Post by Die Fledermaus on May 21, 2007 13:47:52 GMT -4
I posted this comment on the AGS site:
> A few months ago I asked about the likelihood of gerbils appearing
> with long hair, like the GP I have, Lester, who has such long hair he
> looks like a dust mop! But he grooms himself well. As for the gerbs,
> it was basically conceded many years would pass before such hair
> lengths would apear, although there has been bred in France a fancy
> mouse with rosettes!
This response pasted below followed, and it is VERY informative!
. . . . . . . . . .
When gerbils will have the long hair gene has to do with the spontaneous
mutation rate of the gene effecting the hair follicle.
There are so many gene mutations in so many species. You can expect to
see the mutations in the other species show up in gerbils at some point,
it all has to do with the likelihood of that particular gene to mutate-
it's spontaneous mutation rate. As far as I know, the spontaneous
mutation rate isn't known for gerbils but the spontaneous mutation rate
of mice and humans is known. Of course, some genes are more likely to
mutate than others so an "average" instance of mutation isn't the best
thing to consider when trying to predict when a certain mutation is
likely to appear.
For instance, the "a" mutation probably has a lower spontaneous mutation
rate than sex-linked yellow. This is evidenced by gerbils and other
species, the black mutation is usually one of the first mutations seen
while yellow isn't (and still isn't seen in many species). The albino
"c" mutation I would also think has a lower spontaneous mutation rate
because it is seen in many different species, even though it hasn't
appeared in gerbils yet.
As hobbyists considering mutations, we usually only consider forward
mutations. For example, two AA parents have an Aa pup. The mutation of
"A" to "a" is a forward mutation- it is a mutation of the
wild-type/normal gene to something else. What hobbyists don't tend to
consider are reverse mutations. A reverse mutation is when you have two
aa parents and they have an Aa pup. The mutation of "a" to "A" is a
reverse mutation- a reversion of a mutation back to wild-type/normal.
Researchers studying five color loci in mice documented that those
particular reverse mutations were four times more likely to occur than
forward mutations.
I have been very fortunate as a hamster breeder and have actually
experienced two mutations in my hamstery. The first one I had was a
reverse mutation- though it was not a full reverse mutation. In gerbil
terms, I had the "cb" gene mutate to a "ch" gene. I also had a forward
mutation of a recessive pattern gene. I had the "Rd" gene mutate to a
"rd" gene. I wasn't fortunate enough to have any "new" mutations
though- isn't that we all hope for?!
Most mutations are recessive and thus not discovered without
in-breeding/ line-breeding. Here's a fictional example, I have two "KK"
animals and there's a forward mutation creating one "Kk" offspring- the
first "k" mutation. I can breed that "Kk" animal to any other one and
still never know it had a mutation because the only other animals I
could breed it to are all "KK". It would have offspring of 50% "KK" and
50% "Kk". If it were bred back to its offspring or if its offspring
were bred together, by the third generation the mutation could appear.
If the animals were never line-bred and always out-crossed, the mutation
would remain undiscovered until it were bred to another animal that also
had the mutation occur in itself or its lineage or the gene would be
unknowingly lost just due to the odds of breeder selection.
(Before any debate starts- I'm not suggesting that everyone start
line-breeding in the search for undiscovered genes.)
I have been interested in the extreme mottled modifying gene. I believe
this to be a complex set of recessive modifiers. What I think is
interesting is that it was discovered in the US and the UK
independently. I've thought about this a bit more and know that the US
lines are all traced back to a pet store gerbil. This has peaked my
curiosity much more. It is known that commercial breeders do import
animals from other countries. There is a chance that there's a
commercial breeder in another country that had the original modifier
mutation and in the end, their gerbils or subsequent generations
appeared in the US and the UK pet markets. This would explain why the
extreme mottled mutation occurred at the same time in the UK and the US
and seemingly independently. Without any scientist being interested in
it and comparing the genetic coding between the two, it's only a
hypothesis. One thing that disproves the "same origin" thought is the
problems being observed in the UK high whites that has not been
witnessed here. This could just be due to different lines and breeding
practices, or it may be different modifiers altogether- just with
similar appearing results.
I've really gotten a bit off the topic from the long hair mutation. The
long hair mutation is a fairly common one and could be expected to
appear in gerbils at some point (it was just discovered in rats!). Of
course, through selection, breeders could select for longer coats as
they do for longer tail tufts. Even if the coat length was increased a
bit through this selection, it would never be a true mutation and would
not breed true, nor reach the lengths expected with the "true" mutation.
Of course, other fur mutations may appear before the long hair- rex,
satin, the rosettes Tom mentioned, wavy- these are all seperate
mutations that effect the way the hair follicle manufactures each hair.
One more side note on genes while I'm one the topic. The "e" mutation in gerbils isn't a true "ee" mutation. A true "ee" mutation will be a self mutation, not an agouti, due to the way the "e" mutation works- or malfunctions rather.
-Janice
> A few months ago I asked about the likelihood of gerbils appearing
> with long hair, like the GP I have, Lester, who has such long hair he
> looks like a dust mop! But he grooms himself well. As for the gerbs,
> it was basically conceded many years would pass before such hair
> lengths would apear, although there has been bred in France a fancy
> mouse with rosettes!
This response pasted below followed, and it is VERY informative!
. . . . . . . . . .
When gerbils will have the long hair gene has to do with the spontaneous
mutation rate of the gene effecting the hair follicle.
There are so many gene mutations in so many species. You can expect to
see the mutations in the other species show up in gerbils at some point,
it all has to do with the likelihood of that particular gene to mutate-
it's spontaneous mutation rate. As far as I know, the spontaneous
mutation rate isn't known for gerbils but the spontaneous mutation rate
of mice and humans is known. Of course, some genes are more likely to
mutate than others so an "average" instance of mutation isn't the best
thing to consider when trying to predict when a certain mutation is
likely to appear.
For instance, the "a" mutation probably has a lower spontaneous mutation
rate than sex-linked yellow. This is evidenced by gerbils and other
species, the black mutation is usually one of the first mutations seen
while yellow isn't (and still isn't seen in many species). The albino
"c" mutation I would also think has a lower spontaneous mutation rate
because it is seen in many different species, even though it hasn't
appeared in gerbils yet.
As hobbyists considering mutations, we usually only consider forward
mutations. For example, two AA parents have an Aa pup. The mutation of
"A" to "a" is a forward mutation- it is a mutation of the
wild-type/normal gene to something else. What hobbyists don't tend to
consider are reverse mutations. A reverse mutation is when you have two
aa parents and they have an Aa pup. The mutation of "a" to "A" is a
reverse mutation- a reversion of a mutation back to wild-type/normal.
Researchers studying five color loci in mice documented that those
particular reverse mutations were four times more likely to occur than
forward mutations.
I have been very fortunate as a hamster breeder and have actually
experienced two mutations in my hamstery. The first one I had was a
reverse mutation- though it was not a full reverse mutation. In gerbil
terms, I had the "cb" gene mutate to a "ch" gene. I also had a forward
mutation of a recessive pattern gene. I had the "Rd" gene mutate to a
"rd" gene. I wasn't fortunate enough to have any "new" mutations
though- isn't that we all hope for?!
Most mutations are recessive and thus not discovered without
in-breeding/ line-breeding. Here's a fictional example, I have two "KK"
animals and there's a forward mutation creating one "Kk" offspring- the
first "k" mutation. I can breed that "Kk" animal to any other one and
still never know it had a mutation because the only other animals I
could breed it to are all "KK". It would have offspring of 50% "KK" and
50% "Kk". If it were bred back to its offspring or if its offspring
were bred together, by the third generation the mutation could appear.
If the animals were never line-bred and always out-crossed, the mutation
would remain undiscovered until it were bred to another animal that also
had the mutation occur in itself or its lineage or the gene would be
unknowingly lost just due to the odds of breeder selection.
(Before any debate starts- I'm not suggesting that everyone start
line-breeding in the search for undiscovered genes.)
I have been interested in the extreme mottled modifying gene. I believe
this to be a complex set of recessive modifiers. What I think is
interesting is that it was discovered in the US and the UK
independently. I've thought about this a bit more and know that the US
lines are all traced back to a pet store gerbil. This has peaked my
curiosity much more. It is known that commercial breeders do import
animals from other countries. There is a chance that there's a
commercial breeder in another country that had the original modifier
mutation and in the end, their gerbils or subsequent generations
appeared in the US and the UK pet markets. This would explain why the
extreme mottled mutation occurred at the same time in the UK and the US
and seemingly independently. Without any scientist being interested in
it and comparing the genetic coding between the two, it's only a
hypothesis. One thing that disproves the "same origin" thought is the
problems being observed in the UK high whites that has not been
witnessed here. This could just be due to different lines and breeding
practices, or it may be different modifiers altogether- just with
similar appearing results.
I've really gotten a bit off the topic from the long hair mutation. The
long hair mutation is a fairly common one and could be expected to
appear in gerbils at some point (it was just discovered in rats!). Of
course, through selection, breeders could select for longer coats as
they do for longer tail tufts. Even if the coat length was increased a
bit through this selection, it would never be a true mutation and would
not breed true, nor reach the lengths expected with the "true" mutation.
Of course, other fur mutations may appear before the long hair- rex,
satin, the rosettes Tom mentioned, wavy- these are all seperate
mutations that effect the way the hair follicle manufactures each hair.
One more side note on genes while I'm one the topic. The "e" mutation in gerbils isn't a true "ee" mutation. A true "ee" mutation will be a self mutation, not an agouti, due to the way the "e" mutation works- or malfunctions rather.
-Janice