Reptile & Amphibian Forums

Spiders are co-dom like pastels right???also whats the difference in co dom and dominant? What are the chanes on getting a bumblebee from a spider pastel breeding?

To my knowledge, co-dom's are nothing more than visual hets. Spiders are dominant since a spider-x-spider breeding does not produce a "super spider" to date. This may be disproved in the near future but as of right now, it does not produce a homozygous animal. Pastels are co-dom since they produce a "super pastel". Word is still out on Mojave's with respect to them being co-dom or dominate. Hope this helps ya.

Speaking of Mojaves, here's mine (I have pastels as well but haven photographed them yet).

Ron

co-dom example pastel x normal theoretically 50% of offspring will be pastel the other 50% will be normal

dominant example super pastel x normal theoretically all offspring PASTEL

dominant example 2 super pastel x pastel theoretically 50% offspring will be super pastel and the other 50% will be pastel

I THINK I THINK not sure if im right
pastel x spider theoretically 25% bumblebee spider 25% pastel 25% spider 25% can go either way whatever nature decides

if i am wrong someone PLEASE correct me i dont mind admitting a mistake

"dominant example super pastel x normal theoretically all offspring PASTEL"

You are misusing the term "dominant". Dominant describes the mutant gene type and pastel can't be both co-dominant and dominant type at the same time. What you are really talking about here is the genotype - homozygous. A super pastel (phenotype) is the homozygous genotype and you are correct in that it will produce all pastel offspring when bred to a normal.

However the pastel gene is still co-dominant or incomplete dominant (there is a debate on which of these two similar types is the correct word for this case) and not completely dominant with respect to the normal gene at the pastel location. Regardless of if you are looking at a heterozygous pastel genotype (the normal pastel phenotype) or the homozygous pastel genotype (the super pastel phenotype) the mutation type is the same and doesn't change between co-dominant and completely dominant.

With both co-dominant and incomplete dominant mutation types the heterozygous genotype animals are visible morphs however the homozygous genotypes are different visible morphs (i.e. pastel and super pastel).

With a completely dominant mutation type the homozygous genotype and heterozygous genotype would be the same visible morph phenotype. Spider would be determined to be completely dominant if some day a homozygous spider is proven by producing only lots of spiders out of lots of babies bred to normals and that homozygous spider looks the same as the heterozygous spiders.

It's also possible that spider (or any dominant type gene for which we haven't yet proven a homozygous) might be homozygous lethal and a homozygous spider will never be produced. I'm not sure but I'm thinking this might fall under co-dominant since technically the homozygous is different than the heterozygous - it doesn't exist.

"I THINK I THINK not sure if im right
pastel x spider theoretically 25% bumblebee spider 25% pastel 25% spider 25% can go either way whatever nature decides"

Each egg from pastel X spider would have a 25% chance of being a bumblebee (spider pastel), a 25% chance of being pastel only, a 25% chance of being spider only, and a 25% chance of being completely normal for both mutations.

>It's also possible that spider (or any dominant type gene for which we haven't yet proven a homozygous) might be homozygous lethal and a homozygous spider will never be produced. I'm not sure but I'm thinking this might fall under co-dominant since technically the homozygous is different than the heterozygous - it doesn't exist.

FWIW, the mouse geneticists call such mutant genes codominants.

Paul Hollander

OK, the guys excplained the co-dom/incomplete dominant in the above reply, so I won't repeat what they have siad.
The *BEST* example of a dominant gene? NORMAL! A dominant gene, whether the genotype is homo or het is always expressed in the phenotype. That is the definition of dominant as I learned it several years back.
Katrina

Your example of a dominant gene is good if you narrow it down say to the normal gene at the albino location. A het normal for albino (which is also het albino) looks just as normal as a homozygous normal for albino. It only takes one normal copy of the albino gene to completely overpower the albino copy of that same gene.

However, as pointed out in an earlier thread (by Paul?) there are likely very many genes that make up the normal pattern and color. To start with the normal copies of all the genes we have known color and pattern mutations for so far and probably lots of others that we haven't seen mutations of so far. So there isn't just one normal gene.

Excellent point there, Randy. Within the realm of "normal" there are high gold, high white, high orange, reduced pattern, abberant/labrynth pattern, high contrast, granite marked, blurrd pattern, etc etc etc...I know I am missing quite a few. Perhaps I was oversimplifying, but the best example I can think of for a dominant gene is that ofnormal/classic jungle coloration when paired with a homogozygous simple recessive mate. The variety of "normal" colors and patterns tempts me to simply "play" with that "morph" just for the sheer curiosity factor.

The original post asked the difference between dominant and co-dom. You explained the co-dom/incomplete dominance thing quite well, I was just adding the dominant explanation.
Katrina

Randy is right. Humans have between 20,000 and 25,000 gene loci, and snakes probably have a number not very far off that. Sequencing will ultimately tell us how many gene loci snakes have. Dozens must be involved in producing normal color. That is certainly true in mice, and mammals do not have all the pigment systems that reptiles do.

While Mendel would agree that the allele that we call normal at the albino locus is dominant to the albino allele, present-day geneticists would not. The pro fruit fly and mouse geneticists say that the normal allele is not a dominant or a recessive. It is the standard against which a mutant gene is compared to determine whether the mutant is dominant, codominant, or recessive to the normal allele.

There aren't any really good examples of dominant mutant genes in snakes. A good example in feral and domestic pigeons is the spread mutant gene. A normal pigeon has slate gray wings with two black bars on them, darker gray head and breast, a white rump, and a gray tail with a black bar across the ends of the feathers. The spread mutant gene changes the appearance of the pigeon to solid black. This is true whether there is a pair of spread genes or a spread gene paired with a normal gene.

I hope that the spider mutant gene turns out to be dominant to its normal allele. Then we might have a good example of a dominant mutant gene in snakes. But while spider seems to be some sort of dominant, it hasn't been proven a dominant, codominant, or somewhere between the two, yet.

Paul Hollander

It’s an interesting question on how to classify the "normal" copy of any particular gene.

I'm wondering if it should really be treated as a standard different from any mutant. I mean, long ago (hundreds of thousands of years?) the ancestors of ball pythons might have looked quite different and hence the "normal" copies of the appearance genes where different. I'm thinking what we now consider normal is just the conglomeration of mutant genes that are the best to come along so far for suitability to their current environment. What if it turns out that the spider gene isn't homozygous lethal and really does make a super snake that is even healthier and better feeding and in some significant way better suited to their wild environment. In a few millennia the "normal" ball python might have the spider mutation of the gene at that location. That's just an example as I doubt the brighter colors or higher appetite would necessarily be better for the wild although that gene has certainly been successful in reproducing/distributing it's self and gaining market share in the captive environment with different selection pressures.

So the Normal phenotype is simply the absence of any mutation? The resulting combination of thousands of genetic tumblers all dialed to the correct position? With no specific gene loci for "Normal"?

Chris
-----
"I don't know about you...but I find comfort in that." -- Cowboy

I would say that normal is a combination of the most advantageous mutations to come along so far. Basically the best setting of all the tumblers (appearance specific gene locations) for survival in the wild. Normal is definitely not a single gene. A normal has the normal versions of the pastel, stripe, albino, axanthic, clown, piebald, etc. (you get the picture) genes and probably also many other genes we don't yet know about due to a mutant version yet. In general each mutation is it's own gene and hence each has it's own normal version and all are necessary to be completely normal. However it's starting to look like there might be some cases where assumed different mutations are the same gene (lesser, mojave, and phantom for example).

"While Mendel would agree that the allele that we call normal at the albino locus is dominant to the albino allele, present-day geneticists would not. The pro fruit fly and mouse geneticists say that the normal allele is not a dominant or a recessive. It is the standard against which a mutant gene is compared to determine whether the mutant is dominant, codominant, or recessive to the normal allele."

Has this come about in the last 10 years? I will confess I haven't kept up in the last decade. Maybe my understanding of the terms "dominant" and "recessive" are a little outdated, but...

There are different levels of dominance/recessiveness. Take the human example: green eyes are dominant over blue eyes, but are recessive to brown eyes. That has been "proven out" in my own family.

With this in mind, how can a gene be neither? If you have a few links to bring me into the 21st century, I'd love to catch up on this concept.
Katrina

Wild type (AKA normal) is the phenotype that is the most common in the wild. Wild type genes are the genes required to produce the wild type phenotype. There is one wild type allele at each locus. And a mutant phenotype is the change from the wild type phenotype produced when one mutant gene replaces one of those wild type genes. IOW, there is one normal phenotype and many mutant phenotypes. If health is equivalent to the normal phenotype, then there are many different and unrelated illnesses that produce a change from health.

The fruit fly geneticists originated the wild type concept back in the 1920s. The textbooks have been a trifle reluctant to go much beyond lip service if they mention it at all. I did a quickie google seach using two key words -- genetics and "wild type" (include the quote marks when googling) and got over a million hits. Here is just one:

http://math.hws.edu/javamath/ryan/Genetics1.html

Another place is Wilmer Miller's web site. Go to the Contents page, find the "Science & ..." section, and click on "Advances in Classical Genetics". It was published in BioScience in 1995 under the name "Three Neglected Advances in Classical Genetics".

"Dominant", "recessive" and "codominant" either imply or explicitly make a comparison. Mendel made comparisons in a vacuum. It worked for his comparisons, but a standard phenotype and genotype becomes mighty handy when mutant genes at more than one locus affect skin color, for example. What is wrong with this? A snow ball python x albino produces F1 that are all albino. F1 x F1 produces 3/4 albino and 1/4 snow. Therefore, albino and snow are alleles. Albino is the dominant allele, and snow is the recessive allele. Text books make this sort of mistake commonly. It is hard to avoid when using strict Mendelian genetics and fairly easy to avoid when using wild type as the single standard of reference.

Standards are everywhere. The equator for latitude, the longitude that goes through Grenich over in Britain, gas milage for different types of cars, the foot, the meter, and on and on. Is 30 miles per gallon good gas milage or bad? It depends on whether your standard MPG is for an SUV or a motorcycle. Remember a few years ago when a Martian lander made a very expensive crater because one piece of guidance software was calibrated in feet and another in meters?

I will try to post another piece about wild type tomorrow.

Paul Hollander
http://www.ringneckdove.com

The following exerpt is from a paper about poultry genetics. But the same problem is present in ball pythons and other snakes, too.

Paul Hollander

-----------------

Wild Type as Standard in Poultry Genetics

R. George Jaap
Ohio State University, Columbus

and

W. F. Hollander
Iowa State College, Ames

Poultry Science 33(1): 94-100. 1954. (This exerpt is just the introduction to the paper.)

What is the color genotype of the Delaware breed? The answer, as best deduced from research reports and textbooks, seems to be "C C i i Al(Al) S(S) B(B) e e bl bl Mo Mo bg bg La La pg pg Sg Sg A A Pi Pi Pk Pk Rs Rs sd sd sp sp-- -- -- -- --etc." But is this satisfactory? Have we any hope that the vague ending will ever be completed? And is such complexity necessary?

For 30 years or more Drosophila geneticists have had a solution for such difficulties, yet none of the poultry geneticists such as Hutt (1949), Jull (1952), or Cock (1953) has used it. That solution was to specify in a genotype only the differences from a standard, namely the wild type. In this way, genotypes can be complete but brief. Using the red jungle fowl for our color standard, we may answer the query: "The Delaware has three pairs of non-wild-type genes, S(S) B(B) e e." Where it is necessary to show genes of the standard, it is the practice in Drosophila genetics to use simply " ", or the same letter as the "mutant" gene with a superscript.

This method was recommended in the genetics of mice by a committee headed by L. C. Dunn (1940). Although Hutt (1949) referred to this committee's report and suggested uniformity of gene symbols, he did not make use of this simple expedient of designating genes according to the deviations from a standard (wild type).

In our experience use of this approach has greatly simplified teaching both elementary genetics and poultry breeding classes. There is greater retention with less memorizing, and phenotypic effects from gene interaction have become more intelligible. The use of the method in the genetics of pigeons has been satisfactory (Levi, 1941). Use of a wild-type standard is desirable for identification of all genes; however, to limit the scope of this paper, we have chosen some of the better known color types of the domestic fowl, turkeys, ducks, geese, and pigeons.

For simplicity--the license of the elementary teacher--it will be assumed that the varieties are homozygous, unless otherwise noted. Probably some greater errors are included, since inadequate information and difficulty of interpreting some published reports have been handicaps. The actions ascribed to genes are, to some extent, our deductions and will need further examination for accuracy, or validity, and revision.

For each species we have chosen the wild type which seems to have contributed most to the ancestry of the domestic forms.

Familiarity with the wild type coloration is essential for its effective use as standard. It should be carefully examined--"memorized"--for purposes of comparison. Not only the adult but all stages of development should be included, as well as both sexes when dimorphism is present. Since the actual wild-type specimens are not easily available at present, domestic counterparts may suffice, as for example the ordinary bronze color variety of turkey.

The deviations produced by single genes (heterozygous or homozygous) may be used as indications of the action of such genes. For example in the chicken the "Silver" coloration of the silver gray or duckwing is produced by a single gene difference from the black-breasted red. The gene responsible, S, appears to cause failure of production of most red or yellow pigment (phaeomelanin). The S female however, has the salmon-colored breast like the wild type. The wild-type allele, s* (s with as superscript--PH), may be a vital link in the processes of complete phaeomelanin synthesis. This mode of reasoning is the same as that used for "biochemical mutants" in Neurospora (Beadle, 1945).

That excerpt was informative, Paul. Thanks for posting it