Mendelian inheritance and evolution. Part III

We've discussed some problems with the idea of Mendelian inheritance as a misleading legacy from the kinds of work that Mendel had to do, that has persisted deeply into modern thinking in ways that we think are misleading at best, or even plain wrong for several reasons.

First, because genetic units, not traits are what is inherited.  A fertilized egg doesn't have legs or a brain nor pollenated pea seed have color, wrinkles, or plant-height.  What is inherited are genetic variants that affect these traits in the adult organism.

Mendelism was wrong because most variation, the variation that enabled the modern synthesis to unite discrete Mendelian genetic inheritance with gradual Darwinian evolution, was generally minor relative to Mendel's purposes.  Clear discrete states and dominance are not the general ground state of biology.  In a population individual genes have many more than 2 alleles (variant sequences) and the effects of their paired combinations in individuals (plants and animals) is associated with more than two trait states (yellow or green).  Even at single loci, even when some alleles are in the traditional sense dominant relative to others, the dominance is usually not complete or invariate.

Mendelism was wrong in that the key to uniting discrete genetic inheritance with gradual variation in traits and their evolution, was that many different genotypes--combinations of alleles--yield the same trait.  When many genes co-contribute, as is widely the case, the trait can be called complex or 'polygenic'.   This is because the individual effects are generally small relative to the variation in the trait.  Small basically 'additive' effects predominate, rather than strongly determinative ones.  We had to give up on notions of Mendelian inheritance were then (and still widely are today) widespread.  But that this was the key to the modern synthesis was not widely perceived in these terms.

One could object that oh, yes what we say applies to multigenic traits, but not to single-gene traits.  Aren't there hundreds of these on the books, in human disease and in other species as well?  We'd respond that in real life most clear dominance or single-locus traits are much less dichotomous or simple that in general perception or in the textbooks, and  adaptation and complex function are demonstrably cooperative and multigenic rather than singe-factor competitive.  Complex organisms couldn't really function or evolve if they were just a bag of individual dominant, Mendelianly inherited traits.  And not only are most traits multi-genic, but genes, no matter how our definitions what a gene is change, are multi-allelic in natural populations.

Once we realize this, we have to accept that in general, statistical dominance, which we explained in an early post in these series, is a population rather than biologically inherent property of individuals.  It is the exception, and only a partial exception that is classically Mendelian: partial, because often even in these cases we overlook variation because it may not be great relative to our pragmatic purposes (such as diagnosing the presence of a disease).  But pragmatic considerations like this often turn out to be wrong and science is about understanding nature.

The problems mainly follow from falsely confounding inheritance of genes and with inheritance of traits, and from using the extreme of a distribution--the few nearly-dominant examples--to characterize the whole distribution of the effects of individual genetic variants. 

At the time of the synthesis, not enough was known about genes (or, at least, seriously and widely enough accepted) to recognize the implications of polygenic inheritance.  But now there is no excuse for clinging to theoretical concepts that are misleading and, at best, inaccurate ways to understand life. Doing so has led us down the paths that we imagine will promise simple answers of immediate clinical or commercial value. Each approximate 'hit' entices us to go deeper into the woods of our dreams.