The factors are called promotor, transcription factors, packing of chromatin.

if you have two genes and two promotors, both have a chance of being expressed unless a product of one inhibits the transcription of the other.

Actually epigenetics is the only factor, which can totally turn off some gene, look e.g. for X chromosome.
Although they will have different promotors, probably won’t be any turned for 100% off, just the expression will be different 😉

What’s exome? All exones?
Just look for CDSs or mRNAs/cDNAs 😉

i think it does mean the dominant allele has a stronger promoter

that’s what i think.

dominance of allele and strength of promotor has nothing common

Are you sure about this comment? ‘nothing’ in common at all? No possiblility that a strong promoter can cause an allele to be dominant in its expression?

now guys please post stuff that you are 100% sure of. i am getting confused. why doesn’t a stronger promoter mean a dominant allele?

kolean: imagine one allele, which is truncated, but has strong promotor and other one, which has weak promotor, but the polypeptide is functional. Do you really think, that the first one will be dominant?
I don’t say, that there can’t be some relevance, but it’s more about co-dominance, than dominance/recessivity. That is achieved by the polypeptide.

JB: interesting argument. First I was not under the impression that we were talking about truncated alleles, or a mutation at all. Also I have a tough time with eukaryotic strong vs. weak promoters in the first place. I think enhancers and the chromatin modeling around each of the alleles is what really makes the alleles stronger than the other one.
You talk about the polypeptide being functional. Do you not need to look at the mRNA first? If the allele with the strong promoter has the mRNA being made into massive quantities, but the truncated form doesn’t even get out of the nucleus to be translated into polypeptide (i.e. – no poly(A) site) then it is all for naught as you pointed out. But what if it has been truncated in a way that it can exit the nucleus saftely, but it is not regulated by miRNAs (i.e. – no let-7 miRNA regulatory sites in the 3’UTR), and so the mRNA is translated into massive amounts of polypeptide, while the weak one is regulated heavily due to feed-back loops?
Expression of an allele, in a eukaryote at least, is getting more and more complicated than just using Mendelian’s genetic terms of co-dominance, dominance, and recessive. At least for me it is after studying epigenetics, genomic imprinting, and many other maternal influences (maternal miRNAs now? oocytes are getting to be some a heavy developmental influence).
I just have a habit of pointing out that one should not say a word like ‘nothing’ or especially ‘never’ (one of my personal pet peeves) when talking about anything in the universe.

by truncated I meant some premature STOP codon, not truncated mRNA 😉

Well, my point was, that there can be but does not have to be a correlation between the strength of promotor and allele dominance. So I used an example taken ad absutio. But still, just take some polypeptide, which has low catalytic speed and other, which is very strong (no matter, which one is original and which mutated;), the first one has stronger promotor, but it catalyze basically nothing, whereas the other one is in the cell only in few copies, but still so strong, that it can override the more-expressed one 😉

The classical examples of dominance and reccessivity are usually based on one gene not working and thus interrupted pathway. In such a case, you can have as strong promotor as you wish, but it will be still reccessive. Or vice versa that can be accomplished by functional allele but non-functional promotor.