Definition of a responsible Breeder

[Homemom]

My understanding is no...

Gene pairs are made up of alleles which are what turn on and off to give different traits. Even identical twins are technically not identical - they may have subtle differences even if it is only just fingerprints.

If you take the DNA from a Holland and compare it with a Fuzzy, they will be the same. You can check for genes but not for what alleles turn on and off. It is amazing how many animals can carry for a long coated gene.

VERY BASIC: When creating a new breed (and I will see if I can get an answer from ARBA as to if the "no sprout" rule ever passed. It was around the time I let my membership laspe) you take traits from different breeds, do various crossings (and have to get enough of a gene pool) to try and fix those traits. Recessive traits are easy to fix - dominant ones are harder as there may be hidden recessives. And when you toss is modifiers - it is really messy! It can take many generations and decades to even get a fairly true breeding strain, then you have to prove it can breed true.

This is why cloning is a myth. You can never guarantee and identical clone because though the genetics may be the same, you cannot determine what alleles will turn on and off.

Each gene has a spot on a chromosome called a locus. Each locus (loci plural) hold two genes. The dominant and rescessive (simplify here) genes are alleles. It gets messy when you deal with modifiers, partial domimance, etc.

So say I have a black rabbit (recessive to agouti pattern) and compare a DNA sample of it to an agouti rabbit. I cannot tell what rabbit is what color because I cannot tell what alleles are present - just that the sample is from a domestic rabbit.

The more alleles present for a trait - the more confusing it can get. In many species, the albino gene is not devoid of color, rather it MASKS all color. And it is NOT always linked to deafness - even in blue eyes animals - these are otehr traits. Albino recessive to regular color, chinchilla and himilayan. You can never get a colored rabbit from breeding two albinos. But if you know the genetics behind the albino, it can be used to create other colors. But there are something like five or six modifiers from full color through the shades of chinchilla down to the himi and finally albino.

Now, once a gene is indentified and isolated for specific traits (like genetic diseases in humans), this is different. So when my husband was looking for genetic issues when doing human research into hereditary infertility. He knew what markers to look for.

Mendelian genetics as most of us learned in high school and basic biology in college are very basic compared to reality.

I still have to ask my husband or mentor to reexplain things.

This is actually a fun page (note there are some illustrations of naked people but it does a good job of basic explanation of some terms and is interactive!)

http://www.virtuallaboratory.net/Biofundamentals/lectureNotes/Topic5-2_LifeCycle.htm

And this is from UC Davis on horse genetics:
http://www.vgl.ucdavis.edu/~lvmillon/

The United Kennel Club has classified the White Shepherd Dog as its own breed as they have developed enough differing other traits from the GSD (not as severe hip angulation is one). This happened recently.

And Sue Bowling is one of my favorite genetics writers. She deals with dogs but her stuff is very easy to understand - as far as genetics go!



http://bowlingsite.mcf.com/Genetics/Genetics.html

I have a headache now and am going to watch a horror flick while little one naps!

 

[Access]

Yeah that is sure more compicated than what I leared in high school biology. I saw one recent case where they tried to make a flower more purple by turning on all the purple genes at once, but that caused the RNA inhibitors (RNAi) which act as part of the anti-viral immune system to activate and all the flowers came out white (no color at all).

 

[C&K]

If you take the DNA from a Holland and compare it with a Fuzzy, they will be the same. You can check for genes but not for what alleles turn on and off. It is amazing how many animals can carry for a long coated gene.

I know, I was shocked a few months ago when I found out that Dalmations (dogs) have a recessive long hair coat gene. Also their spots can come in different colours then just black or liver. I think after the Disney movies came out, that the backyard breeders really propogated these "faults" and brought them to the surface, as more serious breeders usually would not breed dogs that have these faults in their lines intentionally.

This is why cloning is a myth. You can never guarantee and identical clone because though the genetics may be the same, you cannot determine what alleles will turn on and off.

I remember hearing back in the late 90's of a tricolour cat being cloned, but the cloned baby did not have all three colours... Only 2. Apparently the allele for the third colour did not turn on, or was masked, bottom line was they where genetically the same, but looked different as far as coat was concerned.

The United Kennel Club has classified the White Shepherd Dog as its own breed as they have developed enough differing other traits from the GSD (not as severe hip angulation is one). This happened recently.

I remember hearing this, I just forgot about the UKC, I was only thinking of the CKC and AKC... Still though, the WSD is a "sprout" isn't it? I remember reading that either the first male champion GSD was a white shepard, or his father was? And that the reason why they disqualified the coat colour was they where finding the White genes where causing the GSD to loose its dark colouring? Basically they where hoping to breed the white out of them altogether, but some white GSD lovers refused to give up on them?

I have a headache now and am going to watch a horror flick while little one naps!

I have to go do other things too, hope your head improves...

 

[Homemom]

Genetics gives me a headache - and the more I study and learn over the years, the more risky I realize how many things are.

There are a lot of "so you want to be a breeder" type articles out there - many barely TOUCH on genetics other than testing for a few issues. I wonder if it is time for one to be written regarding other genetic issues many are not aware of? I was pondering this at about 3am. How many are not aware of some color genetics and lethal or disabling issues? Honestly, not a lot. Heck I did not know about piggies roan genetics until here. Far more severe than double merles and coloes that could be called roans in dogs! Writing for the women's online gives me a lot more freedom to touch on thought provoking issues (though I do need to sometimes lighten it up). I have one pending publication on pets as presents in Nov and have one sizing a cage for small animals and retracting lead dangers. I think a general genetics issues topic may be a solid consideration... Hard part is narrowing to two to three pages maximum!

I am definitely going to contact the ARBA and ACBA regarding the skinnie issue. I just know too many who are still in piggies up north who would just capitalize on it if skinnies get get recognzined and they can sell through the fair.

 

[salana]

Heck I did not know about piggies roan genetics until here. Far more severe than double merles and coloes that could be called roans in dogs!

Yes, different species seem to be more or less affected, even by defects in the same gene. Hamsters have the anophthalmic white problem, which is very much like lethal white for guinea pigs and also caused by the roan gene (for them, roan is also caused by MITF). Anophthalmic white hamsters usually die, and are generally worse off than lethal white guinea pigs, and also have more internal defects, such as sterility. Mice also have a variety of mutations in MITF, from mild to severe (including osteopetrosis and sterility). On the other hand, humans with mutations in MITF have Waardenburg Syndrome Type 2 or Tietz Syndrome, which are comparatively mild, just coloration problems and deafness.

 

[Homemom]

Yes, different species seem to be more or less affected, even by defects in the same gene. Hamsters have the anophthalmic white problem, which is very much like lethal white for guinea pigs and also caused by the roan gene (for them, roan is also caused by MITF). Anophthalmic white hamsters usually die, and are generally worse off than lethal white guinea pigs, and also have more internal defects, such as sterility. Mice also have a variety of mutations in MITF, from mild to severe (including osteopetrosis and sterility). On the other hand, humans with mutations in MITF have Waardenburg Syndrome Type 2 or Tietz Syndrome, which are comparatively mild, just coloration problems and deafness.

Can you give me some decent references for this? (not doubting, but I like to give references in articles for those who want to learn more). I really am giving this topic a lot of consideration and want to be able to give general examples to get people thinking.

I have talked a lot of people out of breeding dogs, now I can target other species writing for a more general audience! I am also brushing up on feline genetics...

 

[naturestee]

In rabbits you get lethal babies from dwarf genetics. "True" dwarfs are heterozygous for the dwarf gene. Nondwarf purebred Nethies and such have no dwarf gene and are considered breeding but not show quality. "Peanuts" have two dwarf genes and are either born dead or die soon after birth due to severe defects. There is a second "Max Factor" gene that is more rare in dwarfs where heterozygous is good and homozygous for the gene is fatal.

I don't see how you can purposefully breed an animal (at all at most times) when you know you have a 25% chance of dead/dying kits. I have heard some breeders use the nondwarf females to breed with dwarf males so they don't get peanuts, but most don't as it increases the number of unshowable kits.

 

[C&K]

I think your article sounds great! I hope you can share it when you are done, or at least point us in the direction where to find it.

 

[Homemom]

I think your article sounds great! I hope you can share it when you are done, or at least point us in the direction where to find it.

I am roughing out notes now.

 

[salana]

Homemom, I lost all my links because they're on my old laptop. I can try to dig them up or re-find them but it'll take time. Try http://scholar.google.com - here's some of the first links for the search mitf hamster

http://www.genetics.org/cgi/content/full/164/3/1035

In the Syrian hamster, one dominant mutation in Mitf (W241X) has been reported and designated as anophthalmic white (Wh). It is predicted that this premature stop codon leads to a truncation of the protein in the loop between helix 1 and helix 2 of the bHLHzip region. It prevents the protein from dimerizing or from binding to its DNA target sites (HODGKINSON et al. 1998 ).

So maybe you could look up Hodgkinson et al. 1998 for more info.

 

[Homemom]

Homemom, I lost all my links because they're on my old laptop. I can try to dig them up or re-find them but it'll take time. Try http://scholar.google.com - here's some of the first links for the search mitf hamster

http://www.genetics.org/cgi/content/full/164/3/1035


So maybe you could look up Hodgkinson et al. 1998 for more info.

Don't worry about it. As long as I have trait or disease names, I can look them up and I am pretty good at determining the good from the bunk out there. We had a computer crash a few years back and I lost dozens of behavioral references that took me ages to find again! Don't even go there for me, please!

I have notes roughed out and am already just about at my page limit (OUCH!) without adding references. Narrowing things down is going to be tough.

I am basically doing bullet notes to get the thought process going and then will add a for more reading list at the end.

 

[Access]

I don't see how you can purposefully breed an animal (at all at most times) when you know you have a 25% chance of dead/dying kits. I have heard some breeders use the nondwarf females to breed with dwarf males so they don't get peanuts, but most don't as it increases the number of unshowable kits.

I saw a documentary a little while ago on the history channel about animal breeding. Most of the animal breeders interviewed said they expect that, for any given generation, 90% of their animals will be 'terminal' and 10% will go on to breed. Whether an animal is terminal or goes on to breed depends on a complicated formula put into a computer, every animal is catalogued in the computer and its applicable traits measured or tested. The ***** of desireable animals is frozen and preserved for future generations. What happens to the terminal animals depended on the type of breeder... for cattle breeders the terminal animals are seperated from the rest of the herd and fenced in, allowed to grow to maturity and then sent to the slaughterhouse. For pet animal breeders, terminal animals are treated much worse, the sellable ones are offloaded to pet shops / auction / pet owners, the others are killed in numerous ways -- suffocation (using custom-built gas chambers), microwave irradation (placed into a microwave and cooked alive), released into alien habitats where chances of survival are nil, etc.

Also this 90% terminal / 10% breeder formula is only attainable with sophisticated computer models and thousands of dollars of computer software and the like.. additionally freezer facilities for artificial insemination (another great expense) -- these tools are far more than the average small animal breeder has. Realistically without the tools the percentage of breedable animals is even less than 10%. If 90% or more of the animals are terminal from the start, 25% is a relatively small number, that is only 1 in 4 compared to 1 in 20. Some efficiency-minded breeders no doubt prefer the 25% lethal rate since most lethals are born dead or die shortly after birth, relieving them of the duty of having to dispose at least a portion of their terminal animals using other methods. 500+ cavies is not unusual for a cavy breeder, if you remember the thread a while back about the breeder who died and all his pigs were being auctioned off to pay for his services... and he was said to be one of the 'better' breeders compared to the rest. Breeding is a "big numbers" game, when only 5%-10% of your animals can be re-bred you need to produce 100+ animals per generation to get 5 desireable ones... then those breedable animals have to turn out another 100 in the next generation to get another 5, and so on. If you are skilled in genetics and biology the idea is that with each sucessive generation you will get a slightly higher percentage, but if commercial breeders with the best tools say 10% is average, I would not expect that a small animal breeder without those tools can get close to that, much less exceed it.

 

[naturestee]

Hi Access!

I am familiar with how that system works as I grew up in a farming area. The difference here is that these animals have somewhere around a 99% chance of dying before reaching maturity. Homozygous dwarf and max factor babies die, often painfully if not euthanized, within a few weeks of birth. This is not a nonshowable versus showable choice except for when breeders choose to use nondwarf does. And that just increases the proportion of nonshowable babies, as nondwarfs can not be shown and to breed they still need appropriate markings and other physical characteristics. I'm not as bothered by the result of nonshowable but living kits, I'm bothered by the intentional creation of babies born to die painfully from their birth defects. It just always seems to me that this is overlooked and considered unimportant when people talk about breeding rabbits. If that happened in cats or dogs there would be an uproar.

 

[Access]

What is the genetics behind those though? If the lethal gene is recessive, you have to breed two carriers to have a 25% chance of getting a lethal. If the lethal gene were dominant, a carrier would most likely die before it reached breeding age. So it really comes down to two possible outcomes...

1) Parents are carrier (Gg) and normal (gg) - offspring has 50% chance of being a carrier, 50% chance of being normal.

2) Both parents are carriers (Gg) - offspring has 25% chance of being normal, 50% chance of being carrier, 25% chance of being lethal.

For cavies both roans and dals (dalmations) carry a recessive lethal gene. If you breed [roan] x [roan], [roan] x [dal], or [dal] x [dal], one in four (25%) of the offspring will be lethal. 3 in four (75%) of the offspring will either be normal or a carrier.

A breeder who specialises in roan or dalmation will do (1) or (2) and not really care, either way they have 50% any given offspring being a roan / dal to begin with.

In case (1) the other 50% they would immediately consider terminal, be either offloaded for an immediate profit, or killed if they could not be offloaded. Of the remaining 50%, at best 10% of the 50% is breed quality (5% of the total), and the remaining 45% is at least within the breeders specialty, ie. what the breeder has a reputation for and can get a good profit for -- so they can be raised a few weeks then possibly sold to owners.

In case (2) the only difference is that instead of 50% being outside the breeder's specialty and hence labelled immediately terminal, 25% are lethal and 25% are outside the specialty.

The sad thing is, logically, we can deduce that a roan / dalmation breeder who dislikes having to kill or dispose of animals outside their area of specialty; they are more likely to favor case (2), even if only unknowingly or subconsciously, since in case (1) they have to dispose of 50% of the offspring, in case (2) they only have to dispose of 25%, the other 25% is either born dead or most likely will die in the first few days.

This is why just about everyone who feels any kind of connection to cavies despises breeders so much... breeders are only hurting the far majority of their animals for their own sake.

 

[salana]

Actually, some roan/dal breeders also maintain lines of selfs (or tortoiseshells, or whatever the normal babies wind up being) for showing. Perhaps they're more likely to breed Rnrn x rnrn (dal x self) because then they might get more nice selfs for showing too.

Still, dumping nonshowable roans on the pet store is pretty irresponsible in my opinion.

I've been reading some old works on cavy genetics and perhaps in the early 20th century there was a non-lethal roan gene floating around in the US. The one author even called the lethals another researcher had gotten "anomalous". It seems that the lethal roan gene has taken over the population, though.
http://scholar.google.com/url?sa=U&q=http://www.genetics.org/cgi/reprint/32/2/115.pdf

 

[Homemom]

I wish other animals would catch up to dogs (which really have far to go in regards to genetics work but are far more advanced than other species in many respects), in regards to health testinging and published genetics materials.

Dr George Padgett did a lot for the dog world and debunked hybrid vigor in the cross bred dogs. But other keep the myth gping...

It blew my mind when I was breeding rabbits over a decade ago how FEW people understood even basic color inheritance and had no idea how many genes can be involved in various things. My favorite was you can never breed a red or blue eyes white to a colored animal because you will get white toe nails. Gee, white nails is not really related to coat color in that respect. Yes nail color is related to coat color but not mismarked nails. How many breeders did I know who did not breed whites or broken patterns or have the genes in their lives who were still having white nail problems? Many. Yet they were still insisting it was something else. No, they were breeding rabbits that carried for the gene and that was it. But try to explain to them that their rabbits carried for the DQ and should not be bred. Clueless!!!

Let's not even get into health! Truy to explain that a predisposition to sore hocks can have a hereditary basis as well as a sign of poor management.

In piggies, the better roan breeders I knew of bred roan or dal to self and never the two together. But they were few and far between. Most I knew avoided those colors.