🚀 go-pugleaf

On Thu, 31 May 2001 14:23:15 GMT, ogier <ogier@optushome.com.au> wrote:

>Let me see if I understand this part right:

Oh dear.  Here we go ;-)

>The presence of the heterozygous Pearl gene (Pepe) is only
>visible with the presence of the homozygous mink gene (mm) and
>the heterozygous agouti gene (Aa).

Not quite.  The heterozygous Pepe can only manifest itself on a homozygous
recessive mink (mm) gene.  That's the only time it can show up.  If an Agouti
gene is involved, it must be Aa heterozygous.

>The only references I've seen of the pearl gene link it
>to mink, but not Agouti. Are you saying that it cannot be 
>shown with the presence of homozygous agouti (AA)?

That was what Robinson observed in his results. I am currently mating several
Cinnamon pearl does with an Agouti buck to determine this. (one reason why I
prefer berkshires, "cardigans" and selfs to hoods, there is much more colour and
therefore colour variation apparent.)  

Wouldn't mind having an Irish ot two, but I'm already over taxed keeping the
pets I have.  I don't want to become too objective and lose the attachment to my
babies.  That defeats the purpose of both the Society and the show standards
which I hope will remain in favour of the ratties' health, temperament and
well-being, above all else.
/--end rant

If there is a heterozygous Aa, then the Pepe can show up so long as the rat also
has the homozygous recessive mm.

So, homozygous dominant agouti rats, AA can "carry" a heterozygous Pepe, without
it showing.  Rats of other colours except those influenced by the homozygous
recessive mink, can also (theoretically) carry the Pepe heterozygote.

>Regarding your notation of the pearl gene, you referenced that
>PePe is lethal and Pepe shows pearling on mink (mm) rats.

Let me check Robinson's paper again, but yes, that is what was studied and
notated.  The results of my breeding Cinnamon pearl with Cinnamon pearl and
losing 100% of the litter would support that.  

Pearl is dominant to Mink, and the Pearl phenotype can only manifest on a mink
background.  The hassle with breeding dove to dove, is the great variation in
the effects of the pearl... it can show up as proper tips on a white or very
pale coat, or can be so profuse in its 'tipping' as to confuse with other
phenotypes.

Hence I bred a heavily Pearled buck to an apparently Dove doe, only to lose the
entire litter because I hadn't examined her coat closely enough.

>I have found many times that the pearl gene is referenced as PePe
>meaning it doesn't show, Pepe shows with mink, and pepe is lethal.

I'd be curious to hear the sources for that, as it is the other way round to
Robinson's observations.  Mink is recessive, and can only affect the phenotype
as a recessive homozygote, mm.  Pearl is dominant, like Agouti and three of the
four rex genes.  Pepe will show on mink, and also if there's a heterozygous
agouti, (AammPepe).  The dominant homozygote PePe is lethal.

>This went against my conception of the workings of the pearl gene
>until I read a passage which went something like this:
>
>The pearl gene is recessive, except in the presence of mink
>where it becomes dominant, if the homozygous recessive form of 
>the pearl gene is present, this is lethal and causes reabsorption
>of the fetus within the womb.

Again, I'd be interested to see those studies.  Robinson observes that aa
'Black' rats can apparently carry the Pepe heterozygote, which will become
apparent in the F1 or F2 generations when bred back to mink rats.

>On tonights internet research alone, I have seen Pearl gene described
>both ways, so regardless of the case used, as long as the effect is
>understood, it doesn't matter. But for some reason I still like the
>description used above as this describes the dependence of mink, and
>why pearl is not seen on non-mink rats.

Yes, the pearl phenotype is definitely dependent upon "a mink background" as
Robinson puts it.

>The last thing I'd like to leave with you is some observations of
>my own breeding. One of my first rats was a silvered black male.

Silvering appears to be quite different from Pearl.  The silvering gene came
from the Wistar labs and was studied by Castle and King in 1945.  Silver
expresses its affects in a homozygous recessive form (ss) and was found to be
linked to the Brown (Chocolate) b gene.

The silvering becomes more and more apparent with successive moults, according
to King and Castle.

>(aaMM) His coat was black, with the exception of the guard hairs 
>being silver (white). This boy was bred to a mink girl (aamm),
>producing black babies which carried mink (aaMm). None of these
>offspring show the same silvering as the sire, but instead have 
>hairs with a white base and black tips with black guard hairs.

This is where having the pedigrees of the rats comes in so handy.  What are the
odds of your silvered black boy being aaMmss?  

Another possibility is that the black and white effect you describe is caused by
the "roan" marking gene.

If there is the possibility that your rats carry the silvering gene, ss.  Black
is the best bet to bring it out, unless we should discover the Brown (Chocolate)
bb recessive homozygote in Australian R. douglasii any time soon.  Silvering of
Mink rats is much harder to pick and the recessive silvering homozygote is more
closely linked to the Chocolate and Black phenotypes than Mink is.

If the colouring fades during the rats' maturation and is quite a bit lighter
after 12 months than appeared at, say, 2 months at weaning, then it might be
worth considering a careful line breed to see if these rats aren't actually the
European "roan" H^re.

The difficulty with that is that the H^re homozygote causes infertility in the
bucks, so again, breeding needs to be very carefully planned and the pedigrees
of the animals taken into consideration.  You knew it couldn't be simple, didn't
you?  ;-)

>The thing which has me thinking is that the Pearl gene causes
>an effect similar to what I see on these black rats, which all
>carry mink. I am theorizing that the presence of a Pearl gene
>is causing this with the carried mink in presence, but I cannot
>find any research to support this theory, or find any coinciding
>theories.

Heh, neither have I.  The Pepe gene is so closely linked to the mink mm
homozygote that it cannot express itself otherwise.  My observations of a dozen
of my rats bred for the pearl gene shows that it is a combination which must be
carefully planned, unless one is prepared to allow for 25% to 50% or even 100%
loss of the litters due to the lethal PePe homozygote.  

The silvering in your black rats is, according to the papers I presently have,
accounted for by either the ss Silver recessive homozygote or, much less likely,
the H 'restricted' gene, which causes some 'roaning', but in homozygous H^reH^re
results in the bucks becoming infertile. 

I've gone back through my records and pedigrees and found that I can account for
most of the "lost litters" as being due to linebreeding for the Pearl phenotype,
and ending up with the PePe dominant homozygote which is, as I now know, lethal.
In five cases I was successful.  Too successful.

This is a great shame, since golden ginger ratties with their gorgeous colour, a
gentle and friendly temperament make great pets, not to mention show animals.
Still, now that I'm aware of the lethal PePe homozygote, I can plan my breeding
and hopefully avoid the homozygous dominant PePe.  

That can only mean that I end up with a 50/50 litter of Cinnamon and Cinnamon
pearl, both gorgeous colours, or 50/50 Mink and Pearl.  Again, they're both very
attractive and showable colours.....  now we get down to the pattern
inheritance.  *grin*.  A whole new kettle of fish.

Thanks Oggie, I hope this has made some sense.

Cheers, Ana