[QUOTE=grayarabpony;7202663]
Stoney you’re getting into the realm of expression of genes versus inheritance, which is another matter ON TOP OF Mendelian genetics and gene linkage.[/QUOTE]
Not exactly. Inheritance either occurs according to a Mendelian model or it doesn’t. Expression of traits and its variability is directly tied to the mode of inheritance and the linkage of genes. My evidence for this was provided.
Inheritance of GENES occurs according to the Mendelian model, when genes are not linked. Expression of genes is an entirely different story.
Just look at the inheritance and expression of BRCA genes in humans. Some men who have one of those mutations get cancer, some don’t (I do not know the percentages, only that those genes are associated with several different types of cancer). Not every woman with one of those mutations is going to get breast or ovarian cancer (although I do not know the percentage of overall cancer incidence). According to the National Cancer Institute, roughly 50 per cent of women with one of those mutations will develop breast cancer by the age of 70. Suppose a woman develops breast cancer at age 75, and then lives to be 90. She has a sister who died of breast cancer at the age of 45. Both tested as having the same mutation in the same gene, different expression.
Maybe I have gotten too caught up in describing my ideas in terms of expression and phenotype, fair enough. I have gotten way off course of the original and only 2 points I intended to make anyway.
Yes, I believe that allele frequencies are inherited in the way that you say, however I was unaware we were talking about allele frequencies since it was being said that an offspring of a carrier and a carrier has 25% of having disease ect…since this is referring exclusively to expression. They may have 25% chance of having the alleles that may lead to disease, but the actual expression of disease relies on many more factors (such as penetrance and epigentics). GAP’s breast cancer example highlights this.
I only wished to say initially that there are processes that would render 25/50/25 inaccurate at both the allele level as well as the expression level and that these processes become more common in a highly homozygous (inbred) population. These processes are mostly non-mendelian and involve epigenetics, which yes I know revolve mostly around expression and I had already assumed incorrectly that we were talking about phenotype of said disease instead of allele frequency alone, but also include things like genomic imprinting which is inherited and not reliant on expression. In the population of horses I think that keeping in mind epigenetic expression is just as important as the alleles inherited since methylation patterns are also inherited and do not rely on expression, since the actual DNA is altered (albeit reversibly in some cases). This may occur far less commonly than traditional inheritance, but since we usually deal in small population it bears mentioning and is important to keep in mind.
The other thing I wanted to say originally, which most of us invariably know anyway, is that a trait (which is inherited as a trait regardless of expression…for example height) is more complex than: Stallion A has big neck, mare B has tiny neck and resulting offspring C has 25% chance of big neck, 25% chance of tiny neck and 50% chance of a heterozygous neck. In addressing this we must consider co-dominance, incomplete dominance, multiple alleles, incomplete heritability, ect. in addition to epigenetics and other environmental influences on expression.
ETA: Sorry everyone for the sidetracks. I know even though I enjoy talking about this stuff with GAP and others, some people may find it tedious. It is, however, what I consider when breeding my mares 
Yes, we were basically “cross talking” about genes and phenotypes. 
It’s not known in humans, much less in horses, how often epigenetic expression is inherited and how persistent it is over generations. The Dutch Famine study shows some changes over two generations, but that’s a pretty extreme example.
The Russian fox studies are interesting as showing how genes are interrelated. Breed for a given interior trait and you can also affect the phenotype substantially.
I’m certain that the foxes used were substantially inbred.
[QUOTE=vineyridge;7202944]
The Russian fox studies are interesting as showing how genes are interrelated. Breed for a given interior trait and you can also affect the phenotype substantially.
I’m certain that the foxes used were substantially inbred.[/QUOTE]
I only recently found out that deafness is attached to bald faces with blue eyes. I guess it’s similar with other species as well.
Regarding linebreeding in order to reliably reproduce desired characteristics – It seems to me that the wiser choice might be to choose unrelated stallions and mares who both have those characteristics one is trying to reproduce. I say this because genetic weaknesses will almost always come with the strengths when inbreeding. The Friesian breed, for example, has several “tendencies” which are almost 100% certain to be from inbreeding/linebreeding. Granted – the breed has a closed studbook. But if one is not working in those confines, why risk genetic weaknesses? You can’t know that a given stallion or mare may have a genetic link to a somewhat weak circulatory system, or poor disease resistance, or tendency to have weak ligaments, etc, etc, etc especially when certain genes are doubled up through line/inbreeding. Nature will almost always give the advantage to those with genetic diversity. I think the key is to maintain genetic diversity when breeding for certain traits. Just my opinion.
[QUOTE=jdeboer01;7204444]
I only recently found out that deafness is attached to bald faces with blue eyes. I guess it’s similar with other species as well.
Regarding linebreeding in order to reliably reproduce desired characteristics – It seems to me that the wiser choice might be to choose unrelated stallions and mares who both have those characteristics one is trying to reproduce. I say this because genetic weaknesses will almost always come with the strengths when inbreeding. The Friesian breed, for example, has several “tendencies” which are almost 100% certain to be from inbreeding/linebreeding. Granted – the breed has a closed studbook. But if one is not working in those confines, why risk genetic weaknesses? You can’t know that a given stallion or mare may have a genetic link to a somewhat weak circulatory system, or poor disease resistance, or tendency to have weak ligaments, etc, etc, etc especially when certain genes are doubled up through line/inbreeding. Nature will almost always give the advantage to those with genetic diversity. I think the key is to maintain genetic diversity when breeding for certain traits. Just my opinion.[/QUOTE]
Back years ago I was a dalmatian owner and was fascinated by their genetics. Now I’m probably remembering this all wrong, but the stem cells that produce color are the same stem cells for the little fibers in the inner ear that are activated by sound waves. If for some reason the embryo doesn’t make enough color cells to migrate to the inner ear, it will be deaf.
[QUOTE=jdeboer01;7204444]
I only recently found out that deafness is attached to bald faces with blue eyes. I guess it’s similar with other species as well.
Regarding linebreeding in order to reliably reproduce desired characteristics – It seems to me that the wiser choice might be to choose unrelated stallions and mares who both have those characteristics one is trying to reproduce. I say this because genetic weaknesses will almost always come with the strengths when inbreeding. The Friesian breed, for example, has several “tendencies” which are almost 100% certain to be from inbreeding/linebreeding. Granted – the breed has a closed studbook. But if one is not working in those confines, why risk genetic weaknesses? You can’t know that a given stallion or mare may have a genetic link to a somewhat weak circulatory system, or poor disease resistance, or tendency to have weak ligaments, etc, etc, etc especially when certain genes are doubled up through line/inbreeding. Nature will almost always give the advantage to those with genetic diversity. I think the key is to maintain genetic diversity when breeding for certain traits. Just my opinion.[/QUOTE]
Thank you, especially for the part in bold.
Breeding always has a risk. I don’t understand why breeders would want to ratchet up risk with close inbreeding. I’m sorry, I know I must have written that more than once already, but I just know that someone will come back with “Well, breeding is risky!” as though there is no difference between normal risk and then adding additional risk on top of that.
[QUOTE=vineyridge;7204494]
Back years ago I was a dalmatian owner and was fascinated by their genetics. Now I’m probably remembering this all wrong, but the stem cells that produce color are the same stem cells for the little fibers in the inner ear that are activated by sound waves. If for some reason the embryo doesn’t make enough color cells to migrate to the inner ear, it will be deaf.[/QUOTE]
You might be interested in reading this paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2871368/
This article too: http://purinaproclub.com/Dog/ResourceLibrary/HealthGeneticsTraining/Genetics/2987d207-2fe2-49cb-914b-710b74ca67eb
This article is also interesting regarding linebreeding, inbreeding, prepotence and ‘how close is too close?’ though it as about dogs, not horses.
http://dpca.org/BreedEd/kb/index.php/component/content/article/92-illena-a-the-seven-sires
Progeny proves the pedigree…
Also known as hind sight is 20-20.
I think if some checked the closebreeding in pre-WWII stock of their own preferred horse breeds they would faint away.
Then let them go back another 50 years to pre 1880, my that does get interesting!
[QUOTE=vineyridge;7202944]
The Russian fox studies are interesting as showing how genes are interrelated. Breed for a given interior trait and you can also affect the phenotype substantially.
I’m certain that the foxes used were substantially inbred.[/QUOTE]
If you haven’t, you ought to search for gene knockout sequences in rats/mice studies. If I wasn’t on my phone I could pull the exact study, but I can’t copy/paste. IIRC, scientists were knocking out certain genes in a rat (maybe fear? I can’t remember it’s been a while) and found when they knocked out a certain gene, it caused other differences in personality and phenotype. I THINK it was they were trying to knock out fear or something and ended up with exceptionally aggressive and dumb rats.
[QUOTE=D_BaldStockings;7205947]
This article is also interesting regarding linebreeding, inbreeding, prepotence and ‘how close is too close?’ though it as about dogs, not horses.
http://dpca.org/BreedEd/kb/index.php/component/content/article/92-illena-a-the-seven-sires
Progeny proves the pedigree…
Also known as hind sight is 20-20.
I think if some checked the closebreeding in pre-WWII stock of their own preferred horse breeds they would faint away.
Then let them go back another 50 years to pre 1880, my that does get interesting![/QUOTE]
Faint away? No. I’d hope people have more sense nowadays and realize they aren’t stuck with the stallion up the road.
[QUOTE=vineyridge;7202944]
The Russian fox studies are interesting as showing how genes are interrelated. Breed for a given interior trait and you can also affect the phenotype substantially.
I’m certain that the foxes used were substantially inbred.[/QUOTE]
Are you talking about the behavior study? In this case, they selected one group for “interest towards humans” on test day (index of domesticity) and the other group they randomly bred foxes. Over time, selecting for foxes that simply approached humans pulled down other traits such as body type, bone structure, facial coloring, etc. Interesting. It is also well known in the mouse world that gene knockout phenotype often varies with the background strain of the mouse. Linebreeding over time is also known to be disasterous in mice and emphasizes rare genetic recombination.
[QUOTE=J-Lu;7205980]
Linebreeding over time is also known to be disasterous in mice and emphasizes rare genetic recombination.[/QUOTE]
Not sure what you mean by “disastrous.” The “inbred” mouse strains are defined as the descendants of products of IIRC 20 consecutive generations of littermate crosses. The results are certainly viable, however many of their great-great-great aunts and uncles didn’t make the cut.
Sometimes a narrow gene pool is not without its attractions, depending on how selection of the foundation stock is done.
If you want to produce a cheetah, for example.
http://www.ncbi.nlm.nih.gov/pubmed/21183613
http://www.earthtimes.org/nature/knocking-spots-off-cheetahs/2192/
Or if you throw a relatively small population into a difficult environment and cull the non-performers…like North America during the 18th and first half of the 19th centuries, from settlement to the Civil War.
Or most of Europe during the first half of the 20th century.
Sometimes that ‘stud next door’ is the best there is, not just the closest.
And anyone who doesn’t think horses moved around in the past might consider they were the mode of transport for humans pre-automobile and changed hands at every battle where horse and man parted company.
Byerly Turk was a spoil of war, for instance, to name just one.
The Darley Arabian embarked from Aleppo, Syria for England; Dutch horses came to England with the Flemish weavers ‘imported’ for their expertise with wool influencing Fell and Dales, and likely Welsh and Shire gene pools.
Outcrossing for desired traits that are lacking, followed by real world performance, then inbreeding to smoke out the recessives and set type is how generations have been breeding livestock since Bakewell.
linebreeding most horses is a far cry from the intense inbreeding for 5-6 generations that it takes to set genetic lines in experimental rodents - which foundation stock was itself inbred for ten or eleven generations to begin with.
At 8-10 years per horse generation if performance is taken into account, that would be -50 years of inbreeding? Piled upon 500 years (oops! math would be 110 years, 200 yrs for 20 generations) of intense inbreeding?
I don’t think that will ever be likely as human lifespans and culture turn over and evolve more quickly than that.
Using the fantastic genetic tracing tools we have today and searching for more into the future, should allow an intelligent breeder to maximize their odds of producing a good horse -IF there is disclosure of genetic mapping, and of surgical repair of breeding animals, and realistic tests beyond simple beauty contests.
Cheetahs are highly vulnerable and in extreme danger of extinction – and that’s without factoring in humans and habitat destruction. They are a highly inbred species and are all near clones of each other. Their fertility is abysmal, and they only live between 8 - 12 years even in captivity. They show classic signs of inbreeding depression.
http://www.animalwelfareintergroup.eu/2011/12/21/the-cheetah-and-its-race-for-survival/
[QUOTE=D_BaldStockings;7206005]Sometimes that ‘stud next door’ is the best there is, not just the closest.
[/quote]
Yes, this is the case with the Friesian breed. The group that founded the studbook in the late 1800’s thought they were “saving the breed” with their aggressive culling (oftentimes solely based on color or a bit of white on the legs) and heavy use of “ideal” stallions. We now know that the single stallion line they culled the breed back to in order to set phenotype carried dwarfism. At this point in the game, if all Friesians that carry dwarfism were to be eliminated from the breeding population, it would do more harm than good, as it would likely half the gene pool again!
“Smoking out deleterious recessives” isn’t as easy at it sounds. Genetics are so complicated, and oftentimes, the causes of diseases aren’t known. Sometimes, no known disease is present, yet early death has may have it’s roots in inbreeding depression. Sometimes horses just show an overall tendency to get sick, take a long time to heal, or have other vague issues with no nail down-able cause. For example, some experts theorize that some of the root causes of certain issues with some Friesians (i.e. aortic rupture, megaesophagus, excessive sidebone, stomach rupture, etc.) may be due to collagen structure. That’s really not something that can be “tested” for. Nor can it be said that every horse with collagen abnormalities will develop problems. But the size of the gene pool is almost certainly the underlying source of the problem. Yes, linebreeding and inbreeding has been done for generations, but today, we know for a fact that doing so has more downsides than upsides. Continuing to use those methods in this day and age knowing the risks is truly nothing more than laziness, IMHO. I still firmly believe that breeding unrelated horses with similar desired traits (if at all possible) is the safest bet.
From an in depth study of the Friesian horse:
http://www.fenwayfoundation.com/pdf/Boerma%20et%20al.%20EVE%202012.pdf
[I]It may be that several of these disorders are related to
one common feature which has been intensively selected
to obtain the breed specific postural characteristics: a
baroque type appearance with a vertical neck and a
hyperflexing and hyperelastic ‘dancing’ locomotor
pattern (Halper et al.2006). In particular, the latter fits
with the suggestion that many of the problems
are collagen-related and a systemic collagen-linked
abnormality plays an important role. This supposition is
supported by a recent study of tendon properties. It has
been shown that there is a significant difference in tendon
properties between dwarf Friesians and normal ponies
leading to load failure of the stay apparatus (Gussekloo
et al 2011); normal Friesian horses had properties in
between the dwarfs and ponies and tendons were more
elastic than reported in Thoroughbreds. Another indication
of a possible abnormality of collagen is demonstrated by
the predisposition to rupture of the aortic wall:H&Estaining
of these lesions revealed significant presence of
degeneration, collagen fibre fragmentation, necrosis and
inflammation (Ploeg et al. 2011). Abnormal collagen
formation together with aberrant elastin properties has
previously been demonstrated in Belgian draught horses
with verrucous pastern dermatitis (De Cocket al. 2009)
[/I]
All I can say is- wow- on the level brainiest of the conversation! What an amazing resource you all are!
Each choice of breeding relationship has its place; depending on the goals of the breeder.
Outcrossing, especially to an established inbred group of horses (Thoroughbred, Arabian, Icelandic, etc. - what most would call purebreds) and choosing on phenotype and performance of the family as well as the individual is what created the super-performer in many cases.
Continuing to breed outcross to outcross unfortunately often leads to regression and unpredictability after the 2nd generation: the very diversity of genetic material to work with often outputs an ‘average’ animal that has lost the hybrid vigor (assuming one was lucky enough to have that expressed, sometimes crosses do NOT combine the best of both…) and here comes a generic ‘feral’ type that is functional as a horse, but most unstylish and unmarketable.
Outcrosses to succeed generationally must be back-crossed to the pure foundation, linebred within their family group, or inbred to a particularly exceptional (usually 2nd or 3rd generation) result of that first outcross.
Would Irish Draft, Fell / Dales, Welsh Cob, Andalusian, Lusitano, Old style Morgan… be included in ‘similar traits to Friesian’ and so be a ‘correct’ outcross?
Or is the goal to instead create ‘black and hairy and high-headed with big trot and kind temperament’ in a metabolically non-Friesian body form that the modern WB and /or TB is closest to?
The difficulty with closed registries (you can’t breed to x mare or stallionbecause it isn’t in our book) is also part of their salvation.
They are retaining the small gene pool as a resource for the future where you will only pick up XYZ if breeding to a registered animal.
At some point opening a registry becomes necessary, but remember the German Coach horse / Gelderlander viable mare base pre WWI is no more. They have been completely absorbed and homogenized into the European Sporthorse registries, leaving remnant populations too small to perpetuate.
The guiding force of a registry board is a powerful and dangerous director of genetics when ‘voting -AKA inspections’ limit breeding stock to narrow, often prejudicial selection.
In short, if you breed yourself into a hole, you can get out - by outcrossing.
If you’ve found the ‘charm’ you might be able to retain it for a few generations by inbreeding.
If you have sturdy stock of useful and beautiful type and can do lots of research, you can do very well linebreeding the best of your families.
You can also undo the good that generations of breeders that came before you accomplished with just a few generations of foolish choices.
DBaldStockings, don’t be silly. Of course horses were moved around in past centuries – but not to the extent that they are. And that certainly wouldn’t include the semen.
I just hope that all breeders truly realize that no matter how much research you do, close inbreeding can still result in some very unpleasant surprises, up to involving the type of culling that involves the death of the horse – because you do not have a genomic map and do not and cannot know everything in that horse’s genes. Picking out the examples that have worked out with close inbreeding isn’t the whole picture.
And sometimes two beautiful people have an ugly child. But usually, they don’t. 
And most often two athletic people will have athletic kids. Or very high IQ parents will have very intelligent kids.
[QUOTE=D_BaldStockings;7206751]Outcrosses to succeed generationally must be back-crossed to the pure foundation, linebred within their family group, or inbred to a particularly exceptional (usually 2nd or 3rd generation) result of that first outcross.
[/quote]
I think it depends on what a breeders’ goal is. Outcrossing, then backcrossing to pure stock is exactly what I’m doing in my own program. I’m not completely disagreeing with you regarding linebreeding. I just think some breeders take it too far or rely on it too much.
[QUOTE=D_BaldStockings;7206751]Would Irish Draft, Fell / Dales, Welsh Cob, Andalusian, Lusitano, Old style Morgan… be included in ‘similar traits to Friesian’ and so be a ‘correct’ outcross?
Or is the goal to instead create ‘black and hairy and high-headed with big trot and kind temperament’ in a metabolically non-Friesian body form that the modern WB and /or TB is closest to?
[/quote]
Again, depends on the goal of the breeder. My beef with the Dutch Friesian registry (and other closed studbook breeds – even dog breeds – where inbreeding depression is apparent) is that they absolutely refuse to do any outcrossing whatsoever – despite the fact that not doing so is an obvious detriment. Their obsessed with the idea of “purity”, which makes no sense whatsoever. It’s enough to leave a bad taste in one’s mouth regarding incessant “linebreeding”.
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