Thread: Dominant/Recessive traits?

What makes certain physical characteristics dominant over another (what's called a recessive trait) when their only defining characteristic I'm aware of is their preponderance in human populations as a whole. How is it inferred that a dominant trait would necessarily be dominant over a recessive trait? Look at this picture I came across the internet of a mixed-background couple. Take into account that I don't know much about genetics, I'm just an amateur observer curious about these terms.

Dominant and recessive can be often be as simple as the presence or absence of a particular gene product.

So, for example, imagine a simple plant that had red-coloured flowers. If the gene encoding the red pigment was faulty then there would be no red flowers; perhaps they'd be white instead. If you then mate this white-flowered plant with a red-colured plant then the offspring will all be red since the missing gene product is supplied by the other parent. We could say that the red trait is dominant over white. This is not to say that red is superior in any way, just that the white trait in this case is defined by the absence of something - a pigment. (I cut some corners with this example, to illustrate the point).

Real world examples can obviously be a lot more complicated.

Dominance and recessiveness can also be detected by looking at the pattern of expression of a trait in a population - if a man with black has children with a woman with blonde hair, and all their children have black hair, it's possible black is dominant to blonde. The more examples you have that show this the more likely this is to be true. And then if one of those black haired children mates with someone who is blonde, and approximately 1/4 of their offspring are blonde, this also makes it more likely, because the recessive allele from the black haired child met one of the two recessive alleles in his/her blonde mate.

As to knowing exactly how one dominates the other, as Zwirko said, will vary from gene to gene.

twain, I suggest you get your hands on an introductory genetics text book. You can get a used one for a decent price and it will clarify a lot of these basic issues for you quite nicely.

many traits are the result of a set of genes/genetic regulators.

So don't try to focus too much on the simple picture. It's only valid in a minority of the cases, although these are usually the ones ending up in text books for the simple reason that they are simple.

Originally Posted by spuriousmonkey

many traits are the result of a set of genes/genetic regulators.

So don't try to focus too much on the simple picture. It's only valid in a minority of the cases, although these are usually the ones ending up in text books for the simple reason that they are simple.

That's a good point, true Mendelian inheritance is pretty uncommon.

Originally Posted by paralith

That's a good point, true Mendelian inheritance is pretty uncommon.

Did Mendel just get lucky then, or did he know in advance what he was looking for? I recall some statistical analysis a while back that suggested the numbers he came up with were too close perfect to likely have been arrived at by chance. Could his selection of variables that turned out to be controlled by a single gene have been influenced by a prior strong suspicion that these were the such characters?

Originally Posted by John Galt

Originally Posted by paralith

That's a good point, true Mendelian inheritance is pretty uncommon.

Did Mendel just get lucky then, or did he know in advance what he was looking for? I recall some statistical analysis a while back that suggested the numbers he came up with were too close perfect to likely have been arrived at by chance. Could his selection of variables that turned out to be controlled by a single gene have been influenced by a prior strong suspicion that these were the such characters?

Yes, it was largely a combination of luck and the fact that he noticed bimodal traits in the pea pods. Before he started his crosses, he bred straight lines for a single trait for a long time to make sure they were "pure."

I've also heard some rumors that he may have "tweaked" his results. Experimental rigor wasn't quite as important as it is now.

Have one too many tall stalks and not enough short ones? Just *snip*, and there you go So I think he had a preconceived idea of what the "correct" results were, which sort of biased how he ran the experiment. Especially on subjective traits.

Originally Posted by John Galt

Originally Posted by paralith

That's a good point, true Mendelian inheritance is pretty uncommon.

Did Mendel just get lucky then, or did he know in advance what he was looking for? I recall some statistical analysis a while back that suggested the numbers he came up with were too close perfect to likely have been arrived at by chance. Could his selection of variables that turned out to be controlled by a single gene have been influenced by a prior strong suspicion that these were the such characters?

Mendel was actually very unlucky. You see, Mendel was a true believer. He didn't like his results at all on the peas.

There is a reason Mendel's laws were 'discovered' in the 1900s instead of at the publication of Darwin's evolution theory. We would think that his work was essential to Darwin's theory since it would suggest a mechanism.

But apparently a whole scientific community thought otherwise back then. Were they stupid?

Of course not. We are stupid to think people back then were thinking the same as we are.

So what were they thinking?

One thing is certain. You can't find a single thing on the hypothesis of paired alleles in his work in any form whatsoever. That is purely our modern interpretation. Some may claim it is obvious, but apparently not even Mendel noticed it. Or the other scientists who read his work back then.

Mendel was actually thinking in terms of inheritance by 'elemental'.

So he would describe a dominant trait as capital A.

But what for heterozygotes and recessive homozygotes. Did he write Aa and aa?

No. He wrote A or a.

No coupling of traits whatsoever in his work. He just didn't see it, nor did anyone else at the time.

At one point in time Mendel switched to another plant (Hieracium). It is claimed that the famous biologist Nägeli instructed him to do so and that this caused Mendel to be led astray.

Was this really the case? Interestingly there is no mendelian inheritance in this plant due to its genetic characteristics.

Was Mendel disappointed?

Absolutely not. Mendel was part of a very contemporary group of researchers who were interested not in inheritance theories, but the question of the formation of new plant species in nature.

Mendel actually was doing this as an alternative to the evolutionary theories. All species are created by God. Evolution is one theory that explains the emergence of new species. What mendel was doing was the opposite.

He was looking into the matter of crosses producing new forms, and hence 'species'. Perfectly compatible with religion since the new forms were just the result of crossing the existing creation. God could allow for that.

His pea work didn't get him any decent results on this theory. His crosses didn't give him new forms after all that remained stable after crossing them again. But once he switched he was a happy chappy. His new plant species generated lots of new forms, some of which seemed almost stable. Imagine his joy.

His work was therefore rather boring and normal for his era.

The true biologists here can correct me on the details of this one but my understanding is that, in their expression within the cells, it's simply that both the dominant and the recessive allele have their proteins (or whatever) constructed, but it's just that those produced by the dominant allele tend to be the ones that make a difference. If I haven't made myself too clear, consider my favourite example - blood groups.

Traditionally, we think of four different blood groups/type:

A
B
AB
O

In fact, given that there are two of each, the real types are:

AO and AA (both expressed as A)
BO and BB (both expressed as B)
AB (one each of A and B)
OO (both are O)

Here’s the thing: O was so-called more for zero than the letter O, because that blood group does not produce a certain marker protein (call it an antigen if you will, because that’s how it acts in certain circumstances).

Those with the allele for A (one or two copies), produce a certain version of this protein. They do not, of course, react to it themselves, but if blood containing this protein is transfused to anybody without the A allele, then it will be treated as an antigen and attacked – hence the dangers of cross-transfusion.

Those with the allele for B have the same situation, but with a different variant on that protein (which may provide some mild protection against malaria, hence its preponderance in South Asian populations).

Now it is possible to have one A and one B allele, in which case BOTH protein variants will be produced and neither will be treated as an antigen. That’s why AB is called the “universal recipient” – no other blood (within the ABO scheme) can cause an antigenic reaction.

Since people with the neutral blood type, O, do not produce any such protein, whenever they encounter it – either A or B type protein – they treat it as an antigen, which is why people with blood group O (OO actually) can only receive blood from others with O. BUT, as O itself produces no such protein, none of the other types ‘see’ an antigen to react to, hence O’s ability to be the “universal donor”.

If you know your blood group and those of your parents, it is frequently possible to tell more exactly what yours is. For instance, if your father types as B, your mother as O, and you as B, then your are guaranteed to be BO (though you cannot tell whether your father is BB or BO).

I don’t know if this helps explain the differences, but in this context you can see O as the recessive allele inasmuch as both A and B show as the type in people with the AO or BO combination, and therefore the O in that combination remains invisible to tests for blood group. Therefore A and B are dominant and, since both proteins ‘show up’ to other blood types and on our tests, they are co-dominant: Mendelian with a twist!

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shanks