how a SNP in a 'junk DNA' region can affect the formation of a protein without having its 'coded' information extracted by the protein building process in some way.
It's obvious that you don't really know what you are talking about, but I'll try. Please pay attention.
It has been know for about 10 years that variations in the promoter region of the stromelysin-1 gene (the MMP3 gene) has been linked to coronary artherosclerosis. Prior to this finding, this region was called "junk". It turns out that the variation is a single nucleotide polynmorphism (SNP) 1608 bases upstream of the transcription start site for this gene. Nothing is "extracted". It is a binding site for at least three different proteins. These proteins form a complex that, in asociation with other regulatory factors, determine how much mRNA will be transcribed (still with me? I'll wait). It turns out that the nature of the disease pathology is in the amount of mRNA made in response to SNP in this upstream NON CODING region. (Incidently, this region is no longer called "junk").
Feel free to use whatever semantics you wish to avoid the admission that there is any 'coding' going on, but it's not a CODE for anything. It's a regulatory binding site (do you understand the difference?) and try to avoid letting on that the existence of a pertinent piece of the protein building apparatus in a 'region' automatically revokes the 'junk DNA' label. I'm not avoiding it, I'm drawing attention to it. You're avoiding it.
The thread began with the 'claim' that an unrelated 'junk DNA' SNP, on it's own, caused a specific variance in a physiological characteristic. Here's a link to a relatively easy article about genetic causes of disease that are due to polymorphisms in "junk" regions. (Remember, once ID'd they are no longer "junk") Try to catch up. www.biology.duke.edu/wraylab/papers/Rockman2004CB.pdf
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