Some alleles are dominant while others are recessive; an organism with at least one dominant allele will display the effect of the dominant allele
We know there is such a thing as incomplete dominance, but the general principle is still amazing.
But why does the Law of Dominance happen in terms of molecules? I googled around, and I didn’t get any clear hits.
In the case of Mendel’s green and yellow alleles for pea color with Green being the dominant allele, does the yellow allele not get translated at all? Seems there has to be some regulatory computational type control to somehow say, “this is a recessive allele, if there is a dominant allele, express that, if not, express this recessive one.”
Maybe there is info on this, but I don’t recall reading anything on this.
The closest related thing I saw was dosage compensation via the XIST lncRNA which shuts down one of the X-chromosomes and the outcome is a calico cat, BUT this isn’t exactly the same thing as what the Law of Dominance is about. It is relevant only in as much it shows one of the many mechanisms to shut down expression of an allele.
Generally, recessive alleles represent loss of function or lack of function.
Alleles don’t get translated, mRNAs do. For mRNAs with nonsense (premature stop) mutations, the early stop actually promotes degradation:
I think that you just stumbled upon an ID hypothesis. It’s false, of course.
Maybe you aren’t very well-read when there are even Wikipedia articles addressing what you don’t recall reading anything about what was discovered more than 40 years ago…
To give some speculative answers - biology is messy, and things work different ways in different organisms - …
I expect that many recessive alleles are loss of function mutations - there’s been a frame shift, or introduction of a premature stop codon, or loss of the promoter site, or whatever other mechanism has escaped my attention.
So the recessive allele either does not produce a protein, or produces a non-functional protein which just floats around the cell until it gets degraded by the normal cellular mechanisms that recycle surplus proteins. Take the case of plants with red flowers as the wild type. A loss of function mutation that disables anthocyanin synthesis produces white flowers in a double recessive. In a heterozygote either anthocyanin production is lower, giving pink flowers, or the cellular regulatory network boosts synthesis of the dominant allele, giving the wild type red flowers. (Perhaps something of the lines of produce the protein that binds to the regulatory site and promotes synthesis of the relevant target protein until the level of the pigment has reached the normal level.)
Assuming that you’ve recalled the situation correctly, in the case of yellow versus green peas I’d guess that the dominant allele is a gain of function mutation. Chlorophyll synthesis is often disabled in seeds, or at least seed coats, presumably as a result of it being unneeded, and therefore energetically wasteful, leaving whatever other pigments are produced to colour the seeds. If the mechanism by which this is achieved is broken then chlorophyll production is turned back on (I am assuming that chlorophyll production is the default state) and the chlorophyll masks any other pigments present giving a green coloration.
Differences in activity and expression can also play a role. An allele with really high gene expression can result in a different phenotype than two low expression alleles. A protein with 10x’s the activity can swamp the lower activity of two recessive phenotypes.
We report a new mechanism for allelic dominance in regulatory genetic interactions that we call binding dominance. We investigated a biophysical model of gene regulation, where the fractional occupancy of a transcription factor (TF) on the cis -regulated promoter site it binds to is determined by binding energy (–Δ G ) and TF dosage. Transcription and gene expression proceed when the TF is bound to the promoter. In diploids, individuals may be heterozygous at the cis -site, at the TF’s coding region, or at the TF’s own promoter, which determines allele-specific dosage. We find that when the TF’s coding region is heterozygous, TF alleles compete for occupancy at the cis -sites and the tighter-binding TF is dominant in proportion to the difference in binding strength.
Note that it says “new mechanism”, implying that other mechanisms are already known. The article then goes on to give references to papers describing other mechanisms. One citation is to a 1934 paper, though admittedly that was theoretical rather than empirical.