Another indication that you have an immature male is the angle of the gonopodium relative to the fish's body. As the fish matures, the remnants of the fan-shaped caudal fin will disappear, allowing the gonopodium to be flush, parallel to the body.

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Karl

I was initially surprised when you indicated that the Nigra (N) gene was carried by Bleeding Heart platies because N is dominant and the Bleeding Hearts that I have seen don’t have any black pigmentation. I also suggested that this might be explained by the fact that the N gene is not 100% penetrant, which means that in some genetic backgrounds, presumably in Bleeding Hearts, the N gene will be present, but no black spots/pigmentation will be apparent. In the hybrids, the N gene, now in a new genetic background, would be expressed resulting in black pigmentation. The N gene is also closely linked to genes that specify late sexual maturation which likely explains the large size of the hybrids. They are very attractive fish.

Roy

Chromedome

Allow me to clarify my previous statements. In regards to Xiphophorus sp., a "sailfin" gene distinct from the Simpson hifin gene may exist, but I have seen no evidence to support that idea. Given that, I think of "sailfin" as a trait that is associated with a wide, flowing dorsal fin, and not with the expression of a specific gene or set of genes. The origin of the Chinese "sailfin" is not well documented, but my understanding, and I could be wrong, is that it resulted from intensive selective breeding and not from a new mutation analogous to the Simpson hifin. In my hands, the Chinese "sailfins" behave similarly to conventional hifins in that the trait is dominant, and there is considerable variation among the offspring (when the cross is between a "sailfin" and a fish from a non-"sailfin" line) in terms of dorsal fin width and length, although maybe not as much variation as seen with conventional hifins.

The appearance of a hifin, whether the hifin is due to the expression of the Simpson hifin gene or a distinct "sailfin" gene, is dependent upon modifiers that control the length and branching of individual dorsal fin rays. In "sailfins," the appropriate modifiers are clearly being expressed. This could have resulted from the accumulation of these modifiers by rigorous selective breeding or possibly from the expression of a new "sailfin" gene which leads to the expression of these modifiers in a single or at least in a reduced number of steps. However, it seems unlikely, but certainly not impossible, that a single "sailfin" gene could both increase the length of the normal dorsal fin (which is what the Simpson hifin (H) gene does) and also affect the expression of all of the modifiers needed to produce a wide, flowing hifin.

Again, I may have misspoken by indicating that a unique "sailfin" gene does not exist, but until there is genetic or molecular evidence of its existence, I remain skeptical.

Roy
http://www.xhifin.org/

CharlieO

"Saifin" is a popular term coined by hobbyists to describe a hifin that is wide and long. There is no "sailfin" gene (see below). The hifin gene, the gene responsible for the extended growth of the dorsal fin and originally found on Simpson swordtails, is a dominant gene. Classically, breeding two hifins should produce 2/3 hifins and 1/3 lowfins because embryos containing two copies of the hifin gene die. However, hifin genetics is apparently more complicated than this simple scheme because there is a wide variation in the percentage of hifins that can be obtained from a mating between two hifins. With some matings, I have obtained 100% hifin offspring, whereas with others, the percentage can be quite low.

The appearance of the hifin can also vary considerably from narrow to wide and from short to long. All hifins derived from the original Simpson swordtail, regardless of their appearance, express the hifin gene. The appearance of the hifin is determined by a set of accessory or modifier genes that specify fin width and length. "Sailfins" express the hifin gene plus a specific set of modifier genes that enable the rays of the dorsal fin to branch extensively resulting in a very wide, attractive hifin. Other modifiers specify the extended length of the hifin. Many genes are therefore required to produce a "sailfin" which explains why it can be challenging to produce a true breeding line of high quality "sailfins."

Roy
http://www.xhifin.org/

Melody and Darrell:

This albino mutation may still have been in the "classic" albino gene (tyrosinase). However, it may be a somatic mutation that occurs in the early embryo, but is not in the cells that will become germ cells (sperm in this case) and therefore is not passed on to the babies.

Roy

Hi Copper:

We should have a permanent feature on the website or in Livebearers based upon your readings, “Copper’s Believe It or Not.” I especially like your euphemism that the daughters will “go weak in the fins” over their prospective mate.

Actually, the possibility that the mother can pass on her mating preferences to her offspring seems reasonable. Gil Rosenthal and others are studying these types of inherited mating behaviors.

Roy

Is that the Twilight Zone music I hear in the background? Seriously, I find it very difficult to believe that sufficient numbers of free-swimming sperm would be able to find and enter the genital tract of a female resulting in a productive pregnancy.

Roy

Darrell and Copper:

I wish it were true that crossing blacks or red jets with albino swordtails could prevent melanoma formation. Unfortunately, that is probably not the case. The gene that is responsible for albinism is tyrosinase which is needed to make black pigment. Albinos still have melanocytes, but they are usually not black. Albinos can develop amelanotic tumors in which the non-black melanocytes keep growing. It’s possible that Frank Grainer's albino swordtails with black pigmentation cannot develop melanomas, but it’s probably not just because they are albinos. The albinos with black pigmentation that I’ve raised often develop melanomas. In my previous posting I optimistically wrote that it might be possible to obtain healthy blacks and red jets. I left out the pessimistic part that inactivating the Xmrk gene is probably a rare event and that we’ll have no way of knowing by looking at a fish whether Xmrk is inactivated or if its offspring will be melanoma-free.

Another possibility is that other genes or pigment patterns might suppress melanocyte growth. I’ve noticed that my black swordtails containing a large number of blue-iridescent scales throughout the body and especially near the base of the caudal fin, where my fish frequently develop melanoma, don’t seem to develop cancer. This might be worth exploring.

Roy

Copper, Alex and Darrell

Much of what is known about the genetics of melanoma in Xiphophorus sp. comes from the work of Manfred Schartl and his colleagues. They identified a gene called Xmrk that stimulates black pigment cells (melanocytes) to grow uncontrollably, producing melanomas. Darrell is correct that a modifier gene plays an important role in this process, but in this case the modifier gene (R) acts to prevent melanoma formation. Wild platyfish (X. maculatus) have both Xmrk and R so even though they may have black spots, they don’t get melanomas. When they were crossed and then backcrossed to wild swordtails which lack Xmrk and R, eventually black offspring arise that have Xmrk, but not the R melanoma-suppressor gene. This results in uncontrolled melanocyte proliferation and cancer. Most of the colorful domestic swordtails available today have platy ancestors, so almost all contain the Xmrk gene and are therefore prone to developing melanoma. Other genes and gene modifiers that control pigment pattern (e.g. tuxedo) may also affect this process. The good news is that Schartl found fish in which the Xmrk gene was lost or inactivated by mutation, and these fish were melanoma-free. It may therefore be possible to produce all black and red jet swordtails that do not develop cancer.

Roy