Willy, because at the heart of the matter, no matter the species, we are all a result of some very similar biological process.
Today, however, I would like to state for the record that there is a grey area caused by our basic definitions in simple genetic models. When we define a blue mutation, we assume three things. 1) a mutation expressing no psittacin, 2) a mutation at the blue locus, and 3) a mutation recessive to the wildtype. When we define a parblue, we say that it is first and foremost 2) a mutation at the blue locus, which necessitates that 3) should hold, while being lenient towards 1) so that the bird is partly devoid of psittacin.
In the above lies the problem. Not with either model of the emerald mutation does all of the above hold true. We have definitions that are not perfect, limiting our scope for reasoning. What prevents us from saying, that when we fix the locus (say at the blue locus for context), that some alleles of that locus will be recessive, while others are dominant over the wildtype?
A case for emerald as a parblue or second blue:
For background, I refer to Peter Bergman's article on Yellow face budgerigar.
http://web.archive.org/web/200203252309 ... ace01.html
In this article, Peter highlights the fact that a blue mutation does not in fact remove psittacin, it prevents psittacin from being produced in the first place. This is a very important point, as the two are distinctly different. The first implies that psittacin has been produced, and then taken away.
"In a Green bird the gene for Green (designated B) codes for an enzyme which is responsible for the production of yellow pigment. The b1 allele is a mutant form of the B gene therefore it produces a slightly different version of the enzyme
. This (b1) enzyme is defective so no yellow pigment is produced and we have a Blue bird, but it is important to note that the enzyme is still there
Here I'd like to point out the following, for both the Wildtype (B/B), and the heterozygous blue (B/b1), the action of just one B gene is sufficient to produce enough enzymes/psittacin to make the bird appear like the wildtype. So the wildtype actually creates much more than is needed and saturates. This is why green/blue appears green and we call it recessive. We are very familiar with the blue mutation, and (b1/b1) deactivate the second gene and no psittacin is produced. However, at 3 weeks old when feathers start developing, some type of psittacin is already present in the wildtype. Recio refers to it as even psittacin. It is independent of age/hormonal action and is non-fluorescent. This is the specific type of psittacin/enzyme/protein I will be focusing on.
Now let's introduce a second allele of blue (or a parblue), called b2 (this is emerald, b2 is not the best code, but it's just an example). We go on the assumption that the genetic code of b2 acts very similarly to B (wildtype), but modifies the enzyme responsible for psittacin production (as any blue locus allele will do) in such a way that the later molecules/pigments synthesised have a fluorescent sensitive material (unknown which, but lets say phosphor) as part of the molecular structure (not to be confused with keratin based feather structure). This results in a less effective psittacin with the distinct possibility of being able to fluoresce. Here we could very well also reason that the enzyme is completely defective in terms of producing a yellow pigment, but that remains an afterthought.
On that basis, let's look at the first (easier) case, the (b2/b1) EmeraldBlue bird. Here b1 deactivates half the psittacin production power, and b2 results in a modified even psittacin visible in the first feathers, but with a new fluorescent component of the phosphor atoms present. It explains the phenotype of the heterozygous bird, and the (b2/b2) df Emerald produces even more of the modified fluorescent, but ineffective, psittacin. When UV light is applied, those P atoms will fluoresce, irrespective of whether they are located in the pigment, or in the keratin of the feather structure. The observer would see exactly the same thing irrespectively. Depending on exactly how effective this psittacin still is, we could deal with potential difficulty of sf/df emerald(blue) being very close in phenotype as well.
Recio can develop further how the presence of b2 could prevent hormonal changes expressed in parblues (bpr1 "turquoise" and bpr2 "indigo").
Now, let's explore the wildtype and split birds. We know that (B/b1) will produce half the enzymes responsible for psittacin, with b1 deactivating the other half. Yet, it is still sufficient for the wildtype phenotype. What will be the effect of green / emerald, (B/b2)? Here we have the B gene creating half the enzymes responsible for psittacin, and we know it is sufficient again to appear like the wildtype. But does b2, like b1, completely deactivate psittacin production? The answer is NO. b2 will, once again be responsible for ultimately the psittacin granules "loaded" with phosphor in deposited in the feather cortex. However, this time, unlike as with EmeraldBlue (b2/b1), these granules will be competing with psittacin granules of the gene B, which we know is extremely dominant. However, in this case, not completely
. The astute observer, potentially also somebody blessed with above average sensory awareness, could pick up underlying tones of that beautiful sheen differentiating the phenotype of blue and EmeraldBlue, even in the wildtype. The fact of the matter, and the crux of Peter's article is this, the (B/b1) removes half the enzymes for psittacin production and adds nothing with the other half of useless enzymes for b1 (recessive), while (B/b2) produces half the enzymes for psittacin production, plus another half of enzymes for a modified fluorescent psittacin, which should be distinctly different under UV, and could be seen with low penatrance in the wildtype (esp. under UV), thus dominant. b1 = recessive due to inactivation, b2 = dominant due to activation of something different.
I know of one counter argument to this, but not for today (from me).
In this example/model, once again, it is our definitions that have failed us, in that, at a specific locus, if one allele is recessive, then all alleles should be recessive. That is why we can not get over the bridge, and we won't until we modify our definitions.
It could be that what we actually see with b2 is 100% due to UV from the sun falling onto the bird, being absorbed by the fluorescent sensitive material and we are seeing photons released at a wavelength close to yellow. I.e. (b2/b2) is actually a blue bird with fully defective enzymes for creating yellow pigment, but reflecting UV light at a shifted frequency we can observe. Thus, we are dealing with something that has nothing to do with feather structure, nor anything to do with specifically yellow pigments (will require transparent pigment); the premise lies with the presence of a fluorescent material exposed to light. This is a very strong argument for a second type of blue. Consider a fluorescent tube, it works on the premise that UV light is created from Argon gas if I recall (so not normal light) and stimulates phosphor, which then fluoresces in the visual spectrum closer to yellow (i.e. a change in wavelength from UV). Thus we have a "UV to visual light converter" in phosphor. So emerald could actually just be a blue, with no psittacin, but with a "fluorescent tube" effect turned on. If this is the case, the original article can be revisited, and we shouldn't think of no psittacin (as that would never be deposited), but rather transparent psittacin that gets deposited in the cortex, but not visible, until we include phosphor in b2.