The origins of satins in the US come from radiation experiments decades ago; I have been told that in the UK the satins have a different origin, but I don't know what that is. US satins have a tendency to have health problems because of damage to the genes that regulate digestion, blood chemistry, and immune system weaknesses on top of those. It can be hard in some parts of the US to find healthy satins if you want to breed them. It took me several years with lots of heartbreaking problems before I found a good buck, but once I found him, I was able to eliminate most of the problems.
History of Satin Mice
I know satin is recessive, the genetics I understand. But I found out that the first Satin mouse was bred by Tony Cooke in 1973... and that's all I know. Does anyone know more about the history and background of satin mice? I have a couple I just got, and I'm interested to know more of how they came about.
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Well, that explains a couple things... I have one sub-adult satin that's smaller than my others, and one baby satin that's smaller than his littermates... The satin is why they're small?
It very well could be because of that. Many of my satins were about 25% smaller than my standard coated meeces in the first few years after I finally stared my line, but I out-crossed to larger standard meeces and now my fawn satins are among the largest meeces I have. I used to have small litters, and that is no longer the case. I used to have congenitally weak babies that would cease growing at about 2-3 weeks, look prematurely aged, and die. I rarely have that anymore; that's something that can happen in any litter of any type of mouse, especially if the parents are too young or too old. I think that meeces of the proper breeding age (3-8mo. old) provide better quality genes. One of the more disturbing things to see was fuzzies of two to three weeks of age ranging around the tank, trying to find something to eat that would satisfy the hunger, as they were unable to digest what they ate. Now I know what that is, and what to do about it, but fortunately, don't often have that problem anymore.
Tony Cooke was a industrial chemist, and had access to laboratories etc world wide, setting up industrial plants all over the world. He found the first satin in a lab and brought it home to petersfield. The mouse was very sick and had to live on a windowsill at his home untill it got better. It eventually mated some PEWS and this led to the production of the black eyed golds and silver ( rejected by the nmc), and eventually all the satins in the uk.
I knew Tony well, even through the cavy fancy, a pioneer, have not seen him for a number of years, hope he is well along with jill his wife .
I knew Tony well, even through the cavy fancy, a pioneer, have not seen him for a number of years, hope he is well along with jill his wife .
I had been told (by a US fancier) that Tony was no longer with us. His work has proven invaluable to me and I am ever thankful for his contribution to the modern fancy as we know it.
Satins in the US are not any more sick as a whole than any other mice. Only poorly-bred satins are, yet that is true for poorly-bred mice of any coat type.
Satins in the US are not any more sick as a whole than any other mice. Only poorly-bred satins are, yet that is true for poorly-bred mice of any coat type.
I didnt say he was still around. I said I havent seen him for a number of years and hope he is well.
Well, my satin buck is too young to breed, but I just put my satin doe in with a standard male. I'll probably cross both my satin doe and one or more of her daughters with the buck when the babies are ready to breed.
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