# Poodle Genetic Diversity Profiles from UC Davis: Results and Discussion



## CharismaticMillie (Jun 16, 2010)

This VGL report is an example of how COI and actual genetic diversity are not necessarily directly correlated. This puppy bitch has a COI of 12.5 and is the result of a first cousin breeding. She is relatively outbred for a standard poodle with an IR of -.03. Her dam actually has a COI of +.09.


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## sophie anne (Feb 17, 2015)

CharismaticMillie said:


> This VGL report is an example of how COI and actual genetic diversity are not necessarily directly correlated. This puppy bitch has a COI of 12.5 and is the result of a first cousin breeding. She is relatively outbred for a standard poodle with an IR of -.03. Her dam actually has a COI of +.09.


So interesting!

Is there a way for me to easily calculate what Ari's COI is? It would be interesting to have that alongside her VGL report. I can't seem to figure out how to do it on the poodledata website, perhaps because I don't have permissions as a "breeder".


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## ArreauStandardPoodle (Sep 1, 2009)

We tested 6 or our eight puppies to help decide which pups to keep to breed on. If I can get my other computer to cooperate I will post at least some of the results. The variance in the results of all the reports to pups born to the same two parents is astounding! Our keeper girl Krystle has phenomenal diversity, with good haplotypes ( 1001/1005) an IR of -0.19% and only six homozygous alleles. If this link works, you can view the results of all six pups if you scroll down to the post made by Jessica Zehavi. We have also kept Joel for our breeding program because though he carries 1007, which we are hoping to work away from, he also carries 1004, which along with 1005 is thought to be protective.

https://www.facebook.com/groups/720587391398080/


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## peppersb (Jun 5, 2011)

I had Sam done. See below.

As I just mentioned in the In Breeding thread, the following presentation is fabulous:
Genetic Diversity Test for Standard Poodles - Poodles de Grenier

It explains the new diversity test and how it is used in making breeding decisions.


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## Viking Queen (Nov 12, 2014)

I think this must all be quite fascinating......if you undersand it all. I read it and my eyes cross and roll back in my head trying to understand it. I always thought I was a fairly bright person, but......

I truly hope these advances are able to help those of you who are responsible breeders accomplish their goals.

Now I think I have to go study up on this so I don't feel so inadequate. Yikes!

Viking Queen


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## lily cd re (Jul 23, 2012)

VQ here is a short "genetics lesson" to help make sense of what is being discussed. Every animal (all species with exception of some insects) has pairs of chromosomes in its body cells. These pairs, called homologues are alike in size and shape and have gene loci (genes) for the same genetic traits in matching locations. One member of each pair is inherited from each parent. In other words each sperm and each egg have one of each of these types of chromosomes and fertilization restores the states of having chromosome pairs. 

The actual specific information encoded at a locus on a chromosome may match or be somewhat different from the corresponding locus on the homologous chromosome. For instance if a person has type AB blood then the loci for blood type on that person's pair of chromosomes is different. They are heterozygous for blood type meaning one chromosome has a gene that encodes an A protein and the homologue has a gene that encodes a B protein at that same locus.

Many genetic disorders are only expressed (visible or able to cause signs of illness) when an individual is homozygous (having two matching gene loci on homologous chromosomes, e.g. a person with type O blood who lacks the ability to make the A or the B protein on either chromosome). Examples of human disorders that generally require the presence of two dysfunctional genes at a single locus include cystic fibrosis, Tay Sachs disease and sickle cell disease.

It is generally the case that being heterozygous reduces the expression of diseases with that pattern of inheritance (referred to as autosomal recessive). There are though some disorders that require an individual to only have one defective gene copy (autosomal dominant) as for example Huntington's disease. So the measure of heterozygosity being high is an indicator that the risk of those diseases that are only seen on homozygotes is lower.

Humans have a set of gene loci that encode proteins used for communication among the immune system and other body cells. It is called the HLA complex, with HLA standing for human leukocyte antigens. Dogs have a comparable system known as the DLA. HLA and for that matter DLA typing is the basis for matching organ donors and recipients. Because these antigens also allow communication by the immune system with itself and other tissues we recognize that certain combinations of HLA and DLA types are associated with elevated risks for things like autoimmune disorders and even the risk of developing rheumatic heart disease after a strep infection. Similar risks for autoimmune diseases also seem to correlate to a lack of genetic diversity in DLA proteins (genes). Also, knowing the profile of which DLA genes are present can give an indication of whether there are risks for certain disorders.

That may be more complicated than helpful, but I hope it helps at least a bit.


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## mamalion (Aug 8, 2014)

Genetic Diversity Test for Standard Poodles - Poodles de Grenier


Peppersb provided this link where a breeder, Natalie Tessier, I believe, does a wonderful job explaining the Davis testing. I have read her website several times over the last year or so. It pertains mostly to standards, but is good background knowledge for any one involved in poodles.

I am so happy to see this thread.


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## Pudellover (Sep 8, 2014)

If you register on poodledata you can input your dog and the pedigree and it will calculate the COI for you. It will take a couple weeks for it to process.


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## Theo'sMom (Mar 23, 2011)

Enjoying this thread very much. So, reading the slides on N Tessier's website and then the facebook discussion that Arreau links to, why would a poodle with a low IR be more prone to Addison's and a high IR be prone to SA. Doesn't that undermine the theory that more genetic diversity leads to greater health?


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## sophie anne (Feb 17, 2015)

Theo'sMom said:


> Enjoying this thread very much. So, reading the slides on N Tessier's website and then the facebook discussion that Arreau links to, why would a poodle with a low IR be more prone to Addison's and a high IR be prone to SA. Doesn't that undermine the theory that more genetic diversity leads to greater health?


For context, this is what I think Nathalie said that you're referring to:


> Because Addison's has been shown to be more common in dogs with lower IR while SA has been shown to be found in dogs with higher IR. So if dogs carry the 1007/2006 haplotype that has been associated with Addison's (can't say it causes it, but it's seen significantly more often in dogs with it) then you go with the higher IR till you can breed it out. For SA, which has the same relationship with the 1006/2004, you would go with lower IR instead. There are perfectly healthy dogs with these haplotypes, of course, but they are worth watching. Given a choice, I'd pick the dog without it, but if there's no choice, I'd go with the higher IR. I also like that Joel has the 1004/2002 which may be protective.


My take: (and I'm a geologist so *disclaimer* I may be very wrong! lol)

Here is the abstract of the study I believe N Tessier was referring to:
The effect of genetic bottlenecks and inbreeding on the incidence of two major autoimmune diseases in standard poodles, sebaceous adenitis and Addison's disease.

From the results section:


> Genetic diversity statistics based on genomic STR markers indicated that Standard Poodles from North America and Europe were closely related and reasonably diverse across the breed. However, genetic diversity statistics, internal relatedness, principal coordinate analysis, and DLA haplotype frequencies showed a marked imbalance with 30 % of the diversity in 70 % of the dogs. *Standard Poodles with SA and AD were strongly linked to this inbred population, with dogs suffering with SA being the most inbred.* No single strong association was found between STR defined DLA class I or II haplotypes and SA or AD in the breed as a whole, although certain haplotypes present in a minority of the population appeared to confer moderate degrees of risk or protection against either or both diseases. Dogs possessing minor DLA class I haplotypes were half as likely to develop SA or AD as dogs with common haplotypes.


Basically, the dogs with the "lower IR" that end up with Addisons still fall within the "inbred" 70% of the standard poodle population. So this doesn't undermine the theory that more genetic diversity leads to greater health, so much as suggest that there may be slightly different genetic factors driving each disease. Variations in the distribution of the causative alleles and haplotypes causing SA vs. AD could explain this...

For example (over-simplified of course)...
... if a very common stud many generations ago carried the mutation for AD, over many generations this could lead to a broad distribution across the whole spoo population of the genes for AD. Thus, AD would crop up most commonly in dogs with slightly lower, but still relatively inbred, IR values. This would be expected in a population that has undergone a bottleneck, of which the spoo population has seen a few. 

In contrast, if a less commonly used stud and/or a more recent stud carried and contributed the mutation for SA, the genes may not be evenly distributed across the population but would still be confined to certain lines (because they haven't had sufficient time to spread/there was no bottleneck). Dogs with higher IR values related to the stud with the SA mutation would be the ones that would be most likely to get all of the alleles necessary to express SA—the more outbred/the lower the IR, the more "diluted" the SA alleles would likely be, thus leading to a correlation between high IR and SA.

I'm not saying that either of those scenarios is what happened, just hypothesizing about how those results could be achieved.

I hope that makes sense. If it doesn't and/or I'm completely wrong, let me know! The only thing I like better than being right is being wrong and learning why! :act-up:


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## sophie anne (Feb 17, 2015)

oh, duh, the next paragraph of the above linked study says this:



> Ancestral genetic polymorphisms responsible for SA and AD entered Standard Poodles through separate lineages, AD earlier and SA later, and were increasingly fixed by a period of close linebreeding that was related to popular bloodlines from the mid-twentieth century.


The above scenarios I described are good, oversimplified explanations of what the much-more-qualified-than-I researchers think might've caused the relationship between very high IR and SA and lower IR and AD.

I'm a genius! Now if only I finished reading the article before posting the first bit... sigh.

:doh:

ETA: Thanks for asking that very interesting question Theo'sMom, I wondered the same thing when I read N Tessier's comment a few weeks ago.


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## CharismaticMillie (Jun 16, 2010)

Addison's is set in the breed, so a low IR is not enough to reduce the risk. The way I think of it is that you have to try to dilute it by introducing diversity from some of the genetic outliers.


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## spindledreams (Aug 7, 2012)

If your poodle is in Poodledata.org then look your girl up, on the 3 generation pedigree page look at the links at the bottom left hand corner and click on the Genetic information link and her COI will be on that page.  I spent hours clicking and using the back button on the site one day


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## sophie anne (Feb 17, 2015)

spindledreams said:


> If your poodle is in Poodledata.org then look your girl up, on the 3 generation pedigree page look at the links at the bottom left hand corner and click on the Genetic information link and her COI will be on that page.  I spent hours clicking and using the back button on the site one day


Yeah, she isn't on PoodleData nor are her siblings yet. I do not have the permissions to enter new dogs despite having an account.

Anybody know how to get full permissions on the database?


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## spindledreams (Aug 7, 2012)

*Got my tests back*

I had two dogs tested by UC Davis. Both had the Diversity Testing done and I got a few surprises. Color testing also revealed some surprises. 

My brown dog has a MASK of course since h is brown the mask is also brown and you can't see it but if he had turned Cafe' as predicted he would have still had a solid dark brown face. Sigh he also does carry cream so IF we use him for breeding we will have to pick the females carefully. 

Here are the UC Davis certificates and the SPD data Rebekah Shyre ran for me.

Phoenix is moderately inbred but is also very typical of the breed with only a few rare alleles. 








[/url]phin vgl cert by spindledreams, on Flickr[/IMG]

phin vgl by spindledreams, on Flickr


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## spindledreams (Aug 7, 2012)

*and this is for Windswept's I'm A Rocket Man*

There were a couple of surprises from his testing. While he is highly inbred (we suspected that) at the same time he is an UNUSUAL due to the number of rare alleles he carries and his location on the bell curve. 

My blue dog also carries recessive black! That was a surprise as it is considered a rarity. This form of black looks like the normal black but can pop up when breeding two brindles, sables, or phantoms. 

Here is his information:
apollo vgl cert by spindledreams, on Flickr

apollo vgl by spindledreams, on Flickr


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