What makes an allele recessive, dominant, or codominant? Watch

futuredoctorVSB
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I've tried searching, but no real good explanations found. I know the effects of the different allele types, but why are they different in the first place?

My hypothesis is that dominant alleles produce proteins that are specific to recessive allele mRNA, and destroy it (preventing recessive allele expression).

And in homozygous recessive, the recessive allele is expressed, since, there is no protein present to break it down?
Same with codominant alleles?

I know my theory is far fetched, but could someone please clarify the actual mechanism for me?
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Revenged
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recessive, dominant, codominant - are terms used most often as the phenotype that you see. the turns were invented before information of genetics was know. they do not relate to the expression of the genes. dominant and recessive allels are expressed into proteins, it is just that some do not have visible outcomes.
most traits are influenced by a number of genes (so unlike sickel cell it is more complicated)

if you take sickle cell disease, a classic 'autosomal recessive' condition caused by only one gene.

'Normal' people (SS) inherit - 2 'dominant' (s) alleles - they synthesis proteins that cause normal 'disc' shaped red blood cells

'Carriers' (Ss) inherit - 1 dominant (S) and 1 recessive (s) - they synthesis some normal disc proteins (from the dominant allele) and some sicke red blood cells (from the recessive allele)

'Suffers' (ss) inherit - 2 recessive (s) - they synthesize sickel shaped blood cells (from the two recessive) - they have sickel cell disease

[the condition is maintained in the population as carriers have a protection against malaria. this is why you only get sickel cell disease in places where malaria is present (excluding travel), it has evolved out in other places]
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futuredoctorVSB
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(Original post by Revenged)
recessive, dominant, codominant - are terms used most often as the phenotype that you see. the turns were invented before information of genetics was know. they do not relate to the expression of the genes. dominant and recessive allels are expressed into proteins, it is just that some do not have visible outcomes.
most traits are influenced by a number of genes (so unlike sickel cell it is more complicated)

if you take sickle cell disease, a classic 'autosomal recessive' condition caused by only one gene.

'Normal' people (SS) inherit - 2 'dominant' (s) alleles - they synthesis proteins that cause normal 'disc' shaped red blood cells

'Carriers' (Ss) inherit - 1 dominant (S) and 1 recessive (s) - they synthesis some normal disc proteins (from the dominant allele) and some sicke red blood cells (from the recessive allele)

'Suffers' (ss) inherit - 2 recessive (s) - they synthesize sickel shaped blood cells (from the two recessive) - they have sickel cell disease

[the condition is maintained in the population as carriers have a protection against malaria. this is why you only get sickel cell disease in places where malaria is present (excluding travel), it has evolved out in other places]
I get that, but what makes something dominant over something else?
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Larynx.pharynx
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It depends on what protein the gene codes for, and what it does. In the case of diseases, it's alright if you have one bad allele for something, because you have one good allele, and so you are still able to produce the functioning variant of that protein. In other cases, the existence of a bad allele leads to the creation of a protein that causes a disease, as in Huntingdon's.
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Revenged
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(Original post by futuredoctorVSB)
I get that, but what makes something dominant over something else?
They are terms for inheritence of diseases.

sickle cell is recessive - you need to alleles from the both parents to get it.

Huntington is dominant - you only need one allele from a parent to get it.
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Revenged
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(Original post by Larynx.pharynx)
It depends on what protein the gene codes for, and what it does. In the case of diseases, it's alright if you have one bad allele for something, because you have one good allele, and so you are still able to produce the functioning variant of that protein. In other cases, the existence of a bad allele leads to the creation of a protein that causes a disease, as in Huntingdon's.
Yes exactly
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Masoudy
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(Original post by futuredoctorVSB)
I've tried searching, but no real good explanations found. I know the effects of the different allele types, but why are they different in the first place?

My hypothesis is that dominant alleles produce proteins that are specific to recessive allele mRNA, and destroy it (preventing recessive allele expression).

And in homozygous recessive, the recessive allele is expressed, since, there is no protein present to break it down?
Same with codominant alleles?

I know my theory is far fetched, but could someone please clarify the actual mechanism for me?
I will keep it as simple as possible (I am not sure if you have College or Uni experience, would assume you know A levels bio)

Say you have a gene: it has variance in its DNA sequence. This certain variance (e.g. AAGGTTCC) is called variance A or allele A and it expresses brown eye colour

Other variance (call it AAGGTTTT) is called variance a or allele a and it expresses blue eye colour

When you have AA (both homologous chromosomes have gene A sequence) you will get protein A expression or the protein that is responsible for brown eye expression

If you have Aa, one chromosome has A and the other has a (i.e. your mum had blue eyes or a and dad had brown eyes or A) and you will get brown eyes

The magic is here: DNA sequence A (not protein A) masks the expression of DNA sequence a. This is an absolute fact that is well established and have applications over it (search balancer chromosome) the actual masking mechanism I would guess can be done in three ways (based on my year 1 and 2 uni lectures in molecular biology):

1- When the cell reads that it expresses sequence A to an mRNA and to a protein, there would be a biochemical pathway that would recruit transcription factors that would methylate and induce heterochromatin formation over sequence a

Or to rephrase it, the presence of protein A is (probably) sensed by certain transcription factors in the cell cytoplasm that would create a pathway that would eventually lead to the methylation (adding methyl molecules above certain DNA sequences) or coiling of DNA sequence a that would make its expression / translation impossible, as RNA polymerase wouldn't physically see sequence a as it is tightly coiled or hidden under methyl molecules.

2- When sequence A mRNA is transcribed, a transcription factor binds to it and says "sh!t I have to degrade similar mRNAs or stuff bloody methyl groups above similar sequences" then it continues to do the same above mechanism

3- RNA interference where antisense translation of sequence A happens (yes it can happen: from 3' to 5' DNA ends) produce a 'rogue' RNAi that search and destroy the mRNAs of sequence a by binding to them, before their translation

Hope this cleared some clouds
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futuredoctorVSB
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(Original post by Larynx.pharynx)
It depends on what protein the gene codes for, and what it does. In the case of diseases, it's alright if you have one bad allele for something, because you have one good allele, and so you are still able to produce the functioning variant of that protein. In other cases, the existence of a bad allele leads to the creation of a protein that causes a disease, as in Huntingdon's.
(Original post by Revenged)
They are terms for inheritence of diseases.

sickle cell is recessive - you need to alleles from the both parents to get it.

Huntington is dominant - you only need one allele from a parent to get it.
Oh OK I get it! So both alleles will be expressed! Recessive protein is not seen in phenotype because dominant produces a protein that is more normal and can counteract the faulty proteins? Thank you both so much!
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futuredoctorVSB
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(Original post by Masoudy)
I will keep it as simple as possible (I am not sure if you have College or Uni experience, would assume you know A levels bio)

Say you have a gene: it has variance in its DNA sequence. This certain variance (e.g. AAGGTTCC) is called variance A or allele A and it expresses brown eye colour

Other variance (call it AAGGTTTT) is called variance a or allele a and it expresses blue eye colour

When you have AA (both homologous chromosomes have gene A sequence) you will get protein A expression or the protein that is responsible for brown eye expression

If you have Aa, one chromosome has A and the other has a (i.e. your mum had blue eyes or a and dad had brown eyes or A) and you will get brown eyes

The magic is here: DNA sequence A (not protein A) masks the expression of DNA sequence a. This is an absolute fact that is well established and have applications over it (search balancer chromosome) the actual masking mechanism I would guess can be done in three ways (based on my year 1 and 2 uni lectures in molecular biology):

1- When the cell reads that it expresses sequence A to an mRNA and to a protein, there would be a biochemical pathway that would recruit transcription factors that would methylate and induce heterochromatin formation over sequence a

Or to rephrase it, the presence of protein A is (probably) sensed by certain transcription factors in the cell cytoplasm that would create a pathway that would eventually lead to the methylation (adding methyl molecules above certain DNA sequences) or coiling of DNA sequence a that would make its expression / translation impossible, as RNA polymerase wouldn't physically see sequence a as it is tightly coiled or hidden under methyl molecules.

2- When sequence A mRNA is transcribed, a transcription factor binds to it and says "sh!t I have to degrade similar mRNAs or stuff bloody methyl groups above similar sequences" then it continues to do the same above mechanism

3- RNA interference where antisense translation of sequence A happens (yes it can happen: from 3' to 5' DNA ends) produce a 'rogue' RNAi that search and destroy the mRNAs of sequence a by binding to them, before their translation

Hope this cleared some clouds
I get it! So the presence of the A protein induces methylation of the recessive allele that prevents its expression? But if there is no dominant allele, there is no methylation and both recessive alleles are expressed?
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Masoudy
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(Original post by futuredoctorVSB)
I get it! So the presence of the A protein induces methylation of the recessive allele that prevents its expression? But if there is no dominant allele, there is no methylation and both recessive alleles are expressed?
It doesn't have to be protein A. it can be mRNA for sequence A that does this or other RNAs that are transcribed from sequence A and we don't know about them yet.

you would assume all genes (DNA sequences that code for a polypeptide) are expressed unless there is another gene that regulate it (repress it, completely silent it, over express it). It can be the mRNA, the protein or even a scnRNA (scanning RNA) that does this regulation

It is 3 mechanisms not just methylation (I've done a powerpoint presentation about it):
1- DNA methylation
2- Tight DNA coiling (induced heterochromatin)
3- RNA interference

In genetics, we are usually taught that there is only 2 alleles for a gene that one is 'dominant' to another with the aforementioned mechanisms. However, life is always more complicated as there can be more than 2 alleles and it is mostly a cluster of genes that repress another cluster of genes.

And yeah in a co-dominance, both alleles are expressed. In recessive aa homologous chromosomes, only one a sequence is expressed and you would get blue eyes. Even in AA only one A sequence in one of the homologous chromosomes is expressed, just as females get only one X chromosome expression from their XX and we get X + Y expression (males have more genes than females)

But in the female example, a whole X chromosome is silenced and in the Aa example, just the small DNA sequence a is silenced.

I think if you read my two posts again several times you might actually understand it. In biology, answers are usually not straightforward.
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