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Color variants - Testudoalbino

Professional breeding of mediterranean tortoises

Professional breeding of mediterranean tortoises

Professional breeding of mediterranean tortoises
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Tortoises Color variants

Testudo hermanni hermanni albino
What are the tortoise color variants

Every living species, from the simplest to the most advanced, has its own external characteristics, shape, dimensions and coloring patterns. What unites them all is the search for a way to blend in with the environment or, conversely, the exact opposite. To do this, the cuticle, the skin or related structures such as hair, feathers and feathers, have the characteristic of presenting particular designs and colors. They have evolved in order to make specimens of the same species recognizable and attractive to each other, but also in order to blend in with the environments they frequent, both in the case of prey and predators. Then there are animals that instead want to be recognized because maybe they are poisonous and thus warn that it is not a good thing to eat or bother them, or others that imitate them pretending characteristics that they do not consequently draw an advantage in terms of survival. Finally, there are other animals with flashy shapes and colors in order to attract the opposite sex. Known examples are the peacock and many other birds. The selection logic is that a showy specimen that shows itself, in addition to guaranteeing an equally attractive lineage, is evidently the bearer of skills that allow it to effectively escape predators despite the obvious handicaps regarding camouflage and often from clumsy structures that they slow down their escape.
Whatever a particular external pattern is, it is regulated by a multitude of genes which, like all the others, are subject to spontaneous mutations with a certain frequency. Normally, mutations that improve a favorable aspect will tend to spread and maintain themselves, while all the others will have less luck and will tend to remain with a low frequency, or to disappear.
Specifically, we can summarize that for example in the case of pigmentation, there are many variations relating to the type of color, physical and otherwise, white, black, red, brown, green and their shades. Some of these have different metabolic pathways, others are simply a different modulation of the same, examples are red (pheomelanin) compared to black (eumelanin) in the first case, and brown/yellow always compared to black in the second.
Finally, we must consider, because often mistakenly inserted in speeches of pigment deficiency or amelanic forms, all the gene variants that determine an alteration of a characteristic design. The extreme case is represented by leucism, where the absence of the cells responsible for the production of melanin generates a completely white and white coloring pattern, however the possibility of producing melanin is preserved and remains visible in other structures such as the iris of the eyes. In some cases there are real mosaics with colored point elements due to the sporadic presence of aggregates of healthy cells. Therefore, apparent cases of amelanic animals or with drawings with few or zero spots typical of the species/subspecies, in fact are not forms of albinism, but in any case, going to clearly alter the design and pattern of an animal, we can still bring them back in the category of color variants, if we go to take the organism as a whole and specify the different origin anyway.
Notes and details on the Testudo hermanni color variants
As in all animals, reptiles and turtles are no exception, there are many possible color variations, and their number increases according to the complexity of the design and the pigmentations that characterize them. In turtles we therefore find the negative tyrosinase albinism, indicated as T- in which the coloring pattern is characterized by the complete absence of melanin due to a mutation affecting the tyrosinase gene, the first upstream step that starting from the amino acid Tyrosine , starts the chain of reactions that leads him to acquire the classic black color. A classic example is a yellow base specimen, in which at least at birth the areas where the dark design would normally reside are instead in a pure white form, while the absolute impossibility to produce melanin determines an apigmentation of the iris and the eyes appear red to following the transparency that shows the underlying tissues sprayed with blood. Obviously, it is the quantity of melanin produced and deposited in cellular structures that in the reptiles take the name of chromatophores to determine their degree and intensity, from the most intense and diffuse black, to the shaded brown, almost a faded shade. This is determined by a modulation of melanin production due to mutations that can make the enzyme tyrosinase or any other intermediate/biochemical passage necessary for the aforementioned amino acid tyrosine to acquire color until it becomes eumelanin, the final form of this process. In reality there is also another pigment, the reddish-colored pheomelanin, which follows another metabolic pathway, which may remain and in turn be missing or be present in different grades, but the logic is always the same.

In Testudo hermanni, cases of T- albinism are known, and in some cases successfully selected, albeit with extremely low numbers by virtue of the limited productivity and the long years necessary for reaching the reproductive age. In conditions of captivity, these mutants do not show particular deficits or limitations, if it were not for the greater sensitivity of the eye to intense light, which leads them to behave slightly differently. Another marked difference is the reduced efficiency of thermoregulation. It is known that the sun's heat is more easily absorbed by dark colors, which makes light animals slower to reach physiological temperatures when the climate is less favorable, upon waking up from hibernation, in autumn or in conditions of reduced insolation. It is no coincidence that for example at higher altitudes or in cold climates, that reptiles show an average darker pattern than that observed in hot climates, where the purpose is often achieved by reducing, even to the extreme, the otherwise typical design. The classic Testudo graeca golden, to be clear, that have nothing to do with albinism, but the selective pressure acts to favor those specimens that show a reduced dark design, are a classic example.

Another mutation that has been found in nature in Testudo hermanni hermanni, moreover with a high frequency, is a form in which the typical design of the species turns out to be strongly nuanced to varying degrees, borrowing a word from the supernatural, gost, ghost. Probably, the most appropriate definition is isabella, and it is an autosomal recessive mutation, that is, it occurs only if both copies of the gene that determines it have mutated. In this case, the bearer of a single mutated copy and a normal one will appear in normal color. There are many breeders who will have the first reproductions in the coming years, and it is foreseeable that in a reasonable period of time, this particular color variant will become quite common and widespread. Unlike albino T-, being only a slight modulation of coloring, it has no particular differences in behavior and efficiency in thermoregulation compared to normal specimens.

When instead we find a birth pattern in all respects similar to an albino T-, with a lot of red eyes, but with the growth an accumulation of pigmentation, albeit nuanced, evidently dark yellow tending to caramel, we are faced with a form of partial albinism, where the mutation, always autosomal recessive, presumably affects other enzymes of the chain which from the colorless tyrosine leads to the colored eumelanin. In these cases, animals are defined as albino caramel or albino tyrosinase positive, i.e. present and functioning, T+. Considering that at birth there is no presence of pigment, it is coherent to suppose that feeding is the source of intermediates at the basis of the inefficient color production of these animals. Although this mutation had occurred and selected on other species, such as the caramel albino Testudo marginata and the Stigmochelys sulcata ivory, now quite well known, recently, the mutation was positively fixed only recently also in Testudo hermanni, in particular in the western subspecies, Testudo hermanni hermanni.

Leucism is also present in turtles, and is recognized by a white white pattern and black eye, complete absence or point presence of pigmented areas. I have no news if not sporadic, of births here and there of specimens of the genus, but not of breeding that have undertaken the reproduction arriving at regular births and a real selection. Therefore the survival rates are not known, while it seems obvious that in this case too it is an autosomal recessive mutation.

Finally, I would like to spend a few words, to tell the truth, for those specimens defined as high yellow, quite common in Testudo hermanni boettgeri, which are nothing but individuals in which the dark areas of the drawing appear extremely reduced or absent. Many breeders have tried to reproduce them by consistently obtaining normal offspring, which suggests that the particular pattern derives from a multitude of factors/genes, which to express the character must be in a rare combination. In a single case known to me, but evidently characterized by a single autosomal recessive mutation, it was possible to replicate the particular amelanic pattern.
Testudo hermanni hermanni isabella
Definitions and insights

Albinism: Deficiency or absence of melanin pigment, which in turn has different variants. Erroneously, albinism is associated with the white color and the red eye, however it is not correct, as it can be partial, with a deficit of melanin production, affecting for example only some structures such as the eyes, or simply giving rise to a mosaic. In any case, specifying what the deficit is, we are always talking about a form of albinism. Since the production process of the pigments is complex, there are different pigments that follow often parallel metabolic pathways, we understand how and why nature is full of color variations and why there are infinite possible combinations due not only to the presence or absence of a pigment, but their relationship and modulation.

Leucism: the absence of pigmentation is due to a mutation that prevents the formation of cells responsible for producing pigment, however the possibility remains for structures such as the iris to produce it as the necessary metabolic pathway remains intact and preserved. Not to be confused with albinism, where the cells responsible for the production of pigment are perfectly formed, but a mutation affecting the chain of events that leads to the production of color, prevents it from completing the metabolic pathway.

A bit of basic genetics: the gene is the fundamental and functional unit of the genome, however reducing everything to a single gene when we talk about a particular character is often an understatement. It is enough to know that, although the mutation of a gene is enough to change a particular character, of genes involved in a particular metabolic pathway there can be many and carry out consecutive and chain reactions. So it is clear how depending on the mutated gene, there may be external differences, even if in theory they go to affect the same process, often diverging from each other. Leaving aside the cases in which a particular pattern requires the concomitance of more than one mutated gene, normally in our daily life, the turtles, we inevitably find the case of a single mutated gene, then depending on where the phenotype changes, which has the characteristic to be recessive, that is, to manifest only if both the maternal and paternal copies are present at that time. This is the first important fact to understand, namely that the absence of a mutated phenotype does not indicate the absence of the mutant gene, but that the reverse is almost never true, since these are very rare mutations. I'll explain. The mutated gene is recessive, if in a single copy, the normal and functioning gene completely replaces and the phenotype appears completely normal. This is the case of individuals who, having only one mutated copy of the gene of our interest, are defined as heterozygous for that particular character. They will therefore transmit the mutated gene halfway through their offspring which, when we think about it, in the case of a male, for example, we are talking about often very large numbers. Considering that from the crossing of two heterozygotes 1/4 of the young will have on average both the mutated copies of the gene and a phenotype for example albino, that 1/4 of the young will be the carrier with both normal copies, but above all 1/2 will be heterozygous , therefore 2/3 of babies born with "normal" phenotype, one understands the often highly underestimated importance of heterozygotes in selecting a color variant. In fact, many stop at the mutant itself and this is the reason for the failure of many selections. All in the absence of these very important basics. In fact, many believe that a normal colored specimen cannot give rise to a mutated specimen, but above all that the birth of mutants can be a random event that can arise from any mating. Therefore, clarifying the mechanisms underlying these simple selection processes also allows you to make thoughtful and certainly profitable purchases. Given the lower cost of heterozygous specimens, obviously with the certainty that they are purchased by professional breeders such as Testudoalbino, this is an indirect and economic way to obtain the desired color variant.

Notes and details on the color variations of Testudo marginta
In Testudo marginata, the only color variant currently known and reproduced for decades, moreover present in nature with a certain frequency and recorded, even if not recognized, in some museum collections, is the T + form, called caramel albino. Due to the absence of pigmentation in the early stages/years of life, as in the case of T- albinism, the animal shows a reduced thermoregulation efficiency which, however, with time and color change towards the known caramel, goes to cancel completely. The eye, initially red, tends to remain light hazel, and is normally the first structure that darkens, not creating for other problems of vision at high lights as in mutations where it remains depigmented/red. They are animals now positively reproduced for decades with several generations, 3 at present, which have shown a survival rate comparable to the typical pattern even in nature by virtue of probably a certain advantage in barren soils and with dry vegetation, where they camouflage more effectively . The only forethought, the first years, is to guarantee greater protection by virtue of the reduced thermoregulation capacity until they reach a minimum of pigmentation.

The story about the selection of the albino caramel Testudo marginata

It was a big surprise on September 10, 1991 for me to find a small Testudo marginata white as milk. She was born together with other 8 baby tortoises in the garden. It was a laying that I was not able to identify, while the others were all in the incubator. In a short time, the last remaining eggs of a female marked with the letter N would hatch. A few days later from one of these eggs, one small, white-colored turtle with red eyes emerged. The N Female (her mother) coloring was absolutely normal. She was harvested 20 years before from the area around Olbia (Sardinia, Italy) by some friends that decided to ged rid of her the year before. Thus, they resolved to give her (together with other specimens of the same species) to me. Who could be the father? From the beginning I thought it was a young pale ocher-colored male, with gray eyes, which lacked completely black color on his livrey. He, too, was found years ago in the area of Olbia (Sardinia). It was Albino! In the following years, a total of 14 newborn were albino: of these, today only seven remains, 6 males and one female, born in 1996 and 1997, respectively. In the last year, their father died from a fulminant pneumonia, shortly after waking up from hibernation. A few weeks before he died, I managed to make him mate with the female heterozygote and from 11 eggs laying 5 albino were born, thus proving the male albinism and the female  heterozygosity.

Since then, no animal had born, until September 2003, when two small eggs of a female tortoise, a child of N born in 1996, released two equally small Testudo marginata albinos. Even this female was heterozygous and mated with the albino brothers born in the same year, finally sexually mature. 12 years had passed since the first-born albino and I truly wished I could be able to select the first albino strain of Testudo marginata, which I did. This year (2004) I have been able to fertilize the female heterozygous N and  her 2 years old daughter by 2 albino males born in 1996 and currently I have 28 incubating eggs obtained from both. But the biggest surprise ever was the first laying by the only female albino born in 1997, of which I have 5 eggs in incubation.

Once the incubation period was over, the first eggs began to hatch. At a temperature of 30-32 ° C 58-64 days are needed for a Testudo Marginata to hatch. Of the 8 young female heterozygous fertile eggs laid in late May, 6 hatched and 2 contained dead embryos with normal coloring. As to the new born babies, 2 had normal color and 4 were albino: exactly what I would expect from a normal segregation of Aa X AA genes (heterozygous for albino). The eggs in the second laying were 12, of which only 6 fertilized. From them 3 specimens of normal color and 2 albinos were born: inside the egg that has not hatched I found a small white embryo.

The N female, the mother of the first  albino, has laid 2 times,  with  12 eggs per deposition. In both cases , fertility was  low and   only 8 were fertilized.  Most likely this is due to the young age of males born in 1996   (year   2004).

The youngest and only female albino, born in 1997,  has laid 8 very small eggs at once. Even in this case, only 4 were fertilized: 3 have hatched, giving birth to 3 small-sized albino  specimens (22 mm each); in the aborted  egg I found  a white embryo . Once again, I obtained what I would have expected from a recessive segregation for   albinism (aa X aa).

This is a recessive mutation that follows Mendel’s law. Its peculiarity lies in the fact that specimens start to accumulate yellow light pigments two months after the birth: their eyes gradually turn to light brown color and this makes them less sensitive to UV light, so that they can live like the normally-colored animals. However, they show very pale looks reflecting the coloring of the species, only faded.


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