I would believe most people think that the code that made and maintains their body the way it is, is stored in the DNA, as in the 21 pairs of helicoidal acids. But this can’t be the case since, with exception for the sex chromosome all others provide two answers for the same question. Either your parents were identical twins or some of these answers are different.
If the process of cloning consists of copying only these pairs, a same aged clone of yours would have the same sex but it could be completely different otherwise, depending on how different your parents were.
I assume each part of the chromosome knows nothing about its corresponding pair so where is the code that creates the final answer?
It’s not randomly picked which of the pair determines your traits. For some traits, one is dominant and the other is recessive, so, for instance, if one copy of your hair color gene is dark and one is light, you’ll have dark hair. Others show mixed dominance, so you’ll get a result somewhere in between what either pure genotype would get.
I’m not sure I understand the question. Thats why there are studies comparing fraternal twins vs identical twins for example.
DNA isn’t everything, but it determines 40-80% of most traits. And that is within our agreed upon genetic traits. Like aggression. Human aggression falls under certain ranges and I’m sure like other traits is largely genetic, but our level of aggression is different than a hippo or wolverine, which have a different baseline.
So genetics determines the baseline, but also a lot of variance within the baseline.
I will do my best to parse the OP, please tell me if I have misunderstood.
We have 23 pairs of chromosomes, I assume that’s what you are referring to.
So here the term you are looking for is diploidy. We have two copies of every gene - except the X & Y in males - with one copy inherited from each parent.
So what you’re concerned about is gene expression, i.e. the regulation of exactly when and how much the information in a gene is “read out” to make RNA & protein.
And in particular you’re concerned about the situation when the two copies of a gene are different - that’s called heterozygosity, as opposed to homozygosity when the two copies are identical.
Having straightened out (I hope) what you’re asking, and the relevant terminology, I’ll put an answer in a separate post.
As a preamble, the expression of genes is (of course) carefully regulated. Our cells only produce certain proteins at certain times and in certain quantities, according to the specific requirements of the cell type and in response to external influences. Regulation is mediated principally by a complex network transcription factors, which are proteins that may transduce information about the external environment or cellular conditions, which bind to specific DNA sequences and/or to one another, and which in the right configuration can “decide” that we need to express (read out) a gene, for which they recruit RNA polymerase, the enzyme that copies out the DNA into messenger RNA and thence to protein.
To come to your specific question - what happens when someone is heterozygous for a gene, i.e. the two copies are different? Well, the simple answer is that in general both copies are read out. We see this in the well known example of blood type. If you are “AB”, that means that you are heterozygous at the relevant locus - you got the allele (gene variant) that makes “A” antigen from one parent, the allele that makes “B” antigen from the other parent, and both alleles are expressed - both A and B antigens are found in your blood.
However, it will not always be the case that both copies are expressed in equal quantities, and that’s because the DNA sequence within and around a gene influence the expression of that gene by recruiting transcription factors that bind to specific DNA sequences called response elements. These DNA response elements are call cis-acting elements, since they influence the expression of DNA that is in close physical proximity on the same chromsome. And we may also be heterozygous for the DNA sequence in these response elements. Thus, if two homologous response element DNA sequences on the two chromosomes are different, then the two versions of the gene that they regulate may be expressed in different quantities or even at different times.
Everything that I have described above is determined by DNA sequence, since the transcription factors themselves are proteins that are also encoded by genes. Contra some overhyped epigenetics papers, there is no evidence of any other significant heritable information - the only other informational input is from the environment.
The two alleles (variants of a gene) do not “know about each other” in a direct sense that they get together and take turns. As described, they will both tend to switch on and off at the same time, although sometimes in different quantities if the cis-acting DNA response element sequences around a gene are heterozygous.
However, gene regulation commonly has feedback loops - the cell will make as much of a protein as it needs, and when there is enough of it present in the cell, transcription factors react to that and switch off the gene. There are frequently situations where you only have one good copy of a particular gene, and the other copy is defective. But in many cases, you are perfectly fine with just one good copy. That’s because one copy allows the body to make as much as it needs, even if it takes a bit longer. This is called haplosufficiency, meaning that one good copy rather than the usual two is enough. This is the situtation for the classic recessive genetic disease, where two parents may not be aware that they are both carriers because heterozygous carriers have no phenotype; but a child may get two copies of the defective gene.
There are also situations where one chromsome “knows” about the other because of trans-acting regulatory elements (as opposed to the cis-acting elements I described above). These are DNA sequences that code for transcription factors or other diffusible regulatory molecules such as microRNA. Whichever chromsome copy these diffusible molecules originate from, they will affect both chromsomes equally. So if someone is heterozygous for a transcription factor where one copy is defective and the other copy works fine, the version that works fine will be able to switch on both copies of a gene that it controls.
So I also did a bit of reading and this turns out to be much more complex than I thought.
I also stand corrected on almost all of my assumptions. And it seems that if cloning is just copying the 23 pairs, indeed one would get a very close match.
Riemann describes it as I read although with a lot more jargon, which I appreciate between professionals, but here among us I prefer to avoid when it is not ambiguous. The AB blood type example is a good one but I was focusing more on the traits that are competitive like the dark/fair hair Chronos mentioned. So if I got it right: in general, both pairs are read with equal preference; there is a gene to produce the pigment in both pairs but there are triggers for this gene which say how much to produce or inhibit production. These triggers can also have their own triggers which can come from the same or the corresponding pair. Fair hair can be dominant or recessive depending on the interplay between these genes. Fair hair can be dominant at one age and then be recessive at an older age if the genes say so. Your pigment glands can be killed and your hair go white if you go over the stress threshold defined by your genes. Genes are like oracles. They define your life but are difficult to interpret.
I recall something - maybe Reimann can chime in - that because men have one X chromosome while women have 2, there is a process where often only one of the alleles on an X will express, not the same on both - thus women tend to be a compromise between their two X chromosomes while men get the only one the were stuck with. The thought is that this results in women’s characteristics being less extremely variable - statistically there are fewer women at the extremes of assorted characteristics. (The claim, not sure I accept, is that there are for example more men who are geniuses, but also a lot more men than women who are lower intelligence too.) The sigma in many distributions of characteristics is greater for men than women, for traits that require cooperation by a series of genetic material.
There’s the minor issue that mitochondrial DNA may differ if the selected cell or some of it does not have the full complement when the material is removed from the host for cloning. Not sure how relevant mitochondrial DNA is to determining inherited characteristics.
Actually, hair color works very closely to how ABO does. A person’s ABO group indicates which proteins their ABO-genes express: someone can be A because both genes are A, or because one is A and the other doesn’t make proteins. Hair is protein, and its color is a function of the exact composition of its proteins: each of your protein-hair-making-genes works by itself, but the color of the end result is, for each hair, the sum of the hair-making-genes in its root, and for the whole head (or any other area), the sum of the individual hairs. And unlike ABO group, hair color is one of the items in which for many people and in fact for any hairy animals expression changes with age, and even with time of year (yes, humans change “coat” too).
Yup, the general principles of classical diploid genetics - recessive, codominant and dominant traits - work on the assumption that both alleles are generally expressed.
Yes, I was trying to say that the classical model for single locus genetics is to assume that both alleles are expressed, and under this model you can then have various scenarios where the inheritance scheme is recessive/codominant/dominant:
Loss-of-function allele with haplosufficiency => recessive (e.g. CFTR)
Two alleles that produce something different that coexists => codominant (ABO system)
Loss-of-function allele with haploinsufficiency => dominant (e.g. NF1)
Dysfunctional form causes problem even when functional form present => dominant (e.g. Huntington’s)
etc.
And if we have a mutation in a cis-acting regulatory element that means one allele is not expressed at all, that would usually look similar to the expression of a non-functional gene product, so it would still tend to fit into this kind of inheritance model.