Inheritance of Metallic Trait

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Sherolyn-Basement Bettas

Betta enthusiasts have the deserved conceit of being unusually well informed as the genetics of their fish. That they can do so is grounded in large measure by the relatively large number of single gene effects on form and pigmentation the inheritance of which has been rigorously established. The existence of such information while necessary is far from sufficient. Indeed, the knowledge of zebrafish genetics far outstrips that of any other fish, but this knowledge has had only passing impact on the hobby. Many livebearers, especially the platy and swordfishes, have a long tradition in classical genetics, but it is nonetheless my sense that an appreciation of the theory and practical use of genetics has not penetrated this community to the extent evident amongst Betta nuts.

I suspect the routine use of genetics to plan crosses amongst Betta breeders has several explanations. Gene Lucas, the originator of the column, not only clarified much early work on single gene effects in his Ph.D. thesis, but also discovered two new single genes (opaque and non-red). No less importantly, through the venue of this column he presented the genetics of pigmentation and form to hobbyists in an accessible albeit rigorous fashion. As important as Gene’s personal contribution has been, no less important has been the organization he co-founded, the International Betta Congress. Readers interested in Betta are strongly urged to join and upon doing so you will encounter a culture in which information on how one might use genetic principles to breed fish of the colors and shapes you might favor is available in a number of forms.

Betta breeders will therefore be unsurprised when I remind them that a cross between a green fish and a steel blue fish will yield 100% (royal) blue progeny. Breeders may then be appropriately shocked by the fact that when I bred a green fish to a steel blue fish, I found the spawn equally split between teal-colored fish, and royal blue fish. How can this be? Single gene Mendelian genetics, while often insufficient, is never incorrect! 

Something other gene must be segregating in this cross and altering the appearance of the blue pigment. Regular readers of this column will have little difficulty guessing the source of this effect. Two columns ago, I explained the way in which the physics of reflection in thin films are employed in cells called iridophores to generate color. In my last column I reported a finding of Dr. Rosalyn Upson, Ph.D. and myself that the ‘copper’ phenotype was caused by a spread of an iridophore, heretofore undescribed in Betta, that reflected light in yellow to yellow-green wavelengths. This iridophore produces a shiny effect on the fish above and beyond that produced by the blue gene. Here I report on experimental crosses that establish the transmission genetics of this trait.

I obtained 3 copper fish from Thai breeders and crossed each of these with 3 different fish from my own fish room. The latter were of known ancestry and had no metallic in their genetic background. We can be quite precise regarding expectations if the metallic effect is attributable to a single gene. To do so we need make a few assumptions and introduce some symbolism to help with bookkeeping. Let us designate the presence of a copy of the metallic gene (i.e., allele) as + and the presence of a copy of the same gene that doesn’t produce the metallic spread as nms, for ‘no metallic spread’. Recalling that each fish has two copies of every gene, a fish can have two copies of the spread metallic allele (+ +), two copies of the ‘no metallic spread’ allele (nms nms), or one copy of each (+ nms). 

The three non-metallic fish from my own fish room were known, by virtue of the absence of metallic in their heritage, to be to have the genetic composition, or genotype, nms nms. If we assume that imported fish had two copies of the metallic allele then the expected outcome of these spawns can be visualized in the Punnett square shown in Figure 1. Recall that eggs and sperm are unique cells in that they carry only one copy of every gene, indeed the reason we have two copies of every gene is that we inherit one copy from each of our parents. The columns of a Punnett square give the contribution of one parent, in this case + in all the eggs (or sperm) from the metallic parent. The rows of the Punnett square similarly reflect the sperm (or eggs) of the second parent, in this case nm from the non-metallic parent. To obtain the predicted genetic composition of the progeny one simply combines the allele from column and that from the row for each cell in the matrix. In this case all cells yield an identical genotype, + nms. 

Figure 1. A Punnett square used to determine the expected genetic composition of crosses #1-3. Columns represent copies of genes coming from one parent, rows copies from the other parent. Each parent has two copies of the gene, but only one copy is delivered to eggs or sperm. The shaded cells in the matrix then gives the expected genetic composition of the offspring, when the genes contributed by each parent are combined to form a new individual. Here we assume one parent carries two copies of the ‘spread metallic’ allele (+) and the other parent two copies of the ‘no metallic spread’ (nms) allele. All offspring are found to have the same genetic composition + nms, that is, one copy of the ‘spread metallic’ allele and one copy of the ‘no spread metallic’ allele. 

We know immediately and upon inspection of the Punnett square that all our progeny are expected to be genetically identical with respect to this metallic trait. What is less clear, however, is how those fish will appear, or in genetic parlance, what their phenotype will be. Alleles may be either dominant or recessive. An allele is said to be dominant when a single copy of the gene is sufficient to display the effect, whereas if an allele is recessive, two copies must be present for the phenotype to be displayed. The Punnett square in Figure 1 shows that the crosses I made initially all produce fish with the genotype + nms. Thus, if the trait were indeed determined by a single gene and if the metallic effect was dominant, then we expect all the progeny display the metallic phenotype. Conversely, if the metallic spread was a recessive trait, all the progeny should be non-metallic.

Before announcing the results, it is essential to emphasize exactly how I decided whether a fish does or does not bear the metallic trait. The gross appearance of the fish is often deceptive, especially when the yellow iridescence is combined with blue and green. As such, all data reported here was scored as metallic only if yellow iridophores where observed spread over the body and unpaired fins upon examination using a dissecting microscope. With the microscope the yellow of the metallic effect is distinct from the green, blue, or steel reflectance controlled by the blue gene.

The results of the crosses, designated crosses #1- are given in Table 1. All three crosses generated 100% metallic progeny. These results then are precisely that expected if the metallic effect where generated by a single dominant gene. That said, these results alone are hardly definitive; indeed they could be accommodated easily by other explanation. For example, the fact that I produced 100% metallic fish might be because I fed the fish something that caused them all display the metallic effect.

Table 1 – Inheritance of Metallic Spread

To rigorously establish singe gene transmission, it is necessary to take the progeny of these first crosses and either cross them to one another or cross them with a non-metallic fish. I twice performed the latter test, in both cases with a metallic male and a non-metallic female. The relevant Punnett square is given in Figure 2. Here the columns represent the sperm of the metallic progeny of one of the first crosses. Note that since this fish was derived from the first cross it has the genotype + nms (see Figure 1), individual sperm bore either the + allele or the nms allele. This fish was crossed with a non-metallic fish, which under our hypothesis of dominance for the metallic spread must be nms nms. Filling in the Punnett square as explained above yields the prediction that one-half of the progeny are expected to have the + nms genotype and hence display the metallic effect and one-half to be nms nms, hence lack the metallic phenotype. The results of these crosses, designated as crosses #4 and 5, are presented in Table 1. Clearly the predicted 50:50 ratio was observed, indicating that the metallic phenotype is attributable to a gene that behaves as a single Mendelian dominant.

Figure 3. A Punnett square as in Figure 2 but for crosses #4-5. In this instance one parent has two copies of the ‘no spread metallic’ (nms) allele, while the other is an offspring derived from the cross shown in Figure 2, hence has a genotype of + nms. Note that half of the progeny are expected to have two copies of the nms allele and will be expected not to display the metallic effect, while the other half will display the metallic spread.

We may now return to the surprising result with which this column began. I made this cross with a steel blue mother and a green father so as to insure that all the progeny would display blue reflecting iridophores, but that some would combine the blue with the metallic and some not. The results of adding the metallic effect, attributable to the spread of yellow reflecting iridophores, is to turn a blue fish into a blue-green or teal colored fish. 

The finding that the metallic effect is inherited as a simple dominant gene insures that it can be combined with all other known colors in an entirely predictable fashion. While exploration of the various ways in which the yellow iridophore may be combined with other genes must await latter articles, I will complete discussion of the interaction of the yellow iridophore with the blue gene. We have already seen the absence of the metallic effect in a blue fish yields the traditional blue, whereas its presence produces teal and blue-green fish. When metallic is combined with the green allele one produces an intense green, without the intrusion of blue tones, which have been a common fault on such fish. Combining steel blue gene with the spread allele at the yellow iridophore gene yields the ‘copper’ pigmentation.

Fads can last generations. The fact that the wild Betta splendens (=imbellis) have the spread allele indicates that at some time during the centuries of domestication that the nms (no metallic spread) allele must have arisen and been favored by breeders. Such a scenario strikes me as eminently plausible, since in a world in which all fish had metallic spreads, there would be no pure royal blue fish. Selection to produce the blue would quickly eliminate the wild type or spread allele. Likely what we see today a novel effect obtained by out-crossing to wild animals is just an effect that our forefathers worked hard to eliminate from their lines. 

Source:FAMA Magazine
November 2005

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