Mendel carefully chose strains of basically inbred pea plants that had simple patterns of inheritance: the dichotomous traits 'bred true' from parent to offspring. He knew there were many traits that did not just have two states, or that did not breed true in this simple way. But to understand the effects of hybridization--or we now wrongly say, inheritance--he picked appropriate traits. His seven carefully chosen traits all had an additional attribute that was important in this sense. One of the states was 'dominant' to the other state, which was therefore 'recessive'. These are essentially the terms Mendel himself used.
|The 7 traits of interest to Mendel|
Note right off the bat that there was a very big mistaken conclusion that followed: Mendel was showing the nature of trait inheritance, but it was interpreted to mean the laws of genetic inheritance. It worked only because of the 100% correspondence due strictly to the careful choice of 2-state, highly determinative traits in his experiments. Although even that isn't strictly true (see my 2002 paper in Evolutionary Anthropology), it was close enough that even now we confuse inheritance that strictly applies only to genes, with the appearance of traits in offspring compared to their parents.
Classically, many 'Mendelian' diseases were identified, because they approximately followed Mendel's laws. Modern biomedical genetics began, around 1900, with Archibald Garrod's studies of 'recessive' traits that arose in inbred marriages, that raised the chance that a child would inherit the recessive allele from both parents (because the genetically related parents shared the allele from their common ancestor). Step by step, we built in the illusion that genes were just waiting their transubstantiation into traits.
Until the nature of DNA was understood and we could examine DNA directly we had to work through traits rather than genes, even though we called the field 'genetics'. For decades it was observable traits in experimental species, such as fly eye color, or 'Mendelian' disease, or similar traits in plants. Genetics split into two parts, one dealing with this kind of 'clear cut' particulate inheritance, which eventually led to understanding of how protein-coding areas were arranged along chromosomes, the nature of chromosomes, the nature of genes coding for proteins, and the transmission of DNA from parent to offspring.
The other segment of geneticists dealt with the majority of traits that clearly did not 'segregate' from parent to offspring, the quantitative traits like stature, milk-yield, grain nutrient properties and the like, from which the field of quantitative genetics developed. It was more pragmatic and said that a quantitative or complex trait was due to the inheritance of many genes: we might not be able to identify them, but jointly they were responsible for traits in organisms. The similarities between parents and offspring for complex traits was consistent with this view as well.
|Cajanus Cajan; Wikimedia Commons|
Of course all of this is manifestly a Grand Illusion! Even a fertilized pea ovule does not have peas, wrinkled, green, or otherwise! Once the connection between a gene and a trait becomes less than 100%, or once many genes contribute information about a trait, we see how obviously Mendelian ideas were a badly misleading mistake. They were great for providing ways to set up experiments that isolated genetic effects and led to an understanding of genetic inheritance. But they were, from the beginning, very misleading about trait inheritance.
In the next installments of this series, we'll examine the idea of dominance and genetic effects further, and will eventually ask whether, surprisingly, there really is such thing as dominance in the first place!