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The son of a man who does not have Huntington's develops Huntington's after age 50. His son develops Huntington's in his late thirties. Explain (1) three ways someone can manifest an autosomal dominant phenotype when his father didn't have it, and (2) why this man's own offspring would show symptoms so much earlier than his father.

This trait is one that has low penetrance (this is actually false for Huntington's, but I'm including it here because it might be true for other autosomal dominant conditions). In this case, the Huntington's allele would only cause

Having a separate article on X-linked disorders perhaps makes sense, as the pattern of inheritance is rather different (and differs between sexes) and people sometimes get confused by that, so to explain this clearly in an encyclopedia one may need a separate article. As for autosomal dominant/recessive, I think that should be explained here in general terms, that is, applying to all organisms, not just humans. That is why I think an list of autosomal dominant disorders does not belong in this article: it distracts from explaining what dominance per se is and it is human-centered, whereas dominance occurs in every diploid organism (it was, of course, first discovered by Mendel in peas). Medical genetics belongs somewhere else. As for my reversion, please have a second look at what you did. It was wrongly formatted as a start, went against WP:MOS (the lead should start with "dominance is" or something like that, etc. One moment it spoke of "dominant alleles", in the next phrase it was "dominant traits". I am certainly not saying that the current article cannot be improved upon and I apologize if I discouraged you. I'm not sure what you mean by "journals semantics", though. As for merging ambidirectional dominance here, I'm not completely against that, but I am not sure that would not clog the article up in yet another way. As it stands, this article is (or should be) about phenomena at a single gene. (Ambi)directional dominance is something encountered in polygenic situations (and a concept used almost exclusively in quantitative genetics and it may be confusing to include it here. As for the article on "Autosomal recessive", did you actually click on that link? There is no article there, it is a redirect here... A final remark about the "confusing definitions" that you complain about: the current version of the article (although, I repeat, certainly not ideal) came about through heavy editing from an editor who has taught genetics for decades, so I gingerly suggest that the possibility exists that he knew what he was doing.

Did anyone get this question: three ways in which someone can manifest an autosomal dominant phenotype when the father did not have it?

Try this thread: https://biology-forums.com/index.php?topic=35839.0

Unless I am completely off track.... the son only has to get one dominant allele from one parent. So his dad did not have Huntington's....it doesn't say anything about mom. Huntington's is not a sex-linked disease. Males and females can both get it.

The disease allele could have come from his mother. That is, the father could have been homozygous or the son could be homozygous for the Huntington’s allele, giving rise to an earlier onset.  Another reason would be due to genetic anticipation, the original father may have not have enough CAG repeats to cross the threshold of penetrance required to show symptoms of Huntington’s.  More repeats may have been formed in the germ cells down the generational line. And the last would be genotypically, both could be heterozygous but disease onset frequently onsets earlier in later generations that in the parental generation. Theoretically, the father could still in fact begin to show signs of Huntington’s in the future.
The offspring will show signs of the disease earlier than the father mostly due to increased trinucleotide repeats. The penetrance and onset of the disease is increased as the number of CAG repeats increases. The offspring will have increased numbers of the CAG repeats.