This is going to be a fairly rough walkthrough. It probably requires you to have a basic knowledge of genetics and Punnett squares. I will do my best to clarify ball python genetics in both their frequently used terms as well as the genetically correct terms. If you need some clarification, please let me know.
If you see something that is incorrect please send me an ask instead of reblogging! It is incredibly tedious to continually reblog this long post to answer concerns. You followers and my followers will thank you.
Many people use terms incorrectly within the ball python industry. Many people will describe a morph as a gene, when they really mean allele, or codominance, when they really mean incomplete dominance.
In genetics, a gene is a series of code that is responsible for expressing a genetic characteristic. For example, scale color would be one gene. Alleles, on the other hand, are variants of that gene. For example, ball python scale color would be the gene, and Mojave would be one allele. Another allele would be lesser. Usually within the ball python hobby, people use the terms interchangeably, which is incorrect.
Another one of these cases resides in the use of codominance. Traditionally, codominance means the alleles are equally expressed. This is different from incomplete dominance, which is intermediate expression of both alleles. Try to think of it this way, if a codominant red flower and a codominant white flower were to reproduce, the offspring would be both red and white. If an incomplete dominant red flower reproduced with an incomplete dominant white flower, the offspring would be pink. Codominance expresses both phenotypes, or the visual manifestation of the characteristic, whereas incomplete dominance meets somewhere in the middle.
For the remainder of this write-up, I will be using the terms interchangeably, although that is incorrect.
Other useful terms include:
Phenotype: The physical expression of a gene
Genotype: The codes for the gene. They usually appear as two letters, either lowercase or uppercase to signify the characteristics. Sometimes differing alleles will be dictated by a +.
Homozygous: has two of the same form of an allele (for example PP or pp)
Heterozygous: has two different forms of the allele (for example Pp)
When speaking of genes and forming Punnett squares, I like to think that genes are being plugged in. Each individual has two slots for each gene. If we go back to the flower comparison again, imagine that we are looking at the petal color slots of two flowers.
Here we have a red individual whose petal color slots are filled with PP (purple boxes). P means the color expressed will be red. The white individual has slots filled with pp (green boxes). p means the expressed color will be white. Now each parent will pass down one of their slots to fill the slot of their offspring. The red parent can pass down a P or a P. The white parent can pass down a p or a p. The resulting offspring would have slots filled with both a P and a p because each parent passed one slot down.
Now let’s apply that to different gene forms.
Complete Dominance Inheritance
Complete dominant genes (usually just called “dominant”) are always expressed in the phenotype. They are kind of like show offs. If they appear in the coding, they stand out over the other gene. Pinstripe and spider are both examples of dominant genes.
Example: Here are the parents.
Both are pinstripes. Both of the parents are heterozygous pinstripes which means they display the pinstripe gene (A), but also carry the wild-type gene (A+).
When paired, they will produce the following:
Each offspring receives one allele from each parent as depicted by the colored blocks. Try to figure out which individuals will be pinstripe and which will be wild-type in appearance.
75% of offspring will have the pinstripe phenotype and 25% will have wild-type appearance (remember phenotype is the physical outcome and genotype is the code that made that happen). Genotype probabilities are: 25% to produce a homozygous Pinstripe (AA), 50% to produce a heterozygous pinstripe that carries the wild-type gene (AA+), and 25% chance to produce a homozygous wild-type (A+A+).
Dominant genes will still have the same phenotype, therefore their homozygous and heterozygous individuals will look the same. Keep this in mind as this will change depending on the type of inheritance.
Recessive genes hide behind other genes and only show when they are paired up with a letter that looks like them. Recessives only show if the genotype is homozygous for the recessive gene, in other words the are two slots must be filled with the recessive gene for it to have a visual effect. Recessive genes are often expressed with lower case letters. Pied, axanthic, hypo, albino, clown, and genetic stripe are all examples of recessive genes.
Let’s start out by pairing a homozygous Pied (bb) to a wild-type (BB).
The only available genes to pass on are either a b or a b from the pied or a B or B from the normal, therefore all offspring will be visually wild-type, but heterozygous for pied.
The resulting offspring will display the dominant phenotype of wild-type but it hides the recessive gene of pied behind it.
Percent Het for a gene:
Breeders will sell the animals who carry recessive genes as “x% het.” This describes the probability of a pairing to create an animal actually carrying the recessive gene. The options you may encounter are: 100% het, 66% het, or 50% het and each depends on the pairing that was done to produce the offspring. As shown above, if a visual recessive (bb in the example above) is bred to anything, the offspring will all carry the gene. That recessive will pass down to 100% of the offspring.
66% hets are produced by breeding two heterozygous individuals. Let’s take two pied offspring from the previous example and breed them together.
In the first boxes, both parents pass on the dominant wild-type trait, therefore the individual will not carry the recessive trait. The 2nd and 3rd boxes are the same, as one parent passes on the wild-type allele and the other passes on the recessive pied allele. Finally, both parents pass on their recessive allele.
The odds are: 25% of the offspring will be homozygous dominant (BB) and phenotypically wild-type, thusly they will not carry the gene. 50% of the offspring will be heterozygous and phenotypically wild-type, and 25% will be homozygous recessive and phenotypically pied.
*Remember pheno= physical appearance and geno= code to make that appearance
The het percentage comes from the three phenotypically wild-type snakes. ¼ of the offspring produced will be visual pied, so there is no guesswork involved. You know those ones have the pied gene. As for the remaining 75%, you would be unable to tell who carries the pied gene and who does not. ⅔ of the remaining animals could carry the pied gene, while ⅓ would not. So, the probability of a snake from this pairing producing a wild-type visual that is also carrying the recessive gene is 66%. (⅔ * ⅓ = 2/9 = .66)
Finally, if you breed a heterozygous (Bb) to a homozygous dominant (BB):
You get a good ole 50/50 split. The first parent does not carry the recessive gene, so there is no possibility of getting a homozygous recessive from this pairing (and therefore no visual pied), but the recessive gene could have still been passed down by the heterozygous parent.
Here’s a Punnett square if you prefer seeing it that way:
The het parent, being the only one with a recessive gene, can then pass it on to 50% of the offspring. That is where the term 50% het comes from.
Alright, do you think you have a handle on all of that? If you do, we can move onto our next topics. This gets particularly tricky.
So tricky, in fact, that it’s going to take me some extra time to finish the write up. Keep an eye out for part 2!
As always, if you have any questions, my ask box is open!!
So… it’s no secret that I hate Thylacine, it’s wasted as a Tertiary, it really ought to be some form of mutant Primary that touches the wings (ib4 the “But it’s on the Wawawawa-wings!!” crowd. Spines doesn’t touch the body or the wings and it’s a Tert instead of apparel for some reason, your logic is a drunk duck). …
Alright yall VOTING TIME
Would you either have… 1) 67 + shitton more to come colors of neat natural spikes on your dragon 2) probably max. 10 color sets of small fake spikes that take up an apparel slot
Scientists Discover That Eyes Are Windows To The Soul
The eye is the window to the universe, and some would say they are also windows to the soul… We have heard this phrase get passed around before: “The eyes are the windows of the soul”. People usually say this when they can see pain, anger, or some other emotion in somebody else’s eyes. But recent research gives a whole new meaning to this phrase. Eyes not only windows to emotions, they are windows to the soul.
Our engineering team has been working on new tools to help us generate and implement genes in a much faster and more efficient manner that does not sacrifice the image and color quality we’ve come to value as part of our site’s style. These tools are being developed to make future gene implementation much easier, but also come with the added benefit of allowing us to expand our color wheel without also increasing artist workload exponentially.
We are currently working on converting our existing breed art templates into ones that will be compatible with our new tools. Every time we finish 10, we will be revealing a color. Some will be old, some will be new.
To answer your questions:
We are intending to only expand the color wheel once, as we would like to minimize the disruption to player’s breeding ranges.
New colors will go between existing colors on the wheel so that they are in places that make sense for their range. We will not reshuffle the wheel, and your ranges will remain close to the same, but expanded.
New colors will ONLY be able to be bred, hatched, and scattered for.
Example: If you had a Rose to Magenta range, you’re not suddenly going to have a green in there. It will be more pinks.
To remain fair to all of our players, only the original 67 colors will be available during account registration and new dragon creation.
In April 2015, a paper by Chinese scientists about their attempts to edit the DNA of a human embryo rocked the scientific world and set off a furious debate. Leading scientists warned that altering the human germ line without studying the consequences could have horrific consequences. Geneticists with good intentions could mistakenly engineer changes in DNA that generate dangerous mutations and cause painful deaths. Scientists — and countries — with less noble intentions could again try to build a race of superhumans.
There is enough DNA in an average person’s body to stretch from the Sun to Pluto and back, 17 times.
The human genome, the genetic code in each human cell, contains 23 DNA molecules each containing from 500 thousand to 2.5 million nucleotide pairs. DNA molecules of this size are 1.7 to 8.5 cm long when uncoiled, or about 5 cm on average. There are about 37 trillion cells in the human body and if you’d uncoil all of the DNA encased in each cell and put them end to end, then these would sum to a total length of 2×1014 meters or enough for 17 Pluto roundtrips (1.2×1013 meters/Pluto roundtrip).
Elephants have evolved extra copies of a gene that fights tumour cells, according to two independent studies1, 2 — offering an explanation for why the animals so rarely develop cancer.
Why elephants do not get cancer is a famous conundrum that was posed — in a different form — by epidemiologist Richard Peto of the University of Oxford, UK, in the 1970s3.
Peto noted that, in general, there is little relationship between
cancer rates and the body size or age of animals. That is surprising:
the cells of large-bodied or older animals should have divided many more
times than those of smaller or younger ones, so should possess more
random mutations predisposing them to cancer. Peto speculated that there
might be an intrinsic biological mechanism that protects cells from
cancer as they age and expand.
At least one
solution to Peto’s paradox may now have been found, according to a pair
of papers independently published this week. Elephants have 20 copies of
a gene called p53 (or, more properly, TP53), in their
genome, where humans and other mammals have only one. The gene is known
as a tumour suppressor, and it snaps to action when cells suffer DNA
damage, churning out copies of its associated p53 protein and either
repairing the damage or killing off the cell.