Genetics and complementation TBR ques

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viola101

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I need some clarification on complementation theory. this was from a passage in TBR


which of the following mutant type is incapable of complementation ?

1. Recessive mutations
2. Sex linked recessive mutations
3. Dominant mutations
4. Deletion mutations

the answer was 3. Dominant mutations. But I dont understand why having a dominant mutation would make a difference. If a mutant is recessive it will not produce the wildtype gene product but probably leave other parts of the chromosome functional. How does that differ with the dominant mutation. Ultimately its job also is to not make an essential protein product required by the cell. This should leave other regions of the chromosome functional so that complementation can take place if another mutant is involved?

I also dont understand how having deletion mutations would still allow complementation. Wouldn't the gene drastically in this case , thus making normal cell functioning implausible?

Could anyone please help me out here!!!!!!!!!!!
 
I need some clarification on complementation theory. this was from a passage in TBR


which of the following mutant type is incapable of complementation ?

1. Recessive mutations
2. Sex linked recessive mutations
3. Dominant mutations
4. Deletion mutations

the answer was 3. Dominant mutations. But I dont understand why having a dominant mutation would make a difference. If a mutant is recessive it will not produce the wildtype gene product but probably leave other parts of the chromosome functional. How does that differ with the dominant mutation. Ultimately its job also is to not make an essential protein product required by the cell. This should leave other regions of the chromosome functional so that complementation can take place if another mutant is involved?

I also dont understand how having deletion mutations would still allow complementation. Wouldn't the gene drastically in this case , thus making normal cell functioning implausible?

Could anyone please help me out here!!!!!!!!!!!

From your explanation, you don't fully understand complementation. Complementation is due to a different mutations of DIFFERENT steps in the same metabolic pathway. These are loss of function. The mutation is recessive to the dominant wild type allele.

A (enzyme 1) B (enzyme)2 Tryptophan

Now, let's say we have two species that both can't make Tryptophan. Now let's say species one has a mutation in the gene that makes enzyme one and Species 2 has a mutation that makes enzyme 2. When we cross these, it's possible that the offspring will each receive a good copy of enzyme 1 and 2 and thus COMPLEMENT each other and produce tryptophan.

The wording is key here. What TBR was referencing is that the mutation must be a loss of function, that is a recessive allele. The wild type is DOMINANT. They weren't referring to wild type. If the mutation were dominant then Complementation would NOT be possible.

In closing, you only missed this because you didn't answer what they wanted. You are correct in that the wild type allele in these is dominant. However, complementation involves recessive mutations and TBR was talking about the mutations. HTH
 
thanks for the input PhilIvey!

I guess what I am unclear about is the statement that when there are dominant mutations complementation does not work.

For instance , if a mutation is dominant and the alleles A = disease
a = wildtype. then combining two mutants to see if they complement each other would show that we have a smaller probability for coding the functional protein.
cross
(mutant 1) AA/Aa + (diseased mutant 2) aa -----> Offspring are either
Aa or aa

If we were talking recessive mutation, then technically the heterozygous alleles would still work to give us a functional protein code (because A wildtype doesnt induce loss of function).

But if the mutation is dominant then having an A (either homozygous or heterozygous) would yield a defective protein code. so the probability to be diseased increases. That doesn't mean it cannot happen though. As indicated above, we could still end up with " aa" offspring, that would be perfectly functional.


So why do we say that complementation doesnt work in dominant mutations?
 
Complementation involves mating two specimens that both express a mutation but the mutation is caused by two different gene locations. If complementation is present, then one of specimens exhibits the mutation on one gene loci and the other will exhibit the mutation at the other gene loci:

Note: + is wild type.

a/a;+/+ mates with +/+;b/b.

Gametes will be:

a;+ and +;b

These will fuse to create offspring with:

a/+;+/b

The wild type would be expressed in this end result if it is a recessive mutation. But if the mutation is dominant to the wild type then the wild type won't be expressed and no conclusion can be made as to whether complementation exists or not.
 
that was really helpful, thanks jeff0106!

Your welcome.

Also, about the deletion mutation, as long as the deletion is a multiple of 3 and not too large, the organism can survive. So just treat it as the recessive mutation because in both cases, something isn't being coded for.
 
yes, about the deletion sequence: it would only affect 1 mutant allele (in the case of complementation) so the other mutant would provide the healthy wildtype allele for the functional protein. So the ques gives us room to think that this mutation could be either recessive or dominant. So this possibility could work.

I guess this theory was confusing because I was bringing heterozygotes into the pic. Instead of thinking aa/++ vs ++/bb i was considering this
a+/++ vs ++/ b+ to be the parents and then figuring out the offspring's alleles would be too complicated.

So the general consensus then is when faced with complementation, assume wildtype is homozygous dominant...or so i think!
 
what about sex linked? wouldnt that be incapable of recessive complementation in males cuz we only have one X chromosome... but maybe in females it could complement...

And dominant is the answer because the dominant phenotype will be expressed over the recessive wildtype if you cross dominant mutant and recessive wildtype because the dominant mutant phenotype will be expressed regardless. The idea behind complementation is turning a homozygous ind. into heterozygous ind. F1 and reinstating wildtype function with the development of heterozygosity (dont know if thats even a word) in the offspring.

so dominance can be between alleles as well as between copies of alleles... is that right? im not sure im just guessing
 
Don't make this more complicated than it is.

Complementation is simply this: 2 species that are homozygous mutants that produce the same phenotype, but when crossed the wildtype can be restored.

Simple example:

Fly A -- BLIND
Fly B -- BLIND

Cross Fly A and Fly B -- CAN SEE

It is that simple. Now obviously we are referring to a gene that is causing sight.

The simple reason the answer is what it is:

Dominant mutations, BY DEFINITION, can't complement. They must be recessive. Why?

Lets say BLIND gene 1 has a mutation that lowers protein expression, or the protein's new function is not deleterious to the organism, it just can't do its normal thing. BLIND gene 1 could then be recessive.

Lets say BLIND gene 2 has a mutation that causes a new SUPER protein that actually destroys your eyes. That would be a dominant mutation, why? Because when it is around it absolutely obliterates the eye. Obviously when you cross this SUPER protein with anything else, it will not lead to sight because its existence OWNS the eye. It is a dominant mutation and therefore can't complement another blind fly.
 
what about sex linked? wouldnt that be incapable of recessive complementation in males cuz we only have one X chromosome... but maybe in females it could complement...

And dominant is the answer because the dominant phenotype will be expressed over the recessive wildtype if you cross dominant mutant and recessive wildtype because the dominant mutant phenotype will be expressed regardless. The idea behind complementation is turning a homozygous ind. into heterozygous ind. F1 and reinstating wildtype function with the development of heterozygosity (dont know if thats even a word) in the offspring.

so dominance can be between alleles as well as between copies of alleles... is that right? im not sure im just guessing

The key here is sex linked genes possibly can complement.

A woman with: INFERTILITY gene could cross with her husbands X chromosome that had the same INFERTILITY gene and then come out wildtype (or FERTILE).

If you can prove it wrong then it isn't true. Plus sex-linked genes is just a throw off answer, the idea of complementing is crossing to restore wildtype. Sex-linked or not has NOTHING to do with it, the mutations would need to be dominant or recessive. Does it make sense why? You could have a dominant sex linked gene or a recessive sex linked gene. It doesn't address the question.
 
what about sex linked? wouldnt that be incapable of recessive complementation in males cuz we only have one X chromosome... but maybe in females it could complement...

And dominant is the answer because the dominant phenotype will be expressed over the recessive wildtype if you cross dominant mutant and recessive wildtype because the dominant mutant phenotype will be expressed regardless. The idea behind complementation is turning a homozygous ind. into heterozygous ind. F1 and reinstating wildtype function with the development of heterozygosity (dont know if thats even a word) in the offspring.

so dominance can be between alleles as well as between copies of alleles... is that right? im not sure im just guessing

Be careful with your language.

There is no dominant phenotype. There is a phenotype. It is what we see.

recessive wildtype
Wildtype is the original state, before the mutation. Again, not talking about dominant/recessive.

the
"dominant mutant phenotype"
....

again be careful with the language. The dominant mutation leads to a certain phenotype. The dominant mutation causes a particular phenotype always because it is dominant, in other words, its existence dictates the phenotype.

The idea of complementation is NOT making an organism heterozygous. Don't make it more than it is.

If we can restore wildtype via a cross, the genes complement. That is it.

Haploid genomes can complement. They do not need to be heterozygous anything to complement. They just need to complement.
 
I need some clarification on complementation theory. this was from a passage in TBR


which of the following mutant type is incapable of complementation ?

1. Recessive mutations
2. Sex linked recessive mutations
3. Dominant mutations
4. Deletion mutations

the answer was 3. Dominant mutations. But I dont understand why having a dominant mutation would make a difference. If a mutant is recessive it will not produce the wildtype gene product but probably leave other parts of the chromosome functional. How does that differ with the dominant mutation. Ultimately its job also is to not make an essential protein product required by the cell. This should leave other regions of the chromosome functional so that complementation can take place if another mutant is involved?

I also dont understand how having deletion mutations would still allow complementation. Wouldn't the gene drastically in this case , thus making normal cell functioning implausible?

Could anyone please help me out here!!!!!!!!!!!

I want to quickly walk through your logic.

If a mutant is recessive it will not produce the wildtype gene product but probably leave other parts of the chromosome functional.
The mutant by definition here, is producing a certain phenotype. Thinking about other regions of the chromosome is making big assumptions. We don't know if this is a gene that has 50 copies in the genome or only 1 copy. If there is only 1 copy then the rest of the chromosome is irrelevant.

How does that differ with the dominant mutation.
The difference is that the dominant mutation is causing something new to happen. Example like I said before, dominant mutation causes new SUPER protein that starts killing eye cells. Its existence when crossed with anything will lead to killing of the eye cells, or a blind phenotype. MUCH different than having a recessive mutation which doesn't actively cause deleterious effects phenotypically; AND when crossed with a functional copy can restore wildtype.

Ultimately its job also is to not make an essential protein product required by the cell. This should leave other regions of the chromosome functional so that complementation can take place if another mutant is involved?

Who said its job is to make an essential protein product? Define essential? Like, if you don't have it you will die? This is going too deep into a question that is just testing if you know a simple idea:

Can I cross this mutant with another one (same phenotype) to restore wildtype. That is it.

Other regions of the chromosome have NOTHING to do with this question.

Also, you don't even know if the genes are on the same chromosome. It has nothing to do with the idea of complementation.

I also dont understand how having deletion mutations would still allow complementation. Wouldn't the gene drastically in this case , thus making normal cell functioning implausible?

deletion mutations again have nothing to do with the idea. If a deletion causes a recessive trait OR if an insertion causes a recessive trait, it doesn't matter. It could be an inversion, or a transversion or a transition. Whatever it is, it needs to cause a recessive trait. Then you need to make sure the organism is homozygous recessive OR that it doesn't have a working copy of the gene. Now we find another one with the same phenotype.

Now we cross then and try to restore wildtype. See? Nothing to do with what caused the mutation but instead what type of mutation it is.

side note: although rare, a deletion could cause a dominant mutation leading to a new phenotype. It doesn't tell us what the mutation is doing but instead how it arose.
 
hmm...
why have never encountered complementation in my EK Bio??

I'm a little worried. How relevant is this topic?
 
hmm...
why have never encountered complementation in my EK Bio??

I'm a little worried. How relevant is this topic?

not sure. I'm just taking a genetics course, I bet they would explain it if it came up. It is a very simple idea even though by reading this thread it doesn't seem to be.
 
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