genetics in any way on this forum. I find genetics fascinating and plan to continue my studies, in the hopes of being the best, most responsibily informed herpetoculturist I can be. This forum could benefit greatly from more fact-based, less emotionally heated posts such as this. Thank you again.

Ashley,

I'm a non-confrontational type, myself, but considering how often I see genetics questions pop up on these forums, if a few people take interest and further educate themselves, the whole herp world is better off, right? Rarely do I get a chance to be involved in something so intriguing (vs. the "what should my ball python eat" questions).

Congrats to you on your breeding goals, sounds like you are on the right path. JMO.

Below is a link to the start of this discussion, for those who are interested, but you have to read the WHOLE damn thing...
http://forums.kingsnake.com/view.php?id=74713,74713

Your argument is better... you site many points in your counter argument. They are good valid points. I would like to further add.... I agree, however now, and for the past decade (even longer) there have been in excess of 100,000 CH ball pythons exported out of Africa each year. The vast majorities are destined for the US market. If WELL in excess of one million ball pythons (which have a rather long life span) are there, is that not enough of a genetic base for successful propagation of the ball python race?

Come on now, think about it. Population (n)= 1,500,000 !?!?! and we are worrying about a loss of a species due to genetic inbreeding? Maybe in 10,000 years if everyone works really, really hard at destroying them we could. Almost like instead of breeding for genetic marvels such as piebalds we work at breeding terminal genes just so we can kill them off. Genetic shift is a good thing, even if Africa is closed for 50 years it will open again. Guaranteed.

We are trying to make this more then what it is. In our life times (even if your 12 years old) we will not see a marked difference in the genes of a pool. I am assuming only one of our life times (75 years which is maybe 25 ball python generations). If we did it for 30-40 generations in humans (our good 'ol medieval and pre-medieval times with the English empire) before inbreeding forced the extinction of a family, I'm sure a snake will be no problem. Comparison being, genetically humans and snakes are similar (not specific sequences but the acids themselves, etc, everything to do with the basic common genetics) but we are of much higher order and requiring our sequencing to be different. In general we as humans have alot more to worry about with regards to genetic problems through inbreeding then snakes in a quicker period of time.

Point of the story.... both you and Jeff are very correct in your arguments when taken from your specific points of view. Remember....

There are three sides to EVERY STORY

1. Yours
2. Mine
3. and the un-biased, totally informed truth

Just my $0.02

Play nice now,
Dave

Jeff did not just do a quick lookup on the net so he can speak about a particular topic. He genuineley knows his breeding. Just because a person does not work in a particular feild, instead an unrealated one, does not mean they do not know what they are speaking about.

Trust me, if I have learned anything in my 30 years in life is that everyone has a story. You do not know it. Do not assume you know it.

I am a graduate mechanical engineer yet if I choose to speak about kenesiology with respect to athletics or extenous substances used for athletic preformance increase to a physician then I will. My knowledge of these topics well exceeds a general practicioner due soley to the fact that I decided to learn about these topics because I wanted to. If I want to learn about plate techtonics and the resulting geophycial effects then I will pick up a book, speak with people, ask questions and yes, even go on the internet and learn it.

It's what Jeff did. It's what I did, and I would amagine it's what almost everyone that reads this post and surfs this website did.

Agreed?
Dave

Dave,

I usually enjoy reading Jeff's posts. I've gotten the impression that, although brusque at times, he's educated and gives good advice.

The reason I said that (about the Google thing) was that the examples he listed can't be used to support his position. They actually work against him. It was just odd.

I joined the original discussion to have a debate over another hypothesis, and like all discussions worth a dime, it evolved into this. If I didn't think Mr. Favelle was up to the task, I wouldn't waste my time.

Regards,

Kassandra Royer

Kassandra,

I like your and Jeff's posts as well. I really just want the topic aggressively pursued. This way, with more minds the answers come quicker and of better quality (more re-verification, etc). Frank discussion about genetics and all associated attributes will be the ONLY way we can get some credibility to this industry and answer the question once and for all... IS THIS HET A HET?

It hurts the industry. How does the little guy get a foothold? It's tough.

With effort this question could be eventually put to rest once and for all. (Or a governing body or watchdog, that's an entirely different and VERY controversial topic for a different post)
Thx
Dave

Dave,

You are correct. We most likely will not see many problems in our lifetimes. That doesn't mean it won't happen, which was what Mr. Favelle insisted upon. It would happen even faster, if importation of CH or WC animals halted (Mr. Favelle's dream).

Many, many thousands of Ball Pythons are imported each year. How many survive, though? A relatively small percentage. Of them, how many are bred? Only a portion of those. Take into consideration that the rising popularity of morphs makes the alleles that only a few individuals (the founders of those morphs) more and more frequent. So, we are already losing genetic variation.

That said, there is only ONE side to the truth, and unless someone amongst us is a psychic, the best we can do is make an educated guess.

True, based upon the assumption that 1/2 of all the ball pythons will never be bread, we have lost alot of genetic variation right there. Still, with that being said, to evolve a change or create change in an acid sequence is extremely hard to do, we can't do it yet. They exist naturally and also appear sporadically due to other factors such as yes, your theory of inbreeding. We don't hear about the culls in Africa. We get them here. Do a search on the archives and net for birth defects and you will find them. Dormant genes that became active due to the chance that two animals which have some unusual matching bands? Don't know, not enough knowledge to form a more educated guess.

There is always someone out there that does "know" the truth. Gotta be at the top of your game though... and they are hard to meet. Steven Hawking doesn't accept too many phone calls to speak about space/time and general relativity. He's a busy guy. But there is always someone out there, the recognized "leader" in the field. We as common people (not in the particular field) never meet or know whom these types of people are. But remember everyone has a story. They might be the gentleman you bump into in the grocery store. Who knows?

God knows I which I had a genetics lab out back so we could just start now! But I don't, and I'm not a geneticist, so I can't do it at work, either.

Generally speaking, bad genes do exist in a healthy, large population, and they occur with a pretty regular frequency. Once inbreeding occurs, such as what we encounter in morphs even, the chance of two of those carriers (hets) matching up increases.

In the wild, the homozygous animal would likely be picked off by natural selection, if the "bad gene" is severe enough (like we imagine a white snake would be in the wild). Imagine how fast that could happen, if say, a caramel albino also carried a defective gene.

Because of it's color, it will be breed to many females, increasing it's influence on the resulting generations (far above what would occur in the wild...he's be a STUD!) Add to that, he's likely to be bred back to his daughters, which might also carry that gene, and boom, you've just uped that gene frequency in your population big time. Then, start crossing out to other morph gene pools, and the gene starts popping up there too.

Then you have your possible hets, who, regardless of whether or not they carry the caramel gene (unless this particular bad gene is linked to the color gene (YIKES!)) and now you're ending up with normals again that have the bad gene passed down from one single caramel albino male.

From this example, it's easy to see how inbreeding can easily lead to an increase in gene frequency in a closed breeding population.

Regarding your post about education incongruent with one's employment. I truely believe this is the best kind. Our society doesn't promote education for the sake of bettering one's self anymore. Rather, it's all about making more money. Very sad, in my opinion, because there are so many fascinating things to learn about. Plus there are so many people who are miserable doing their jobs! LOL!

Best regards,

Kassandra Royer

I liked that one. Pure agreement. It would seem we need to be the bother's keeper on this one and be responsible for propagation of bad genes as well. Thank god we have practice tracing gene lines due to hets and homos. Good record keeping of CB (the wave of the future) will allow us to stem any problems which may arise. Technology advances so fast I bet you we will see a solution within a couple of decades. Food for thought.

Dave

(as in a previous post... its not the world's greatest idea.... if an HLA test could prove in humans quickly and very cheaply the very most basics in genetic makeup, which is does, why not snakes? Sure it't not proven but time and money, we are not re-inventing the wheel here. It's done for humans which are of a MUCH higher order, should be rather simple for snakes. Just one dozen of the largest breeders could get together and have FAR more than enough resources expendable resources to get this done. How could a small time breeder that has made next to nothing kick in? Maybe it's time to give back to the industry what the industry has given to us?)

Again food for thought.

This gives me one more reason to keep "pedigrees" on my babies, much like that which has been done in the chondropython world. When the genetic resources become available, we can add that to our data. The good news is that ball pythons do live for a long time, so even if it takes 25 years for the technology to be practically applied, we can still add the DNA profiles or whatever we use to the database. Imagine how impressed our great great grandchildren will be that we had the foresight to plan ahead!

Anyone have an online example of the chondro python pedigree? I would like to start something like that for the balls I sell. A lot of work and most people probably wouldn't care but if I start it now it may eventually amount to something.

I just worry that we might see problems sooner rather than later. I've heard of the one eyed albino burms and boas. The bug eyed leucistic TX rats, the poor feeding bloodred corns. With the high price of out breeding mutations (extra generation and luck to get a small number back), especially multiple recessive combinations, we need to be on guard. Sure we have a huge population of imports to work with already but as we make combinations will we really go back and use them?

Piebaldpython, I also have a Mechanical Engineering degree and your spelling affliction. I'm suspect a high correlation between mechanical/mathematical aptitude and poor spelling skills

I'm sure you can find someone with a good example on the green tree forums. I'm setting up a chart for myself that has pics of the individual, the parents, ID#s assigned, notes on the clutch, siblings (like average weight at hatching, health, feeding response,etc.) as well as notes on the parents...average clutch size, etc. Many generations from now, I'm setting myself out to be in a position to pick out trends in a bloodline. Personally, I'm concentrating on developing strong maternal lines, selecting for females that are good feeders and produce good feeders, breed young and breed back to back. Well, that's ideal, I actually only have a few that fit all those qualities, but you can be sure I keep all their female offspring!

Randy,

Glad to hear your an engineer as well (actually I only did the three years for the diploma so no licence, boo, that's what happens when you choose the wrong course when you leave high school, you need to go back!).

Here's an idea I am working on right now. Do you remember what an actual repesentative graph of a power cycle looks like in thermodynamics? Notice the it almost looks like a tan-tan graph? Not really but at a half second (its been 7yrs since I seen one). I've been fooling around with AutoCAD and come up with a few ideas that would allow me to place a snake under this graph (how you can see the snake, etc is a long story) and interwoven graphs may be used to accurately map an animal.

Now we could interpolate certian things such as growth, changing location, but what about change? Change is REALLY hard to deal with. If BP's change then I would have to rethink the idea. Still going to do it in the future when I'm ready to sell hets. I can track the animal for at least a few years. The animal by then will have proved out or not. I purchased a het from a rather established, respected breeder, which was purchased from him not even 6 months ago by an individual, then sold to me (so from the respected, well-known breeder to the individual then directly to me. Have the breeders Bill of Sale, records, etc. The only problem is.... when I called the breeder before purchasing the snake, he could not varify or produce any pictures to varify the animal. Now this is not good. I took the chance and bought the animal anyway. I'll find out in three years if I got burnt. LOL. It was at this time that I decided to start my process of being the consumate professional. Just at like work, I need to preform whatever I do with professionalism and integrity. That is why I'm working harder on how I can garenttee my animals vs. buying all the animals I can manage to "find" the money for.)

Sorry, I'm not following your graph idea. You are talking about identifying characteristics?

Pictures work well for me. A good hatchling pic can be matched to the adult. It might stretch a little but that may just be the way they are laying in the pic and not really changing as they grow. I guess if it was quantified somehow you could make them searchable but for simple verifying "is this the same animal" a good picture works fine.

I did have an idea once to plot gender distribution in a large number of ball python clutches to see if it is distributed normally as would be expected or if clutches really do tend to be clustered either high female or high male with the average even distribution not being the most common. Sometimes it seems that individual clutches are lopsided a lot so if the data supported that we could try to figure out why it might happen. In snakes the female determines the genetic sex of the offspring so maybe it's not random as expected when determined by the male with a larger number of sperm (but I understand even that isn’t always random).

I finished the degree and even passed the PE test but graduated in the last recession so never got to work in the field or go through the PE internship.

BS and MS in Mechanical engineering (2 confrence papers and a real paper and another real paper in progress), I am curently enrolled in a PhD program in biomedical engineering. I am going the distance.
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Derek Affonce
DeKeAff Exotics
dekeaffexotics.com

So Derek, how is your pre-spell checker spelling? Mine's so bad that I often use the wrong word and don't catch it.

ah pretty freaking horific!!! I took the wonderful GREs, uh yeah 770 math 700 analytical (both above average for those admitted into each of the top 50 engineering schools) verbal, uh 440. The minimum score is 200 like the sats. What a wondrful score. I have become better with my verbal skills since I started to handle my brothers care. Writing to the state takes lots of practice, and with practice comes improved skills.
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Derek Affonce
DeKeAff Exotics
dekeaffexotics.com

I tell you the world's greatest thing, unlimited access to information and god only knows who you meet.
Davv

Ha ha, JK. But all that jibberish is greek to me! LOL!

BS = Bull terd

MS = More terd

PhD = Piled high and deep in terd of course
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Derek Affonce
DeKeAff Exotics
dekeaffexotics.com

I'm gonna save that one!!!

BS = Bull terd

MS = More terd

PhD = Piled high and deep in terd of course

oh and gre, is just like the SAT but on steriods. It is what most graduate schools use to determine how stupid a person is. boy did boston university screw up. lol
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Derek Affonce
DeKeAff Exotics
dekeaffexotics.com

Geez buddy, go outside a little more often, looks like you hit the Congressional Library and studied every book you could, wasting time thta could have been spent doing something PRODUCTIVE!!! Instead of melting our brains with this textbook regurgitation, write your own book. Most of us come on here to ask questions, get advice and learn, not re-spew crap you've read in a book. Your post belongs in a really boring, thick, small-worded book, that collects dust at the library. Get over yourself.

good to see you're bettering yourself and contributing something positive.........

Both Jeff's and Kassandra's. Informative and thought-provoking. Yeah, I have a couple 50%PosHetAlb BP's, one's got a clean, mostly banded pattern, the other's black-backed, reduced pattern. I've also got some "farmed" normals with "busy" and banded patterns. I just bred the banded 50%Pos with a farmed "busy" patterned female. I'm going to have fun just learning the genetics of the patterns. Six eggs...All offspring banded? All "busy"? Some of each? All typical with no genetic response to pattern? Won't know for another 45 days, but I'm having fun anyway! And I'll inbreed the 50%Pos banded to his daughters and the 50%Pos reduced to her sons & breed the siblings...ONCE!!! To see if I actually own a Het. If I get an albino, I'll buy/sell/trade to diversify the gene pool within my little world of albinos as much as possible, breed a few seasons,then buy/sell/trade for piebalds. If I don't get any albinos, I've already got a good diversity of nicely patterned "new genes" to continue playing with pattern genetics...no money, no piebald, but still fun!

Geez. My head hurts. Ok, here goes...

I suggested Hardy-Weinberg, gene flow, genetic drift etc etc because these are tools that are used by biologists to determine allele frequency. After school and during school, we used them all the time. SO no, I didn't type anything into Google. These tools were NOT suggested to support my argument. Not at all. I was suggesting that if a person makes an outrageous claim like "Wild Caught Ball Pythons should be purchased over CB Ball Pythons because their genes are stronger NOW and the cons are far outweighed by this"!!! IS that statement not CRAZY? I think it is. And I thought it was.

SO I replied. And then you bring in a theory that dogs have problems so Ball Pythons are going to have problems. I was like "what"? How can you make that inference? That's even crazier!!

Take Womas for instance. How many do you think made it out of Australia? Now many man. How many are in N. America now? Thousands. All from that same founder stock (Founder Effect). Any problems? Nope. Don't you think that that example has 1000 times more weight than a DOG example?

How about Odatria monitors? How many Ackies, Kimberlies, Pimburas, Caudos, etc etc were smuggled out? Not many. How many generations have they been bred together? Lots. No problems. They don't hatch with 3 heads, 10 feet and 90 toes. Why is that? It happens to dogs. Well, not really, but you get the point...

Therin lies the problem.

We are assuming that there are lethal alleles floating around in the BP world. Not sure why we are taking this as fact, but we (not me) are. BP's have probably (note: I say "PROBABLY" been evolving for closed to a few hundred thousand years. Now, what is the point of their metapopulations having bad genes floating around? There isn't. Biology says that most of the bad alleles have been weeded out. By bad alleles I mean things that contribute to poor health. If a field gets burned and there's a race of Pastels that inhabit it, I would say Pastel is now lethal (or at least detrimental) in that ONE area. Doesn't make it a lethal allele in terms of health.

Point is, the design of life has weeded out that crap a LONG LONG time ago. I have no idea why you guys think deleterious alleles are rampant in nature. Inbreeding increase homozygosity. That's it. Nothing more. If the recessive lethal allels aren't there to begin with (my opinion) exactly how is this increased homozygosity going to be detremental?

Well?

.
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Jeff! There you are! I knew that's what you had to be getting at, but I wanted you to clarify. I know you're talking about now, and I'm talking about 1000 years from now, but you and I seem to be in a minority who even give a crap, so I consider you a friend not a foe, nonetheless.

I would agree that now, the ball python is "perfect" for all practical purposes. However, even IF there are no lurking genes, mutation does occur, and down the road (100 generations or more), "bad genes" are likely to pop up.

You and I both agree that captive hatched animals are not superior to captive bred hatchlings. Neither has had a chance to "prove themselves worthy" so to speak. LOL! Some part of surviving is luck, of course, but some part of it is genetic...things we tend to overlook...like slitting eggs. Who knows if they would have hatched? We've all at least heard the phrase "full term dead in egg". Or force feeding...those ones probably wouldn't live to reproduce either.

Now, I don't know much about the history of Womas, but as with any reptile, the captive reproduction is in it's infancy. Reptiles are wonderful, perfectly adapted animals, that's why most of us (well, at least me!) find them so fascinating. BUT, (there's always that but) without the benefit of natural selection, the weak don't get weeded out. It's inevitable, in my opinion, that problems will eventually crop up.

But, (there it is again) I don't expect to see any problems right away. In general, there is still enough variation to go around.

Agreed. The system is closed and problems will only occur through chance. Out of the thousands of genes in a snake, some dormant, some not, thier could be that little something out there that can cause problems. It would be localized to a specific population but could exist. What causes the mutation of our genes to form our friend cancer? Extenuous substances? Don't think so. Can happen if you abuse something (ie: smoking, yet all smokers do not drop dead of lung cancer). Jeff eludes to an assumption that lethal alleles do not exist. I feel as though they do (according to degrees of freedom I must consider it as equal an option as the next until proven/disproven) but just not active. I wish I had more in-depth knowledge of the genobe but don't at this time. Maybe a few things need to happen for an inactive gene to suddenly become active. Could happen. Humans are investigating the possiblilty of cryogenics renewed by the development of the frogs in Canada that freeze solid in the winter then thaw in spring.

Cancer is just cells that have their G-zero lock removed. That is, in a cell cycle, a cell undergoes mitotis (cell division) in ONE part. After that it has a lock in place so that it doesn't divide anymore and can then differentiate into its function (brain cell, skin cell, liver cell, etc etc). but cells that have the G-zero lock removed keep dividing. Its like a gear without any tracks on it. It keeps going and going and that's what a tumor is. Just a bunch of cells that are undergoing unwanted mitosis.

Tons of things can cause the cells to loze G-zero lock. Radiation, free radicals, toxins spicy foods (kidding) etc etc etc
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But the formula for calculating the chance of one eludes me right now. But I do know that its usually results in a HUGE astronomical number. Meaning, its not likely to happen. And inbreeding doesn't CAUSE it to happen. Inbreeding only increases homozygosity. Nothing else.
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Agreed, and I don't know the formula either (but I'm sure we could find it using a Google search! LOL)

It's my opinion, and I know you disagree and that's o.k. we don't have to revisit it again, that there are already "bad genes" floating around, in a heterozygous form (or maybe even polygenic...).

Like I said before, even IF there are NONE now, when they do eventually occur, then inbreeding will take it's toll.

Good job on the cancer bit. I wish they would nail down the "genetic" predisposition to cancer, but even more I wish the general public would reach a level of understanding where they don't believe cancer is some "disease"...it's just your own confused body killing itself.

Thanks Jeff,

With EVERY member of my family on my mother's side dead of cancer and my mother diagonosed, you would think I would be interested and get more info. I guess what people shy away from what scares them.

Thx
Dave

I mean, there's only so much time in the day/week/year/life, so we tend to not think of things that make us scared or sad. I mean, life is so damn short as it is, nobody wants to purposefully have a crappy day right?

Cheers.

We're not foes. Not at all. That's the problem with the Internet. Everyone seems to be way too edgy and quick to be on the defence. I'm glad we've been able to talk, even if it seems there's only 3 or 4 of us interested in this stuff! Oh well. But yeah, nothing here is personal. Its just a discussion. No probs.
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We both agree that 1000 years of inbreeding would result in health problems IF the so-called lethal alleles exisited in the BP populations. I'm no dummy. Lethal recessive alleles inbreeding = increased homozygosity = expressed lethal alleles = health problems

But we don't agree. Heh heh. so the argument continues, yet in ANOTHER direction, ha ha!

I don't think these alleles are out there. Mother nature's design shouldn't allow for it. And mutation is not something to rely on because the odds of it are astronomical. And the 2 Lucy's are said to be the result of spontaneous mutation? Are you sure? Do you know the odds of this? Most likely dormant alleles triggered by others on nearby loci or in connection with them. Its documented.

I'm thinking that if the ball python population has so darn many desirable morph mutations which aren’t necessarily suitable for the wild that it's a very genetically diverse species and there are probably also lots of lethal mutations. In fact, I think I can note two examples. Unfortunately I don't have all the details by a long shot but I THINK that the pearl ball is a homozygous woma ball and that this gene has negative effects when homozygous. There were also two black patternless balls hatched last year that might be another messed up homozygous example of a co-dominant gene (sort of cinnamon looking when het I hear). I think they where missing scales on their noses and had a number of other problems. It's too early to be entirely sure about either of these (plus my not being in the loop on either) but I'm thinking there are probably plenty of bad genes in the captive ball population already.

It would be interesting to know how much ball pythons travel in the wild and how much inbreeding does or does not take place in the wild. I would think that your best chance to naturally weed out most bad genes would be in small isolated populations with lots of inbreeding for a long time but maybe in a big widely distributed population there is enough movement that bad recessive genes are spread widely in heterozygous form without having much pressure to weed them out.

I’m also thinking that heterozygosis in general is a good thing, even with all good genes (I’m assuming there are lots of cases of multiple “good” alleles). Not a scientific study but I remember that some of my best corns where from crossing two inbred lines (bloodred and blizzard). I’m thinking that more genetic diversity even at an individual snake level will generally make a stronger snake that is more likely to thrive and have whatever it needs to overcome as many possible challenges as it can.

Other than albino and Pied, what are the other "mutations" that are bad? I can't see any other colors being all that bad for living life on the wild side, can you? That's 2 morphs to like 20 other ones?

It would be interesting to know how much ball pythons travel in the wild and how much inbreeding does or does not take place in the wild. I would think that your best chance to naturally weed out most bad genes would be in small isolated populations with lots of inbreeding for a long time but maybe in a big widely distributed population there is enough movement that bad recessive genes are spread widely in heterozygous form without having much pressure to weed them out

That's exactly it. Small populations of reptiles inbreed all the time (supposedly). Monitors are best bred when they are rasied as a group of babies from the same clutch. But that's inbreeding?!! Why don't they have problems?? Well local populations probably don't have lethal combinations of alleles. Maybe these lethal combinations (IF they exist) are the PRE-ZYGOTIC barriers that prevent certain races and metapopulations of Balls from getting together to reproduce. Much like the Andes Mountains and all the races of Boa c. imperator and Boa c. constrictor? Maybe they are supposed to be in the process of speciating and we keep catching them from ALL OVER and outbreeding to different races. Species don't become species over night. They are slowly created, usually from said pre-zygotic barriers.

Like if we were to catch garter snakes from all over N. America and ship them to keepers in Africa. They might not all produce healthy babies due to the fact that they weren't meant to interbreed.

Maybe? Maybe not. Ha ha, seems kinda far-fetched eh?

Heterozygosity and homozygosity is neither bad nor good if the genes are good. Its just a combination (if in fact Mendel was right and this is exactly how it works). Heterozygosity is good however in times of rapid-changing habitat(s). It allows greater different combinations of phenotypes to be out there against natural selection with hopefully at least one "type" surviving.

Not sure where we're at now!! LOL!!

I suspect ball pythons don't spend a lot of time above ground and then mainly at night so even albino, piebald, and leucistic probably aren't all that bad in the wild and more subtle color and pattern mutations mater even less.

However, I'm thinking that the pearl and black patternless would be examples of mutations that when homozygous would not survive in the wild (may not even survive in captivity). They just happened to produce visible hets for us to pick up on and inbreed. I would expect that there would be many other genes out there that are lethal when homozygous but don't happen to look interesting when heterozygous so haven't been found yet. More breeding needs to be done with both pearl and black patternless but eventually we'll hopefully know the details and can be sure if these really are examples of single genes that are bad when homozygous and not some other phenomenon like incompatible localities.

Incidentally, if it turns out that the heterozygous pearl and heterozygous black patternless are as healthy as the next snake they might still be very useful for morph breeding alone and in combination with other mutant genes, you just wouldn't want to breed two of them together and risk creating a homozygous. This is the way that the "dominant spot" and Anophthalmic white genes are used in Syrian hamsters (lethal or impaired when homozygous genes). I know it's another species but interesting with many many generations and many spontaneous captivity mutations from a single founder animal less than 100 years ago.

I really wish I knew if ball pythons are now or have been recently a species that tends to have small isolated populations. From what little I've read I think they are now widely distributed in high numbers in farm land. Is the farm land continuous? If so, how long has it been that way? Before agriculture they may well have had more isolated populations.

Also, I'm thinking that captivity qualifies as a rapidly changing habitat. As a group we are always refining our husbandry methods and certainly there are changes as offspring are sold from one breeder to another and as a breeder tries new things or makes mistakes. If heterozygosity benefits the species in times of rapidly changing habitat, perhaps it can benefit the individual as well? I suppose it would require that the heterozygous alleles both be some sort of co-dominant so that both can have an effect to aid the individual when the changing habitat requires it.

I love you guys, sparking so many great thoughts! Anyhow, in a small (isolated) population, the race evolves to suit that niche. Any disturbance in their environment leads to a rapid decline of the race. They are essentially, too specialized, and it would be difficult for a population with a high degree of homozygosity to adapt.

On another note, I've been speaking of genes that would negatively affect the fitness of an animal until now. Now Randy brings up lethal genes. I wish I had examples in reptiles to give, but the science is just not old enough yet. I can add a couple to the list, though.

In dwarf hamsters, there is a dominant color gene called platinum that, in it's homozygous form, causes the death of the embryo in utero.

In horses, a similiar gene exists, referred to as "lethal white", and is the homozygous form of the overo (dominant pinto color gene) that causes the foal to be so unfit that is usually born dead, if not it seldom survives more than a few days, has eye problems and it's internal organs do not function correctly or are not properly developed.

In Australian shepherds, the merle gene (also dominant), in it's homozygous form causes, in most cases, an all white dog that is usually blind and deaf (some are born without eyes) and severe internal difficulities.

To illustrate how little is known about the underlying genetics, even in dogs, which have been domesticated and bred for so long, I've pasted the following exerpt:

"Not only can you sometimes get non-merle pups (which should not happen according to the rules of Mendelian genetics,) worse things can crop up, too. The "cleft palate syndrome" is a rare and isolated Aussie defect that has been the subject of numerous scientific journal articles and symposia presentations. It is a sex-linked (on the X chromosome) defect, in which females have minor abnormalities, like extra toes, while males die of massive skeletal abnormalities and a cleft palate. This disease STARTED with a homozygous merle [bleep] that just happened to be born, and kept for coat color research, when ASCA's genetics committee got started. The odds of a random mutation are high enough by themselves (nothing like this has been seen anywhere in the breed but in the descendants of this [bleep].) The odds of it happening in the very [bleep] who was selected to kick-off color research in the breed, is even higher."

You see, the homozygous merle always has problems, but they are variable, and some live to breed...and (get this) occasionally produce NON-merle pups! Crazy stuff!

It bleeps out the word for a female dog...toooo funny!

I'd also like to know what the normal range of ball pythons is. I would assume, so long as suitable habitat and food are available, a reptile is going to waste as little energy as possible.

Inbreeding in the wild does weed out bad genes as they crop up...it's called gene purging. It only happens in the wild where natural selection is king.

Now this is of course hypothetical, but if there are indeed small pockets of ball python races in the wild, we may indeed have done an injustice by outbreeding. Too late now.

For making me practice my typing! Ha ha, I'm getting quick now! A 3rd finger is into the mix!

Oh no.............. I'm mutating......Ahhhhhhhh......

Ok, it sounded funny in my head.

Anyhow, I'm not suggesting that bad genes are "rampant in nature", but they do exist, and as you said, inbreeding increases homozygosity, and it also increases gene frequencies because there are fewer genes to choose from.

Where I disagree with you is this: you seem to think (correct me if I'm wrong, this is the impression I'm getting) that Ball pythons are not changing, that they are in a suspended state.

What causes a color morph? A gene mutation. Mutation, one of the mechanisms of evolution. I'm assuming you believe in evolution since we are engaged in this discussion. How obtuse is it to believe that ONLY color (and pattern) genes are capable of mutation? We just don't know WHAT else is going to mutate, or when.

...and back to you....

What causes a color morph? A gene mutation. Mutation, one of the mechanisms of evolution. I'm assuming you believe in evolution since we are engaged in this discussion. How obtuse is it to believe that ONLY color (and pattern) genes are capable of mutation? We just don't know WHAT else is going to mutate, or when.

I wouldn't say that mutations cause color morphs. Who's to say that Balls just aren't variable in nature? Are Amazon Tree Boas all mutated because not a damn one looks the same? Mutation is not as abundant as you are making it out to be! Not in the slightest. Variation in nature is NOT due to mutation (all the time. Sometimes it is). Variation NORMALLY takes place as natural selection quietly and slowly works on animals in their specific niches. Just because not all Ball Pythons look the same, don't assume mutation is the culprit!

And for a mutation to actually occur, and THEN ALSO be hereditary is just not likely. Its a very very very very chancy event. More like a miracle.
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O.K. I know we've agreed to disagree on this, but since we seem to be able to talk like adults, I want to respond to this:

You said (in regards to the leucy):

"Most likely dormant alleles triggered by others on nearby loci or in connection with them. Its documented"

All I'm saying is, if this is possible with a color/pattern morph (which is convenient because of the clear phenotypic difference) why not with any other trait?

Once again, I know mutation is not rampant, even if the color morphs are not spontaneous mutation (I'm not convinced they all are, either) than that means, in the variance of the wild population, there are rare, hidden genes, and once again...if it's true for colors, why not anything else?

On a more interesting note....

We assume that most color morphs would be a disadvantage to a wild ball python, but adults are still occassionally found. Due to the (relatively) high number of albinos, ghosts, and pastels found I would certainly agree that there is an established frequency of these traits. Why they are so rare could easily be explained with natural selection, and I could carry that train of thought to other genes as well...

Best regards,

Kassandra Royer

Most likely dormant alleles triggered by others on nearby loci or in connection with them. Its documented"

All I'm saying is, if this is possible with a color/pattern morph (which is convenient because of the clear phenotypic difference) why not with any other trait?

Because nature is not stupid enough to design many things like that. Its too risky. That's like saying, well if colors can be mutated, then why can't snakes mutate to have 5 heads and no eyes. Well the combination just don't exist for that to happen. And for good reason. Its not in the benefit of life FOR it to happen.

Jeff,

I'm not talking about blind hydras here! LOL!

Personally, I've never seen an animal of any species as grosely mutated as having 5 heads and no eyes. However, we've all seen snakes with no eyes (albino boas), "bug eyes" (leucistic texas rats), and two heads (incomplete twinning). I did see a picture of a deer with a leg growing out of it's back...not sure what was going on there....HA!

Nice.

You KNOW the whole 5 heads thing was an exaggeration to prove a point, ha ha.

Don't be mistaken however, 2-headed snakes, bug eyes, etc etc can very well be mechanical damage to the gametes, zygote, embryo, etc etc. They aren't necessarily hereditary and the cause (or effect, I guess) of bad DNA.

At least not in my opinion.
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Honestly I don't know a thing about genetics, but I happen to own a bug-eyed leucistic Texas ratsnake. I have a freind who's been breeding them for years, and when I asked him about this snakes eyes, he told me that its an anomaly that pops up in the leucistics (and then he gave him to me, his name is Magnum P.I. I have also, on numerous occasions, seen baby bug-eyeds at expos being sold with the rest. I have never seen nor heard of it occuring in any of the other morphs (including normal).

-Bulldawger