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Human phenotypic characters & Genetic Plays


sreerag16

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Hi.

im a new member of this community.

i have a doubt in the subject that human phenotypic characers and its controlled genes..

 

ive observed tht many has attached earlobe whereas some has free..

and some can roll their tongue in "u" direction, whereas others cant..

and, some can bend their thumbs backward, while most of the people cant.......

wht is all behind these?

my teacher said me that these are the result of the play of genes..

but it isnt clear to me....

ive also searche the net but couldnt gather any more..

 

can any one of youu tell me the mechanisms involved in these?

which genes on which chromosomes are controlling these?

which stasis is shown by them?

are the sex-linked?

can u plz explain all these phenomena....

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Basically, well it's to do with your genes.

 

You have two parents for example, called Man and Woman.

Man has two genes for the same trait, which means he could have one for Tongue-Rolling ( Dominance ) and one for non-tongue rolling ( Recession ).

These two forms of genes for the same trait are alled Alleles.

 

The mans Genotype ( Genetic Make-Up of that Person ) for the trait for tongue-rolling is Tt, the big T stands for dominance or the ability to tongue roll and he is said to be Heterozygous Dominant(Tt) for that trait.

Heterozygous means different, like in Heterogenous Catalysis, different forms and Homogenous Catalysis where the state is the same for the catalysis. In Homozygous, the genes are the same, in heterozygous, the genes are different.

 

The woman has alleles of tt because she doesn't contain the alleles for the trait. Thus she is said to be Homozygous Recessive for the tongue-rolling trait.

Now if the egg and sperm fuse, so do the genes obviously which gives rise to variation, half from mother and half from father, it's always 50:50. Now the following shuffling occurs between the traits for tongue-rolling.

 

Tt tt

Tt Tt tt tt

Therefore the child will be 50% Tongue-roller and it has 50% of becoming a tongue roller to. We say that whatever physical appearance the organism has is called it's Phenotype.

 

This is the basic process behind these traits, it's all part of Inheritence. However, just because it's 50:50 now, the third or fourth generation stats could be completely different maybe being 75:25 as genes from grand-parents are never lost and always remain and can show up during any shuffling through the generations.

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I have absolutely no idea what gene tongue-rolling is but I do know eye colour, here are some of them:

 

There's a brown eye colour gene named bey2.

There's a blue-green one called gey2.

 

The process involved is quite complex and difficult to explain, but I have an article by Geneticist Dr. Barry Starr who can explain these very well: He wrote the following ,all credit going to him:

 

"To get blue eyes, both of your bey2 and both of your gey genes need to be the blue kind. For example, if both your bey2 are blue but one of your gey is green, then you have green eyes. So to get blue eyes, both genes need to be “right.”

 

I think there sex-linked genes on the sex chromosomes, not too sure, will have to brush up on that but I'm pretty sure it's sex-linked.

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I have absolutely no idea what gene tongue-rolling is but I do know eye colour, here are some of them:

 

There's a brown eye colour gene named bey2.

There's a blue-green one called gey2.

[/u][/b]

 

I think there sex-linked genes on the sex chromosomes, not too sure, will have to brush up on that but I'm pretty sure it's sex-linked.

I had a female friend with one blue eye and one brown who managed to convince two male yanks in a bar in Hawaii that this was the way to tell Australians from other races.

They were amazed and spread the news far and wide. (In loud voices- as they do):)

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I thought Epistasis only occurred on strange genes like Human Histocompatibility Complex', I think this has a role in the immune system, so I wouldn't say that eye-colour nor tongue-rolling are epistasic.

 

" Genetics is so interesting isn't it "

That's if you understand it! :)

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That definition from MSN is actually quite a basic one, I know of very detailed Epistasis and thought you understood it, however this is what it means:

 

Basically it's the interaction involving genes which determine the phenotype. The phenotype is the physical appearance of the organism. In epistasis, one gene on a different locus inhibits the function of another gene hence the epistatic one is expressed, this is not to be confused with dominance though as these terms are completely different.

 

If the genes were expressed individually you would expect a different phenotype, but this occurence causes variation and impossible to calculate. If one would find the genes and the most likely outcome, it would be a completely different one if epistasis occurs. The genes on one locus inhibit the function of the genes on a different locus, as you have probably guessed, mutations can result often from this. The loci is masks as many people say is referred to as the Hypostatic locus that is not expressed and is masked from function.

 

In epistasis, one gene blocks the function of a different gene. In dominance, one allele blocks the function of another allele on the same locus. In one line, one gene on one locus suppresses the function of another gene on another locus.

 

Prolu2007

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...i mean in which gene does this triat lie?

i mean is it in allosomic chromosomes or in sex chromosomes?

have scientists deviced any name for the gene which carry this characters?

In all probability, there is no single gene that controls "tongue rolling" or hyper-bendable thumbs.

 

Genes do not code for phenotypic features. As a general rule, genes code for proteins. For example, you cannot take the genes for a giraffe's neck and insert them into a horse, producing a horse with a long neck. There are no genes for a long neck.

 

But you can alter a gene so that a sequence that normally produces a certain protein, will now produce a slightly different protein -- with a different shape. If this new protein is active in the zygote development, it could seriously alter the eventual phenotypic shape. Usually, fatally. If it is active in later stages of development, it might alter, say, skin color, or the flexibility of certain muscles, or the length of a leg bone.

 

In fruit flies, we know that there are proteins which serve as the anchor for a phenotypic feature, such as a leg. Copy the gene for that protein into a new location of the DNA, and you could get a leg where an antenna ought to be.

 

There are occassionally genes that code for repetitions. A millipede may have one long sequence of genes that produce a body segment with two legs. An associated gene causes that body segment to be replicated 17 times, producing the body of the millipede.

 

The relationship between proteins in various combinations and phenotypic features is very complex and has not been worked out in any detail yet.

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That definition from MSN is actually quite a basic one, I know of very detailed Epistasis and thought you understood it, however this is what it means:

 

Basically it's the interaction involving genes which determine the phenotype. The phenotype is the physical appearance of the organism. In epistasis, one gene on a different locus inhibits the function of another gene hence the epistatic one is expressed, this is not to be confused with dominance though as these terms are completely different.

 

If the genes were expressed individually you would expect a different phenotype, but this occurence causes variation and impossible to calculate. If one would find the genes and the most likely outcome, it would be a completely different one if epistasis occurs. The genes on one locus inhibit the function of the genes on a different locus, as you have probably guessed, mutations can result often from this. The loci is masks as many people say is referred to as the Hypostatic locus that is not expressed and is masked from function.

 

In epistasis, one gene blocks the function of a different gene. In dominance, one allele blocks the function of another allele on the same locus. In one line, one gene on one locus suppresses the function of another gene on another locus.

 

Prolu2007

and prolu2007,

can u explain this with an example which could make us it understand easily..

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IAs a general rule, genes code for proteins. For example, you cannot take the genes for a giraffe's neck and insert them into a horse, producing a horse with a long neck. There are no genes for a long neck.

..............

 

In fruit flies, we know that there are proteins which serve as the anchor for a phenotypic feature, such as a leg. Copy the gene for that protein into a new location of the DNA, and you could get a leg where an antenna ought to be.

 

isnt these statements controversial?

or is it meant that the protiens produced could replace an already existing phenotypic character?

or is it meant that the altered gene sequence in the embryo of drosophila could make the alterations?

 

can u plz clarify my doubt..

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I am not sure there would be one example to make the easy.

 

Lets try:

 

Ok go back to the eye color (for argument sacks) eye color for us is controlled by one gene. These means the 4 alleles contribute to eye color. The combination of all four alleles interacting make you eyes the color they are. Ok that is simple enough, right?

 

Moving on: Most genes and diseases are not simple as say sickle cell for example where you are either have the disease or not. Most proteins and genes are controlled by and interact with a plethora of other gene products. This governs everything from expression to function and can have a wide variety of effects everything from total inhibition to super activation. You can appreciate it if in the above eye color example we now add another color control gene. Now you have 2 genes that may or may not be independently regulated leading to 8 alleles all of which interact with each other, or themselves. Now you can see how complex it has become just by adding another gene, which we did not even mention the variety of genes/proteins that could be involved in the control of the actual expression of each allele. Now consider the control genes being regulated by other genes/proteins and or stimuli. It get complex rather quickly.

 

I am not sure if that is clear it sort of made sense to me as I typed so please ask and I will try and clarify the best that I can.

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