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HorseAdvice.com » Diseases of Horses » Colic, Diarrhea, GI Tract » Colic in Horses » Overo Lethal White Foal SynDrOme: Equine Aganglionic Megacolon » |
Discussion on Lethal white in Tobianos? | |
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Member: Pirie |
Posted on Friday, Oct 11, 2002 - 7:51 pm: Hi Dr O,I have been reading around this topic for a while but I'm finding it difficult to get to the reference you site where 10% of Tobianos were found to have the OLWS gene. Could you possibly give me a link to this paper? I am wondering how the researchers decided what colour the horse was before entering it in the study as many coloured horses are registered incorrectly. I am also curious as to the population of horses they looked at and how many were in the study. I also have a rather worried friend who is a tobiano warmblood breeder (Trakehner) and they are wondering whether Tobiano horses should also be checked for OLWS, hoping you can help, best wishes, Michelle. P.S. I don't know if you remember my foal who got Botulism? She is doing just fine and went with her Mum to the grading where Mum got into the Main stud book and the foal got lots of compliments. |
Moderator: DrO |
Posted on Saturday, Oct 12, 2002 - 9:48 am: Hello DrD,We are in the mountains this weekend so I am away from my library, but try this reference: Am J Vet Res 2001 Jan;62(1):97-103 Incidence of the endothelin receptor B mutation that causes lethal white foal synDrOme in white-patterned horses. Santschi EM, Vrotsos PD, Purdy AK, Mickelson JR. The summary states the incidence at less than 21% in Tobianos so I am not sure this is the one. I placed the summary in the article but hope you might have access to the full article. Did you see the summary this month that found a case in a registered QH foal? It is in the article. Congrats on the foal and am delighted to hear the outcome. DrO |
Member: Pirie |
Posted on Saturday, Oct 12, 2002 - 4:21 pm: Hi Dr O,thanks for the reference. I have traced it as far as I can but the site sadly won't let me see the full text version without subscribing to the journal. I am suspicious that many of the horses in these studies are not the colour they are described to be. There is an article found by this site's search engine (published 2002) that claims to have an overo white foal who is heterozygous for the mutated gene. Both his parents are shown and both are described as being overos. However his sire looks to be a Sabino not an overo. Pointed tops on his back socks is a dead giveaway.(The white is in an upwards pointing V where the sock finishes) and his dam also appears to express the sabino gene as well as the overo gene. Her extensive flecking and roaning is part of the expression of the sabino gene not the overo. This would make the foal a sabino white which is a well recognised phenomenon rather than a surviving white overo. It just doesn't seem right to me that two genes that I believe to be in different parts of the equine genome (overo and tobiano) can both be linked to the same lethal mutation? Hhmmmm? Perhaps I am mistaken in my belief that these genes are located in different places? Would it be possible to read the full text versions of the "incidence" papers to find out how the researchers decided on the colour of the horses they were studying? I also saw the lethal white foal being born to a registered QH mare paper. Again I was only able to get the abstract. There is another paper saying that horses from breeds that do not exhibit spotted patterns also do not exhibit the lethal white mutation. It is also possible for a horse to be genetically overo or tobiano or sabino while being phenotypically solid coloured. This is termed "minimally expressed." You probably already know this! Putting all this together I wonder if the mare is a minimally expressed overo. Since the mutated gene is very closely linked to the overo gene and some authors have suggested that the mutation itself causes the overo coat pattern in the heterozygous state this seems to be the most likely explanation. That the lethal mutation is expressed as white spotting in the heterozygous state certainly seems possible since the mutation interferes with the development of melanocytes as well as the autonomic innervation of the large gut. Interestingly this seems to be a common linkage in many mammals but I guess since it is so early in the foetal development (the neural crest tissue is affected) I suppose this is not too surprising. Phew! Sorry for going on. This is a subject that intrigues me. Best wishes, Michelle. |