🚀 go-pugleaf

Hi there,

Let me see if I understand this part right:
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).

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)?



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

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.

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.

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.


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.
(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.

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.


Cheers + good night,
Ogier.


Ananke wrote:
> 
> Hi all,
> 
> Whew, I had a feeling my first publishing would be about my rats, and would be
> in usenet forum.
> 
> But I thought it would be regarding disease in Australian rat colonies.
> 
> It seems fitting for it to appear here, in this developing aus.science
> newsgroup.  Please excuse my unfamiliarity with the publishing protocols.
> 
> But here goes:
> 
> The Presence and effects of the dominant Pearl gene in Australian Fancy rats.
> L "Ana" Farrall.
> 
> Background:
> 
> The show standards for Fancy rats in Australia has been under development for
> five years.  For the last two, they have been "stable", but the genetic
> information relating to some of the standardised phenotypes has been awaiting
> research.
> 
> There has, however, been variation in several colours which has caused them to
> be considered "guide standards".  These are Dove, Pearl, Cinnamon, and Topaz.
> 
> Materials and Results:
> 
> Rats from my own mischiefs, exhibiting phenotypes typical of standardised
> phenotypes in other countries, bred to assist development of Australian
> Exhibition standards in what is now referred to as Rattus douglasii, because of
> their distinct differences to the wild Norway or Brown rat.
> 
> Mink, aamm, and Dove, which is the expression of the Red eye gene (rr) on mink.
> (aammrr) having been bred for three and four generations to establish a good
> Dove colour for exhibition and Pearl rats, also for exhibition.
> 
> Lines of the highly irregular "topaz" which was theorised to possibly be a ruby
> eyed Cinnamon (A/-mmrr) or ruby eyed Agouti (A/-rr).
> 
> Cinnamon, Argente and Topaz rats which had been bred for four and five
> generations, to establish what the genotypes of Argente and Topaz are, and their
> possible relation to the Cinnamon A/-mm and Mink aamm genotypes.
> 
> In the fourth and fifth generations, five does bred to bucks for this purpose,
> appeared to spontaneously abort.  100% of the litters were lost.
> 
> Robinson identified definite links between the expression of the dominant Pe
> pearl gene in combination with homozygous recessive mink (aamm) and heterozygous
> Agouti Cinnamon (Aamm)
> 
>         He observed that Pepe caused two types of phenotype.  One, the Pearl of
> UK and Australian standards, which is a very pale, almost white hair base, with
> dark "tipping" of the hair.  The pearl Pepe was observed to produce a greatly
> varying phenotype, between a light dusting and a profusion of tipping heavy
> enough to imitate a "roan" colouration.
> 
>         The second he called "yellow pearl" as it had a similar tipping effect
> on the hair, but in combination with the golden or red banding of the hair,
> associated with the phenotype of a dominant agouti gene. This is the genotype
> now referred to as Cinnamon Pearl in show standards.
> 
>         Pearl is dominant to mink and hypostatic to other genes.  It can only be
> expressed in combination with homozygous mink genes.
> 
>         The Cinnamon pearl was observed only in heterozygous dominant agouti
> rats: AammPepe
> 
>         It was also documented that homozygous dominant PePe pearl is a lethal
> gene.
> 
> Discussion:
> 
> If "topaz" is the same genotype as the "lynx" or "lilac agouti", which was
> proposed because of the similarity in the phenotype, and the great variations in
> the phenotype, then the genotypes would be A/-ddbb and A/-ddbbrr.
> 
> If this were the case, then in breeds and line breeds for A/-dd and A/-bb
> colours, as well as chocolate aabb and blue aadd should result.  These genotypes
> have not been observed in Fancy rats in Australia.
> 
> Following comparison of my own breeding and the observation of great variation
> in the appearance of the "topaz", together with the unexpected loss of line bred
> litters, it appears that the "topaz" is actually the genotype A/-mmPepe which
> Robinson identified as the Agouti "version" of the pearl and mink.
> 
> Robinson also observed that all his Cinnamon Pearl rats were observed in
> heterozygous agouti genotypes, hence the homozygous agoutis could be carrying a
> heterozygous mink recessive Mm and a heterozygous Pearl dominant Pepe, without
> expressing either colour, it would appear as a normal Agouti phenotype.
> 
> Given the expression of pearl phenotype only in combination with homozygous mink
> and heterozygous agouti, it would be expected that line breeding to produce this
> phenotype should appear in 50% of the breedings of rats known to be carrying
> both an Aa agouti, mm mink, and Pepe pearl dominant.
> 
> This result, however, was not observed.
> 
> 100% of the 5 litters bred to exhibit the Pe gene in the aammPepe and A/-mmPepe
> phenotypes failed.  At the time, it was considered that a pathogen was likely to
> be responsible for the losses.  In particular the Sendai virus.
> 
> However, three of the does who lost litters had been bred before, and the only
> fatalities were 2 aged rats.  It is still possible that a pathogen contributed
> to the losses of litters, but normal Sendai symptoms would be for only does
> carrying their -first- litter to be at risk of spontaneous abortion.
> 
> It could be possible that some of the rats bred actually carried homozygous PePe
> genotypes, which weren't able to express the lethal effects of the gene, because
> of the lack of a homozygous mink mm to combine with or a heterozygous agouti Aa.
> 
> Robinson doesn't comment on this possibility, since he was breeding from rats of
> known genotype.
> 
> Now that the genotype of the formerly described "topaz" rats, with the great
> variation of phenotypical effect of the Pepe pearl gene causing the variations
> in seen in the "topaz" rats, it can be assumed that the "topaz" phenotype is
> actually Cinnamon pearl AammPepe.
> 
> Conclusions:
> 
> That great care should be taken in line breeding for Pearl phenotype rats, due
> to the lethal nature of the homozygous dominant genotype.
> 
> That further test matings of Cinnamon pearl and mink rats be undertaken to
> provide data for the supposition that there is a possibility of AA and Mm
> genotypes to successfully "carry" a homozygous dominant PePe.
> 
> That Australian Standards for the exhibition of Fancy Rats be ammended to list
> "topaz" as AammPepe Cinnamon Pearl, and "Argente" to be test bred to
> substantiate the probability that this phenotype is actually A/-rr, a red or
> ruby eye dilution of Agouti.
> 
> References:
> 
> Roy Robinson, "Mink and Pearl: New colour mutations in the norway rat."  in the
> Journal of Heredity 1994:85(2) pp 142, 143.
> 
> NFRS Standards of Excellence.  NFRS 1999.
> 
> History of Standards, Nick Mays, NFRS archivist, in conjunction with the
> Standards of Excellence.