naita:
But is that statement really accurate that if you have one copy of the gene for brown eyes, then you will necessarily have brown eyes? I don’t think so the more I read on the subject
If two blue eyed parents have a child with brown eyes then obviously they had a copy of the brown color gene but still themselves had blue eyes.
http://genetics.thetech.org/how-blue-eyed-parents-can-have-brown-eyed-children
As Blake said, there are complexities, but blue eyes is recessive to brown is still close enough. Your latest page explains how, in unusual circumstances, it’s still possible for two blue eyed parents to have a brown eyed child. But that is a quite rare event. Much more common is for brown eyed parents to have a blue eyed child, but no matter which of the genes in question we then look at, this will then still be a case of them being carriers of genes that can give blue eyes.
Let’s back up a bit. This is my area, and I think I can help.
First, a definition. As has been covered already, we have two copies of every gene. One from mom, and one from dad. Sometimes, genes can come in different “flavors”, or alleles. Sometimes, different alleles can be responsible for different versions of a trait. Let’s stick with a hypothetical for simplicity’s sake, and say that there’s a gene that codes for fur color. Two alleles exist that make your fur either white or black, respectively.
Sometimes, it’s possible for an individual to be born with two different alleles. Say a white mom and a black dad mate and the offspring has a white allele and a black allele. We would call the offspring a heterozygote, because he is heterozygous for this gene. It is impossible* for the fur of the offspring to be both white and black at the same time. So what do we get? Let’s say the offspring turns out to be white. If heterozygotes are white, then white is dominant and black is recessive. Black is “hidden” by white in heterozygotes.
That is the sum total of what we mean by dominant and recessive: which trait we see in heterozygotes. You cannot conclude ANYTHING more about the alleles beyond that. The earlier statement that all recessive alleles are nonfunctional is flat-out wrong. You can also not conclude that the dominant allele is more common in the population, which is another common misconception I see all over the place.
What makes a dominant allele dominant? That’s complicated. It all boils down to the biochemistry and molecular biology of the genes and proteins involved. What happens when you’re making two different versions of the same protein? Of if you’re only making half as much as usual? What does that do to the cell and to the organism? Every gene and every allele is a different story. It’s too complicated even to be able to predict - even today, we have to just make the heterozygote and see.
All right. So let’s move on and talk about hair and eye color. So far, we’ve stuck to Mendelian traits (i.e., similar to those traits studied by Gregor Mendel, who figured this all out in the first place): the trait is controlled by only one gene, and only two alleles for that gene exist. Eye color is far more complicated. It is a multigenic trait: there are multiple genes involved in the pathway that makes eye pigment, and for every gene, multiple alleles exist in the world.
When people talk about blue eyes being recessive to brown (and, incidentally, “dominant” and “recessive” are relative descriptors, not absolute. One allele can only be described as dominant TO another allele.) they’re simplifying this complexity. You can imagine two people that are identical at all of the eye color genes except one. At that one gene, we can consider just two alleles, one that produces brown eyes and one for blue. We’ve ignored most of the pathway and reduced the situation to a single Mendelian trait. We can then determine that at that one gene, the brown allele is dominant to the blue allele. Generally speaking, if we do this for the entire pathway, we find that overall, darker color alleles tend to be dominant over lighter color alleles. But when we consider the whole pathway overall, as we’re shuffling many genes and alleles from generation to generation, even though each individual gene acts in a simple Mendelian fashion, the mixing of genes means that we can get some surprising results, and that eye color as a whole tends to be hard to predict in many situations.
Hopefully that makes some sense.
*Not really - other options exist, like stripes or splotches or grey fur, but those are non-Mendelian situations, and we’ll ignore them for now.
Okay, here’s a slight hijack of a question. Suppose a Nordic woman, blonde, blue eyed, born into a long line of similarly described people, marries a man from an African-American family who is light-skinned enough to be totally “passing” for white as an adult. Could they have a child with dark chocolate-brown skin?
This was a plot point on a recent Law and Order rerun I saw the other day, and I think it’s at the very least extremely unlikely. In the story, one’s first guess is that she had an extramarital affair with a dark-skinned man, but the husband was confirmed through blood tests to be the biological father.
Biologically possible, but extremely unlikely. And the longer that line of “similarly described people”, the lower the odds get.
In simple terms, this requires that the (multiple) genes for dark skin entered the lineage at some point, and in every generation every single one of those multiple copies was passed on.
If we assume even 4 genes controlling skin colour, the chance of the F2 generation receiving all 4 copies is only 6%. The chance of the F3 only 0.3%, the F4 only 0.02% and so forth. So even if a 25 yo woman’s great-great-Grandfather (who would have married into the lineage about 1940) was a full-blooded Zulu, the chance of the child being chocolate brown is at best one in 5000.
Since you say a long lineage and we have to assume that someone marrying a black person on the 20th century would probably be known by the family, we have to assume the ancestor was even more remote and/or wasn’t obviously Black. in that case the odds drop off to less than one in a million.
So it’s still possible, but so ridiculously unlikely that it becomes more than a little contrived.
That’s exactly what I thought.
Of course, there’s also always the possibility of a novel mutation. And the odds improve considerably if both of the parents are interracial rather than being Nordic-white for many generations.
There was no history of hemophilia in the royal family until Queen Victoria’s offspring were born. Either she or her mother had a mutated gene for that result.
Similarly, there was no history of albinism in Johnny & Edgar Winter’s family, yet they both were born with that gene.
Genetics is not an exact science.
That makes it even less likely, not more.
Your examples are single gene mutations. To produce chocolate brown skin you need multiple genes. We don’t know how many, but at least 4. The chance of 4 mutations for dark skin spontaneously arising and being passed on through multiple generations is a million-fold *less *than the chances of the genes being inherited and passed on. The chances of multiple genes spontaneously mutating towards dark skin in one generation is less so remote as to be science fiction.
Putting this circumstance into a simple dominant/recessive paradigm is not appropriate. Rather this section of chromosome 15 (15q 11-13) is showing non-Mendalian inheritance patterns due to genomic imprinting.
It is not the defective gene that turns off the allele from the other parent. The genomic imprinting happens regardless of whether there is a defective allele or not. But this imprinting, by silencing one allele, can allow a disease state to manifest if only the defective allele is left active.
Net result, it can seem as if Prader Willi is a dominant condition if the defective allele is inherited from the father and recessive if inherited from the mother. And conversely Angelman Syndrome can seem as if it is a dominant condition if inherited from the mother and recessive if inherited from the father. But since both the maternal and paternal alleles are not both active it is improper to say that one is dominant over the other.
Further PWS and AS need not arise from a spontaneous mutation. Indeed most of the time they do not. The trait can simply be passed on from an unaffected parent of the appropriate gender.
Suppose a man received a defective allele that corresponds to PWS from his mother. The defective allele is silenced by genomic imprinting. The man then has children. (Assume the mother of his children has two normal alleles.)
The man has a 50% chance of passing along the defective allele. He would not be affected. But he could pass that on to his children. Any of his children receiving the PWS allele from him and a normal allele from their mother would have the PWS condition as the maternal normal allele is silenced by genomic imprinting.
Thanks guys for proving my point that most biologists have trouble recognizing the obvious, and drown in esoterics. We get the same in academic engineering. Some have striven to turn simple structural analysis into something akin to general relativity, terming it “continuum mechanics”.
My main point is that students would surely understand better if the basic idea “recessive = no information” were offered. This guy figured it out the same as me and Cecil Adams: Explained: What Makes A Dominant Gene Dominant? — Dominant and Recessive Traits, Demystified
Just a few tidbits re above you can research more:
A defective gene or “weak trait” is the same/similar to “no information”. Call it “nothing useful” or “ineffective”. I did find an old Cecil Adams article where he stated exactly that (can’t find it today).
Curly hair is dominant, according to http://www.blinn.edu/socialscience/ldthomas/feldman/handouts/0203hand.htm Others say several genes are involved. Regardless, it seems to take information to curl the hair.
Regardless, the child’s traits are usually simply a mixture of both parents traits. That is why children of Northern European - African usually have light brown skin and hair with large curls. Of course, it is more complicated, such as some genes are carried on chromosomes that only one sex has or even in mitochondrial DNA (comes only from the mother).
When I said “all babies are born w/ blue eyes”, I meant even African babies. At least, that is what I have heard, and I could hardly tell my newborn from the African-American babies in the hospital, but let someone who works there comment. Blue eyes is not exactly “nothing”, it is just “weak”. It apparently gives some pigment since true recessive is albinism and they have pink eyes. Again, all is a mixture. Some have light brown, hazel, or green eyes (Afgan girl on National Geographic cover).
Of course, A-A’s are hardly pure African anymore. BTW, please don’t fault me in the future if some decide to change the term again and claim “A-A” is now offensive. BTW, I used to throw off students by mentioning that the darkest skin people are actually caucasian - Tamil’s of southern India. That always came up during discussion of “black-body radiation” in Physics, when students always giggle. Even more where I taught at a historically-black college.
Many linguists have commented on the more complicated sounds of SW Africa. I was just relating common knowledge. I am sure this is in the general media - Nova, Scientific American, …
Finally, on a related note, many say that to really understand a culture, you should move there and live with the people. Go even further - make babies with them. That serves science. I did so, marrying a women from the opposite side of the world. My kids wonder why I often observe them closely. Just performing “field research”. I still try that line on my wife when feeling amorous, though past the child-bearing years.
A statement cannot help students understand things if the statement is not true.
Here’s a pair of posers for you: The gene for malarial resistance is dominant over the gene for malarial vulnerability: That is to say, a heterozygote for that gene will be resistant to malaria. Based on this, would you say that malarial resistance is more or less information than malarial vulnerability?
Meanwhile, the gene for sickle cell disease is recessive to the gene for normal hemoglobin: That is to say, a heterozygote for that gene will have healthy blood. Based on this, would you say that sickle cell is more or less information than healthy blood?
Now reconcile your answer to both of these questions with the fact that those are actually the same gene.
Definitely NOT true that all babies are born with blue eyes. My nephew, to take one personal example, had dark, dark brown eyes at birth. Any African inheritance in our family would have been farther back than the 1300s, and we have the geneology records to prove it.
MLS, Perhaps it depends on how late-term the baby is at birth as to whether the iris has yet turned dark. I have heard that African-American babies have blue eyes initially, but one can never say “always”. Someone with more data can chime in.
Chronos,
From what I have read, the tendency for blood cells to “sickle” is an adaptation to fight the malaria parasite, which sounds like something that would require more information, hence a dominant trait. Unfortunately, evolution doesn’t always lead to a globally optimum solution. The downside is that when one inherits too much of the trait (from both parents), they can suffer “sickle-cell anemia”, which happens when the cells sickle even when not helpful. In the best scenario, they sickle only when infected by the parasite (thus killing it). An intelligent designer might have come up with a better solution. I recall an article that calculated the benefits (protects 50%) out-weigh the downsides (25% sickle spontaneously, 25% un-protected) in a simplistic scenario.
I understand that even Mediterranean people have this and similar “tropical” traits. The TV show MAS*H had an episode where an Italian soldier suffered from a new drug that was thought to only adversely affect Africans (historical truth). Might have been a sickling thing, I forget. You can find much better info than I can recall in old Scientific American articles and such.
Sigh…
Terms such as “weak trait” or “no information” have no meaning.
There are dozens of identified alleles at the CFTR locus. A few are terminated transcripts, but most make a protein with differing permeability to the chloride ion. In the heterozygote state this confers some selective advantage in populations exposed to cholera and other diarrheal diseases.
To say that such recessive alleles are ineffective, weak, nothing useful and so on presupposes that the gene has a particular purpose. Evolution does not work that way.
Pointing out that what you have posted is incorrect on every level is hardly “drowning in esoterics”.
No. A student doesn’t understand somehting if they don’t even know about it. What you are proposing is that we teach children that babies are delivered by the stork because that way they will understand it better. That’s just plain wrong. When you don’t know about something, you don’t understand it. When you think you understand something because of an incorrect explanation, you don’t know about it.
There is no such thing as a “weak trait”. It’s a meaningless term. “No information” does have a meaning, but it does not mean what you think it means. I think you should stop using those words. A “Stop” sign contains information, despite the fact that you seem to think that it does not.
As already pointed out to you, this is just flat out wrong. The O blood group is very useful and highly effective in coping with parasites. In no possible sense can it be described as “nothing useful” or “ineffective”. The O blood group is just as effective and just as useful as A or B.
What you just don’t grasp is that it also takes information to straighten hair. You are arguing around in circles here by trying to claim that recessives traits contain no information, and that you can prove it because X is a dominant trait, and so it must require information.
That’s a massive logic fail.
No, that simply isn’t true.
This directly contradicts everything you have posted so far. If the European features are just “no information” then how can the child possibly have skin lighter than the negro parent or hair less curled? A total absence of information can’t result in phenotype change.
So which is it? Is it “nothing useful”, "ineffective and “no information” or is it “just weak”.
You claim that this explanation somehow clarifies the situation for students, but you keep contradicting *yourself *when you try to explain it.
But you have been stressing that recessive genes carry no information at all. Your entire position depends on it. So where does this “some pigment” come from if there is no information for pigment?
Once again, you are contradicting yourself and demonstrating that your easy to understand explanation is impossible for even you to understand.
It’s not hard to throw off students by lying to them.
If you are sticking to a racial classification scheme that includes “Caucasian”, then dark skinned Tamils are not Caucasian, they are Australoid. And they are not the darkest skinned people. That distinction belongs to groups within Africa and Australians. Even the darkest Tamil isn’t anywhere near the extremes of human pigmentation.
A good example of why people should only teach in areas where they have actually been trained.
Then provide some references from those sources.
But none of that answers the question you were asked: which trait is recessive and contains no information and which trait is dominant and carries information? If the gene for malarial resistance the result of information, or is it the result of no information? Is sickle cell dominant or recessive?
The amount of bluster you had to put in to avoiding answering this questions shows, once again, that you can’t even explain your “simplified” explanation without confusing yourself.
Blake,
You are ranting and your intent appears more to stifle discussion than add to it. You haven’t contributed to answering the simple question posed of why some traits are dominant and some are recessive. You basically say, “too complicated to explain”. I explained it clearly and simply for many common traits, as did Cecil Adams and the link I posted.
I will re-state (a little more exact and wordy) just for you - The child gets a mixture of traits from the parents. Traits that are “ineffective” (worst-case being “nothing”) are over-shadowed by a “stronger” trait (or at least “something”). A simple physical example is if you mix clear water and water w/ dye the result is water with dye. Not as dark, but still “dyed”, if that is a yes/no result you require aka Medelian genetics.
I have read that Tamils have the darkest skin of all “races”, but there is no such thing as “race”, i.e. no trait specific to any group of people. Simpletons point to skin color, mostly in the U.S. South where pasty northern Europeans came together w/ Africans (not by choice), so skin color was very noticeable. But, that is probably the least signficant since all races have dark-skinned people. Skin cancer quickly imposes that as people migrate to the equator. I have read of Indians being lumped with Caucasians. Other than dark skin, they look more like Europeans than Melanesians to me, but you be the judge. Migration of pre-historic people is an active area of study. It was recently shown that people did walk around the coast from Africa to populate the East Indies, based on chromosones of one man found on the coast of India. Anyway, my comment was obviously to stimulate thought than set off experts like you.
I did explain that the tendancy to sickle appears to be a dominant trait (requires “something” or at least more of it). I also paraphrased an article about it I recall, probably from Scientific American. Good luck researching that and let us know what you find.
Maybe the clear liquid is making the dye “weaker”, so it’s actually stronger.
Still getting it wrong.
Sickle cell disease follows an autosomal recessive pattern of inheritance.
Cite from National Library of Medicine of the National Institutes of Health
Sickle cell trait is due to a single nucleotide polymorphism at chormosome 11p15 causing a change in the hemoglobin protein so that it may polymerize in low oxygen conditions.
That is not what I said, nor did the article I read (Scientific American). I said that the “tendency to sickle” is a dominant trait. If you get it from either parent, your blood cells will have the ability to sickle, thus helping protect you from the malaria parasite. Please read and understand this before proceeding.
The “disease” (bad inheritance, whatever you want to call it) comes only when a child gets the sickling trait from both parents.
If you live in malarial lands (before modern medicine), it is also bad to not get the sickling trait from either parent, because then you are unprotected.
It may not be that simple. There may be various levels of “sickling tendency”. The article I read simply analyzed it with simple yes/no statistics. For more info, google it, but it was ~20 years ago (pre-internet when much didn’t get uploaded).
Certainly, dominant and recessive is too simple to be the full story. Everything is a mixture. But, it is the simple explanation that Mendel used and a fine start for 9th-grade biology. So why can’t the books state it? Are all biologists really that clueless?
Why does it matter? There are many diseases (better termed “conditions”) that are inherited. Many show “recessive statistics”, which leads us to suspect “something is missing” or “not enough”. An example is that it was recently found that many people have the genes to fight off breast cancer without any treatment, because they have multiple repeats of a gene sequence that seems to give the ability to fight it. Others with only 1 or 2 repeats, need aggressive treatment to have even a hope of survival. But, as the “sickle cell anemia” example proves “recessive statistics” can be caused by a dominant trait (too much of something), so simply noting dominant vs recessive doesn’t always help. In the end, you must dig into the details to find a cure, but I would first look for “something deficient” when the statistics are recessive. I hope this helps. I am just an engineer, and you guys are declared experts.