No I can't top this one!

[xfactor fan]

Any one have a link to photos of these horses? I'd like to see the dilutes.

The usual way to get a dilute is for the cream gene to be present.

Chestnut + Cream = Palomino
Bay + Cream = Bay.

Two copies of the Cream gene:


Chestnut + Cream + Cream = Cremello
Bay + Cream + Cream = Perlino


However there is a new gene that has been identified, a recessive dilute that is being called Pearl. In order to get a Palomino or Buckskin, two copies of Pearl need to be present.

Just looking at the patterns of color, it looks like a recessive not a dominant, and with the degree of inbreeding, any recessives are likely to show up.


Some info links:


http://www.leehorseandcattleco.net/Mate ... epage.html
http://www.newdilutions.com/
http://bridlepath.wordpress.com/2006/10 ... -genetics/

[Lucy]

Any one have a link to photos of these horses? I'd like to see the dilutes.

Photos may prove difficult to find....these horses were bred forty years ago, and the few that raced weren't terribly good at it.

The first spontaneous 'dun', Miss Perrin, was foaled in 1948, and only produced one 'dun' foal, Odd Link, in 1957. Both of these were bred by a Rush Montgomery of Texas.

Odd Link produced three foals that were registered as 'Light bay'- Yellow Cat (1963), Thru Links (1966), and Miss Jose (1967) - but none of those horses produced Thoroughbred Foals. Of her foals that did breed on, it does not seem that any produced odd-colored foals - though by the time they were in production, the Jockey Club was no longer using color designations such as 'light bay' and 'dun', so it's hard to tell for sure.

The female family descending from Litte-Cote is now complete in the database, if you'd like to check it out.

[llbean]

llbean,

I prob. should have specified she was talking about humans!
But you figured that out----
I can ask her for more details. My doctor friend said she saw a hermaphrodite child with both sex organs clearly present.
This was a product of first cousins who were also products of 1st cousins marrying. One side or both, I'm not sure. This also happened in more ditant generations. Other ancestors in the family also had male/femal genitals present at birth.
Then our crabcakes benedict arrived, so we changed the subject!!!

Thanks Toccet,

I think I remember that Hermaproditism can be caused by a Recessive Gene Variant getting doubled; and if it can, then inbreeding to a Known Carrier (aka in this case having two 1st cousins produce offspring with each other when at least one of their Shared Ancestors produced a Hermaphodite) would in the absence of other evidence increase one's calculation of the risk of getting such a child (how much it would increase it would depend of course on how far back the carrier was).

Of course, if two 1st cousins had their Closest Ancestor Known to have been a Carrier (let's say) 3 generations back and there was significant inbreeding to the offspring and descendants of that Carrier without it leading to the disorder, one would GREATLY downgrade the increased risk.

In other words, you can't just look at how far back the shared Carrier was but also how inbreeding to the shared carrier through the relevant sources has fared (its just about exactly like how if you wanted to inbreed to Mr Prospector through Johannessburg, you'd look at how inbreeding to Mr Prospector through Johannessburg has done in the past).

Anyway, I'm quite interested in the subject of inbreeding and any more info would be welcomed.

-llbean

[llbean]

That makes me wonder about the amish in that they do have alot of inbreeding related defects and it seems that many are degenerative. I would think that in itself would "breed out" but apperantly only after a very long period of time.

Hi Kezeli,

It can indeed take a while but the good thing is that once you've got them out they're gone for good in the absence of outside genes getting introduced into the Gene Pool (not at all likely in the case of the Amish).

Also, I've never really seen figures on the % of Birth Defects for the Amish but I strongly suspect its significantly lower than that reported for Pakistanis in England.

Finally, I tend to think extra Amish Birth Defects (assuming there are extra overall) are caused more by their avoidance of travel relative to others living in the modern day as opposed to the relatively limited number of Amish and their practice of in-group marriage (when people don't move around much for generations, relationships build up in particular geographic areas and probably the Amish marry assortively by Geography even once we take into account the strong in-group preference).

-llbean

[camohn]

Miss Chain Link was in fact owned by the family that has her granddaughter now. They bought her/did NOT breed her! They were too afraid to breed her back to a TB for ANY inbreeding and Miss CL was bred to WBs. She is reported to have been/produced quite sound and durable though a bit stubborn. I am told she looked like a dunskin (pale bay or buckskin w/ dun traits). I don't know if they have pics available from ages ago. Her offspring were not dilutes.
There are a lot of Amish up here. The most common "defect" I see is a high % of dwarfism. A lot of the Amish here take bus trips to Ohio to meet Amish/find spouses from out of the area. I am bummed as my Amish farrier (who was very good and very cheap) has moved to the Adirondacks in NY.

[Vindicated]

Why?

Only question I could think to ask is why?

The thought has crossed my mind to breed our stakes mare to a stallion by her grand sire-but I always hit myself and go "duh"