This page: 3. What Darwin Didn't Want To Know
     
3. What Darwin Didn't Want To Know    

And what we have learned since his time

  

3. WHAT DARWIN DID NOT WANT TO KNOW
3.1  Mendel
3.2  What Mendel did not know
3.3  An interchromosomal exchange program
3.4  Conclusions

In this chapter we are going to look at the way in which inherited characteristics are passed on. Mendel discovered how that worked. Darwin knew nothing about it. In fact, he would have none of it! Nevertheless, Mendel’s ideas are know generally accepted and proven. There is apparently a build-in natural mechanism in reproduction which causes (genetic) variation in the offspring.

3.1 Mendel.
Gregor Mendel (1822-1884) lived in the same period as Darwin (1809-1882). In the monastery where he lived, he spent a lot of time researching inherited characteristics in peas. He discovered that characteristics, like the color of the flower or the shape of the peas, were distributed in the offspring in a standard pattern and that the offspring could have ‘hidden’ (later known as recessive) characteristics.
Darwin had also done research into heredity, but Mendel had a mathematical background, which made him better at statistics. He had also planned his experiments carefully, so that he was able to discover this standard pattern. In 1865 (Darwin’s Origin had been published in 1859), Mendel presented his results, but his ideas were not accepted or understood. One group of people thought that the offspring ‘expanded over an infinite field of variety’ (principle of ergence), and another thought that the next generation received the average of the parents’ characteristics. Apparently, Mendel sent his results to Darwin, but Darwin never opened his letter...[1]

Mendel came up with the concept of a gene, although he did not use that word himself. A gene is a ‘unit of influence’, for instance for the color of a flower this could be a gene coding for purple or white. Genes almost always occur in pairs, because the offspring receives one part from the father, and the other part from the mother. Mendel discovered that when he crossed purple flowers with white flowers (the parental pair is designated by ‘P’ for parents), the first offspring (designated by ‘F1’, the ‘first filial generation’) all had purple flowers. However, when he cross-bred the F1’s with each other, then white flowers appeared (in F2, the second generation), but on average in only a quarter of the offspring. The White characteristic was therefore hidden in some way in the F1 generation and the Purple characteristic was stronger, dominant to the White characteristic. But why were only one quarter of the flowers from the second generation (F2) white? With a bit of calculation, this becomes clear.

Figure 1, Genetic Analysis pp. 24;How Mendel carried out his cross-breeding.

Suppose we assign a letter to the characteristic ‘flower color’, for instance the letter A. Purple is the dominant characteristic, so we will indicate it with a capital A. White is the recessive characteristic, so we will indicate it with a lowercase a. If a purple father-plant is AA (all genes occur in pairs), then he makes pollen in which half of his double genes can be found, in this case A. The white mother-plant aa always passes on a to the first generation (F1). And A plus a is Aa, so all plants from F1 have Aa as a characteristic, and since A (purple) is dominant to a (white), all of F1 is purple.
Schematically, this is shown as follows:

P:          AA x aa           (purple x white)

F1             Aa               (purple)

What happens if you cross Aa with Aa? That results in four possibilities: AA, aA, Aa and aa. The first three all have purple flowers. Only the last one has white flowers, so one quarter of F2 is white.

Figure 2, Biology pp. 227.Schematic overview of the heredity
       of the characteristics Purple and White in peas.
       

A list of a few ‘difficult’ terms:
a gene:     the hereditary coding for a certain characteristic, such as Flower Color
an allele:   a variant of a gene, which has a certain ‘value’ for the characteristic which the gene has, or ‘fills in’ the attribute, such as Purple or White. One gene (e.g. for the characteristic of flower color) can have multiple alleles (a purple allele, a white allele, etc.)[2]
homozygote:   having the same two alleles of a certain gene, for instance AA or aa, or perhaps BB or bb
heterozygote:   having different alleles of a certain gene, for instance Dd (Aabb is a heterozygote for A/a and a homozygote for b)
dominant:         the allele which surpresses the other characteristic in heterozygotes, for instance A or D
recessive:          the allele which has a hidden characteristic in heterozygotes, but in homozygotes displays a different characteristic, for instance a or c
phenotype:    the external appearance, for instance Purple (both by AA and Aa) 
genotype:   the internal, genetic makeup, for instance: AA or Aa (the phenotype (Purple) can be the same while the genotype (AA or Aa) is different)

Why was this so difficult for Darwin and his followers to understand?
I see two reasons. In the first place, Mendel was a monk, thus spirituality he was exactly what Darwinism was against (see Ch. 2.2). How could a clergyman, most of whom were against Darwin, produce anything good?
The second reason is that Mendel’s experiments showed that heredity happens according to a standard, even predictable pattern. New characteristics are not actually new, but hidden. In other words: you can’t produce characteristics that weren’t already there. Darwin’s theory depended on the development of truly new characteristics, such as an eye or wings, because otherwise how would everything have been able to originate from unicellular organisms? If Mendel were right, the whole story would be finished before it even took off.

Alfred Russel Wallace (of the principle of divergence) once wrote:

But on the general relation of Mendelism to Evolution I have come to a very definite conclusion. This is, that it has no relation whatever to the evolution of species or higher groups, but it is really antagonistic to such evolution! The essential basis of evolution, involving as it does the most minute and all-pervading adaption to the whole environment, is extreme and ever-present plasticity, as a condition  of survival and adaption. But the essence of Mendelian characters is their rigidity. They are transmitted without variation, and therefore, except by the rarest of accidents, can never become adapted to ever varying conditions. [3] 
(Italics by PMS)

Not until after Mendel’s death at the beginning of the twentieth century was his work recognised, after three other scientists, including the Dutchman Hugo de Vries, independently arrived at the same results. Later, it was discovered how those characteristics were passed on: by chromosomes, by DNA.

3.2 What Mendel did not know

About cells, chromosomes and DNA
Mendel knew nothing about the existence of chromosomes. Chromosomes are very long molecules of DNA which occur in the nucleus of all the cells of a living creature.[4] A human is made up of billions of tiny cells. All of these cells have a cell nucleus. In every nucleus (except in the reproduction cells) there are 23 pairs of chromosomes. Of 22 pairs, each chromosome in the pair codes for the same gene. The chromosomes in the 23rd pair either code for the same gene (XX), which indicates that the person is female, or they are different (XY), indicating that the person is male.

figure 3: different enlargements of a organism from
the whole body till the DNA, genetic analusis, pp.2.

What appears to be the case? Those two parts, those two alleles of a gene each appear to literally occur on one of those two double chromosomes. A gene, or more accurately a gene pair, is therefore made up of two small pieces of DNA on a double chromosome. Furthermore, during the manufacturing of sex cells, those double chromosomes split apart and each half ends up in a different sex cell, so a sperm cell or an egg cell has only half as many chromosomes as a normal cell. When a sperm cell and an egg cell join, another cell is formed with double chromosomes, and from that new cell, a new life grows. A sperm cell which carries a Y chromosome will make the child a boy (Y from the father and X from the mother). A sperm cell which carries an X chromosome will make the child a girl (X from the father and X from the mother).

Chromosomes are actually super-molecules, on which all our genes have a place . A human has a little less than 100,000 genes. Each gene has a fixed location on a chromosome, and there are also overviews in which the genes are mapped. An example of such a gene map can be seen in Figure 6. At this point in time, it is not known where all the human genes are located and what precisely they do, but it is being investigated in the Human Genome Project.

 
     
Figure 4, The human set of double chromosome in a row,
The DNA-makers pp. 203.
  Figure 5, The human X and Y chromosomes,
Scientific American, Sept. 96, pp. 9.

 

  3.3 An interchromosomal exchange program
You could say that a child therefore always receives either one half or the other half of the characteristics of a whole chromosome, but the chromosomes have another trick to play on us!
In order to multiply, cells share with each other and so grow a bit more. During this process, they copy their chromosomes, so that each successive cell has the same DNA. When manufacturing sex cells, the cells also share, and the chromosomes are also copied. But before it is complete, the double chromosomes exchange a piece with each other. Kind of like: you give me that piece, and I’ll give you this piece. Afterwards, they part ways permanently in a cell ision which makes the sex cells.
And what is the point of that? That each new offspring is a complete mix of the characteristics of the parents. Imagine: if humans had 1 double chromosome, there could only be four (2 possibilities from the father times 2 possibilities from the mother) different children. Humans have 23, so there are (2^23=8,388,608) about eight million possible different children. However, thanks to the exchange program, there are an unbelievably large number of possible combinations.
Another reason is that the exchange program ensures that the alleles (the ‘values’ or appearances of the gene) on one chromosome will not stay together forever. In the hard reality of life, certain combinations could be more practical than others.[5] This exchange of pieces of a chromosome is called crossing-over or recombi­nation.    
      
Figure 6, gene map of a human chromosome, Genetic analysis, pp. 143.
 
     

 

Another list of a few ‘difficult’ terms:
crossing-over:   see recombination
diploid:   a cell is diploid if the number of chromosomes occurs doubly. In humans, diploid cells have 46 chromosomes (23 pairs).
DNA:     the super-molecule of which a chromosome is made, which contains the genes and is therefore the carrier of hereditary information
genome:       a complete singular set of chromosomes of a species, in which all genes occur once.
homologue:         chromosomes are homologous if they are ‘equal’, that is to say, they have the same genes in the same order. The alleles may differ (on one chromosome the allele may code for A (Purple) and on the other the allele may code for a (White)).
haploid:        a cell is haploid if the number of chromosomes occurs singularly, so sex cells are haploid. In humans, haploid cells (the sperm and egg cells) have 23 chromosomes.
recombination:   (or crossing-over) two (double or homologous) chromosomes exchange pieces with each other
     

3.4 Conclusions

  • There is a purposeful and goal-directed process which brings about variation, namely the double chromosomes, and the exchange of genes between the two. Which combination of genes will result is coincidental, but the system itself which takes care of this has nothing to do with coincidence. It occurs in all animal and plant life. We shall in future call this process (sexual reproduction; homologous chromosomes; recombination and meiosis (i.e. ision of homologous chromosomes between haploid sex cells)) natural variation (analogous to natural selection!).
  • In natural variation (not ‘natural selection’), there is no mechanism which ensures that new attributes are added to the organism, or that new functions are added (let alone complete organs). Natural variation only ensures that the variation already present in the genes is distributed more or less arbitrarily throughout the offspring.
  • Natural variation ensures that new combinations of alleles appear, not that new alleles appear, which is necessary for evolution.

Mendel and the built-in exchange program, called recombination which was discover later, meant that the evolution theory needed to be rethought. This happened with the mutation theory.



[1]   Source: The Talk.Origins Archive, Introduction to evolutionary theory, Chris Colby
[2]   The use of the terms allele and gene differs in genetics and in popular science. The word ‘allele’ does not occur at all in everyday speech, whereas everyone has heard of ‘genes’. That makes it a bit difficult to handle the concepts in this book. Furthermore, there is a history behind it. For Mendel, it was a ‘unit of heredity’. Later it was discovered to be a specific piece of DNA on a chromosome. It could go two ways. The first would be to say that a gene is a location or locus on the DNA which codes for a protein and therefore occurs twice in double chromosomes. An allele is then a specific variant of such a gene, with the resultant unique order of base pairs. A (double) gene, therefore, always has two alleles, which could be different, and multiple alleles are possible for only one (double) gene. The second way would be to make absolutely no difference between genes and alleles and to speak of ‘different genes’ which belong to the same location in the DNA. In order to avoid the word ‘allele’ as much as possible, I have chosen where I can for the latter option, although that is technically perhaps somewhat less accurate. Compromises like these must often be made in order to keep a book like this accessible for a wider public.
[3]   From a letter to Dr. Archdall Reid from 28 December 1909; James Marchant, Letters and reminiscences, pp. 340, New York: Harper Brothers, 1916; quoted from In the beginning, Walt Brown.
[4]   will leave the bacteria out of consideration. They have no cell nucleus, no double chromosomes, and no sexual reproduction. In that respect, they are entirely another story.
[5]   It seems as though someone has given this some thought!
   
     
 
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