When Line Breeding Where Do you Cross The Line: - Page 2

Bubba: in the case of the UK lines and Epilepsy, the breeding was for gold but not for cookie-cutter looks or aggression - it's been mostly for coats n colours (as many previous threds including the one linked by Sunny have shown).

Alamance: why do you want to know which book it was ? Have you got TIG's copy ? LOL

Sunsilver: its Ballack, there is a whole thred on this, started by Mackenzie, within the last couple of weeks ...

For Alamance and anyone else who may be interested:

Dr. Malcolm B. Willis's two most informative books are as follows:

"The German Shepherd Dog - A Genetic History of the Breed"
first published 1991, by H F & G Witherby (in the UK)
ISBN 0 85493 207 0

and

"Genetics of the Dog"
same publisher
ISBN 0 85493 176 7

Hope this is useful.

Hundmutter I'm lol cause as it turns out Alamance & I did know ea other. We are relatively in the same part of the universe - about 4 hours apart but would see ea other at shows & herding trials. And no she is not the one who walked off w/ the book. That occurred decades ago back in New England.

Alamance Actually it was his first book published back in 1977 https://www.amazon.com/German-shepherd-history-development-genetics/dp/0668040777. Went looking & while some copies are too rich 4 me there were some used ones I might have to find the funds for.  BtW sent u a pm.

[TreasurePomeranians] 1.9.2016 - 17:09

 

● "It says 3% inbred when they are bred together.  And I have other pairing I want to do but it's 7% together since they share two dogs in a 5 generation pedigree. Where do you draw the line?"
Line#1: When your mentor says, "No - that mating is too risky for this, that, and the other." You DO have a mentor with enough knowledge to say that, I hope?

Line#2: When your own background research (preferably using official records, but paying attention to the "gossip-line" when records are inadequate) points out that the common ancestor possessed a "bad allele" that could be passed his/her F1 (children) and/or F2 (grandchildren) and/or F3 (greatgrandchildren) and/or his F4 (greatgreatgrandchildren) dewscendants, and therefore there is a STRONG possibility that the dog and bitch you wish to mate together have each inherited at least one copy of that "bad" allele (or alleles if the mode of inheritance is polygenic).

Line#3: When something goes wrong.
Thanks to generations of culling, almost all the "bad" genes left are recessives, and therefore whatever goes wrong PROVES that the "bad" gene or genes (actually, I should refer to alleles) came from BOTH parents. If the disorder is like Degenerative Myelitis and the "bad" allele can be identified from DNA, either parent CAN be carefully used. but NOT to each other! - ethically you MUST mate to only pooches that are DNA negative for that allele.
If no DNA test is available, you MIGHT get a clearance from blood chemicals, but probably not. In which case those pooches' breeding career is over.
Statistically, a pair of carriers will have 25% of their offspring totally free of the damaging allele and be quite safe to breed from. 50% of the pups will be carriers and will keep that "bad" allele in the breed's gene-pool if bred from, and 25% of the litter will be afflicted.
But with a slow-to-develop disorder such as DM or PRA (Progressive Retinal Atrophy) it was impossible to identify a "free" pooch from a "carrier" EXCEPT by expensive test matings using an afflicted partner or a known producer as the test-mate, and by NOT registering any pup in the test litter. And with litters usually have low numbers of pups, the statistical "accuracy" was dreadful.

I imagine that your litter-pedigrees are in the pdb and you refer to either Wright's or Hardiman's calculations. Of the 2, Wright's appears more logical:   http://www.highflyer.supanet.com/coefficient.htm   but I prefer the modification that genetics professor Malcolm Willis showed in his 1976 GSD book. To account for genes coming from an infinite number of generations, he start from the premise that 25% of an individual's genes came from a parent (so TWO parents supply 50% of each pup's genes), and halves that in each earlier generation. So a P2 ancestor's share of an individual's genes is 12.5%, each P3 ancestor contributes 6.25%, a P4 ancestor contributes 3.125%, a P5 ancestor contributes 1.5625%.
Okay, - like us, a canid has close to 20,000 genes. So if your planned litter shows P4 : P5 line-breeding (which most people shorten to 4 : 5 or the unmathematical 4 - 5) that THAT common ancestor will on average contribute 625+312½ genes - almost 1000 genes. And the same arithmetic applies if the line-breeding is 5 : 4.

But regardless, remember that what matters is identifying WHICH descendants from a spreader of "bad" recessives managed to NOT produce the ancestor's problem and are therefore "better risks", versus WHICH you must avoid because it is proven that THAT line has produced the ancestor's problem in recent litters - the more recently a problem was produced, the greater the risk that it will be passed to one or more pups in YOUR litter. In the simplest situation (a single recessive autosomal allele from ONE parent), each pup has a 50% chance of inheriting the "bad" allele, each grandpup has a 25% chance of inheriting it, each greatgrandpup has a 12½% chance of inheriting it, each greatgreatgrandpup has a 6¼% chance of inheriting it.

 

But I doubt there is a pooch alive who carries only ONE "bad" allele! My own sire passed on genes for alcoholism, astigmatism, diabetes, Dupuytrens contractures, myopia at least - but until the last 10-15 years his GOOD genes took precedence. And only the myopia was revealed by the time he met Mum.


[TIG] 7.10.2016 - 17:10
● "you have to know what’s in the “back forty”"
What "back forty", [TIG]?
I could understand the term were it referring to a large farm, but cannot find any relevance in genetics.
If you meant the closest 40 ancestors, that doesn't make sense, as the 2 parents plus 4 grandparents = 6. Add the 8 greatgrandparents = 14. Add the 16 greatgreatgrandparents = 30, Add the 32 greatgreatgreatgrandparents = 62. Add another generation's 64 and there are 126. So nowhere is there a group of 40 ancestors at the back of a pooch. If you meant to take the pedigree back 40 generations, Chris H might attempt that first time she was asked but, if I've interpreted my pocket calculator's panicked apostrophes correctly, the P40 generation has, all by itself, something like 1,099,511,400,000 names, and so there would be about 2 TRILLION ancestors she would have to trace & write out (no wonder she takes so long finding some of my Bea's ancestors that were in Britain during the crazy between-world-wars period!).
What DID you mean, please?

As for Ballack, I'm not going to trace his pedigree further back than 7 generations, but I thought the BSZSs from 2013 onwards had had no Sieger, no Siegerin - all the VAs being equal, But I see that the SV's results web-page ranks them, so I checked with an SV friend and found that by 2015 the SV had knuckled under to the "We won't enter unless we can become Sieger or VizeSiegerin" crowd who refuse to believe the 'Animal Farm' slogan that "All animals are equal".

No-one should assume that Germany's GSD gene pool is free of the alleles for epilepsy. Of the 48 names in my private datatable of producers or siblings of epileptics, 7 are German studs despite the "clamming up" practised in Germany. As far as I know, Avon Prince got his alleles for epilepsy from his German sire-line.

This 2013 article   http://www.canine-epilepsy.net/cerc.html   showed that much work still needed to be done! And that 71% of the ridiculously small sample of GSDs actually HAD epilepsy.

Those with stamina might care to work through the theories & methods & failures in the 2011   http://bmcgenet.biomedcentral.com/articles/10.1186/1471-2156-12-38   article. The failures make it easy to believe the possibility that there are 6? different genes interacting to produce genetic canine epilepsy.

[TIG] 10.10.2016 - 00:10

● "Alamance Actually it was his first book published back in 1977"
My copy of that "bible" was published in 1976 by K & R Books Ltd. Despite making a couple of wrong guesses as to which gene certain alleles belonged to (he had no DNA sequences available back then) and wrongly claiming that Vello Sieben-Faulen (my obedience bitch's greatgrandfather) had been breed surveyed, it is a very good book. My copy's purple dust jacket disintegrated long ago. I thought that the Yank publisher of the American edition gave it a cover with Manhattan's head but, looking through Amazon, the 1992 Yank edition of the 1991 "The German Shepherd Dog, a Genetic History of the Breed" has a dog that is probably Manhattan.

 

Yes back forty is a homebred expression more along the line of a farm term but I think most people get the idea w/o thinking I mean to check several trillion ancestors.

Never said Germany didn't have epilpesy or any other country for that matter. Also since it's most likely a threshold factor it is possible for an area or a tightly bred pedigree to lack the triggering level but when introduced to new breeding partners carrying those different factors wham bam. (wh/ may be what happened here in the US) Also never said Avon Prince didn't get it from his German ancestors - it is quite likely he did and there are several suspects that would help explain the seemingly greater preponderance in the UK.

Our problem is we don't know the nature of the defect causing the seizures and in fact there may be several discrete processes being lumped together under the epilepsy label (see this in humans and other animals). We could be just dealing with a bag of marbles(genes or alleles) that are all white except for x# that are black and the triggering level depends on the # of blacks you get. Simplest model. Or it could actual be an extra copy or copies or a deleted copy(copies) of an activating protein. In some human epilepsy I believe one of the hypothosized causes is defective nerve sheathing (could DM be related? be interesting to look if both diseases occur in the same lines of at higher levels in pedigrees carrying both). It could be a RNA transcription error that increases overtime thus the late onset of the disease. In short it could be just about anything and all we have to go on now is knowledge of carriers and affecteds and pedigrees which animal breeders have used successfully for centuries but which you seem to want to ignore.

So care to share  the 48 names in your private db to help the rest of us?

Also I would suggest a stroll thru PubMed. Even a quick & dirty search will show you there is not one entity called canine epilepsy. It varies widely by breed in it's expression and it's possible mode(s) of inheritance and responsiveness to treatment.

Finally for some one who tries to come across as Mr. Know it all and a stickler for the "correct" scientific terminology at all time you use the SOD1 test as an example of a dna test for a disease- really??? 1. It is a test for Sod1 NOT DM so label it correctly. 2. Sod1 has not been proven to cause DM instead just the opposite. In their original test group BEFORE running to the market with a test to earn them bouko bucks one bitch tested clear clear but on necropsy was shown to have DM. This has been true of several others since then. In addition there are AAs who do not have the disease. This is BAD money driven science. If they had been true to the scientific method the very first bitch would have told them they had the wrong hypothesis and needed to go back to the drawing board.

Also do your homework about ALS which is where Coates claims she came up with this hypothesis. Less than 10% of ALS is thought to be inherited. Less than 1%  of that 10% is hypothosized (i.e. not proven) to involve the sod1 gene. So for her to annouce she found the cause(& therefore the cure) for ALS was just plain cruelty. Also go out and look at the OFA db and look at all the breeds with very high levels of AAs which are breeds which have never displayed a disease resembling DM. 

What they should have done instead of chasing the midas gold at the end of the dna rainbow is do the basic work on this disease. First GSD DM -historically notated as being only found in GSDs and crosses with - how does it differ from the disease now called DM in corgies & boxers - and yes there are significant differences in expression and symptoms. So b4 looking for a gene or allele gee golly gee might it not have been a good idea to determine FIRST if we are dealing with one disease, two or three. And for that matter those of us in the breed have long understood with DM there are two types - old & slow and young & fast refering to age of onset and progression of the diease. Clemmon's protocol worked with old & slow (I have personal experience with that) but not the young & fast so that again raises the question - just with classic GSD DM is it one disease with two different variants or is it two separate diseases. We have always been handicapped in two ways -1.tests like a contrasted MRI might show another reason for symptoms but if it is DM will cause a worsening of them so the test is often not done and 2 it is a diagnosis of elimination until necropsy and most people will not pay for that. This also makes is easy for the sod1 fraud to continue because most people will not insist or pay for a necropsy especially if they have that little piece of paper saying CC. My very experienced vet has a client with a boxer with all the symptoms of their disease now called dm but the dog tested CC for sod1 so the owner will not believe the dog has the disease and will not treat it appropriately. That is just one side effect of the bad science.

So please b4 you beat all others over the head with the stick of correctness consider that you too might have some failings.

Re the Willis book

I was going to say 1976 but all the copies for sale said 1977 so I figured it was just my graying brain but if I remember correctly the US edition on both books came out about a year after the UK edition which would explain this apparent conundrum. Yes it is Manhattan on the 2nd 1991 book.

Are you in the UK? Do you have copies of the old annuals the "red book" the GSD League put out  that included among other things a yearly report from Willis on things like hip production records of various sires? I have a few. Do they ever come up for sale over there?

@TIG: Les resides in New Zealand (hence the Kiwi). (At least I think he's still in NZ).
I, however, am in the UK; and the answers to your questions are :
1 - No, I don't have the League's Red Book(s) unfortunately, or if I do it is only the one odd year and I can't get at it at the moment to check it. Never been a League member, though consider joining from time to time ! This is not something I have seen come up at boot sales and the like; but I can ask around and see if I can track any down ...
(Les might have some, I get the impression he's a bit of a pack-rat like me with GSD stuff).
2 - Occasionally someone dies and leaves a collected Library, and occasionally some or all of that comes on the market. Not aware of anybody at the moment.Will keep in mind.
3 - Yes, Malcolm used to regularly put out those tables (one of the things I have sorely missed since he died), not just in League Handbooks but in the national magazine and elsewhere. If you ever want to PM me a year or years you are particularly interested in I will see if I can find it and photocopy it for you via e-mail.

Linda.

TIG, this is my copy -- The German Shepherd Dog Its History, Development and Genetics published 1977 by Arco Publishing Co  Printed in Great Britian  The cover color is purple/pink behind the printed head of a GSD.

Is this the best version of this book?

TIG

English written official reports are very difficult for me to read ( obviously because of my lack of English ) -
I tried to understand http://www.canine-epilepsy.net/cerc.html  .

Did they ask for samples of affected dogs and their immediate family members or did they use ANY samples? That´s a major difference...

Susie, that research asked initially for "affected" dogs (all breeds), ie those with presenting seizures. And for close relatives (siblings,parents etc). How much that made up the total of over 10 thousand dogs studied isn't clear at first glance, particularly if you understand, as I do, that such studies should ALSO look at a number of UNaffected dogs as a 'control', (which is what we are always asked to provide among GSDs these days for any such projects). Or maybe they thought non-fitting relatives was enough ? I am assuming research methods Stateside are similar to those in the UK ?

TIG, any thoughts or info which could clarify for us ?