Collyer’s sixth claim, “[t]he variations within each species
are all explicable by Mendel's laws of genetics, and variations are limited, as
any breeder of plants and animals knows.” is confusingly written. Is he arguing
that there is a limit to evolution which prevents speciation? If so, then he’s
wrong since speciation has been observed. Furthermore, the fossil record of
large-scale evolutionary change is unarguable.
Where he is wrong is in claiming that all variation within
species is explained by Mendelian genetics. Non-mendelian genetics is required
to explain some features such as mitochondrial inheritance, imprinting and the
phenomenon where diseases such as Huntingdon's disease which are autosomal
dominant become more severe with passing generations. Basic mistakes such as
this once again highlight his ignorance of the subject he criticises.
Once again, we have already seen documented evidence of
speciation, as well as evidence of how genetic variation can occur, which
ranges from point mutation to genome duplication, horizontal gene transfer and
endosymbiosis. Species are not immutable biological concepts, as one can see
from the fact of common descent – all life is related via a process of descent
with modification.
There is another problem with Collyer’s sixth point, and that he has blundered badly by claiming variation within species is explicable by Mendel’s laws of genetics. They are not, as demonstrated by the existence of non-Mendelian genetics. Non-Mendelian genetics [35] describes the following medically significant phenomena:
There is another problem with Collyer’s sixth point, and that he has blundered badly by claiming variation within species is explicable by Mendel’s laws of genetics. They are not, as demonstrated by the existence of non-Mendelian genetics. Non-Mendelian genetics [35] describes the following medically significant phenomena:
- Mitochondrial inheritance: mitochondrial DNA is almost always inherited only via the maternal line. The existence of mitochondrial disorders such as myoclonic epilepsy with red ragged fibres and Leber’s hereditary optic neuropathy makes non-mendelian genetics anything other than an abstract concept. Cells contain more than one copy of mitochondrial DNA. This, along with heteroplasmy (cells contain a mix of normal and abnormal mtDNA) and homoplasmy (cells contain only one sort of mtDNA) complicate mitochondrial inheritance.
- Multifactorial inheritance: arises from the combined influence of multiple genes, augmented by environmental factors. One will often see familial concentrations without a particular pattern of inheritance. There is also often a significant variation in the severity and expression of the phenotype.
- Somatic mosaicism: occurs when there are cells with more than one genotype in the body. Most commonly, this occurs when a mutation occurs in the embryo after the first cleavage post-fertilisation. A less common form of somatic mosaicism occurs when two embryos in utero fuse to form one embryo, with cell lines from two different individuals being present. Clinically, this can result in people with disorders such as Downs Syndrome presenting with a less severe version of the disease than those without somatic mosaicism.
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- Gonadal mosaicism: occurs when only some of the gametes (sperm or ova) carry the mutation. Clinically, this results in patterns of inheritance that are not expressed in a Mendelian pattern. One classic way in which gonadal mosaicism presents is when two or more children present with an autosomal dominant disorder in the absence of any family history. This implies that one of the parents has a gonadal mosaicism for the mutation.
- Genetic imprinting: this is a phenomenon by which genes are expressed according to the parent of origin. An imprinted gene will not be expressed, resulting in only the non-imprinted allele inherited from the parent being expressed. Imprinting is vital to understanding the genetics behind disorders such as Angelman syndrome and Prader-Willi syndrome. The same region of chromosome 15 is involved in both syndromes, with the difference being in which parent the affected genes are imprinted. In Prader-Willi syndrome, paternal copies of the genes are silenced while in Angelman syndrome, maternal copies are silences via imprinting.
- Genetic amplification: also known as anticipation, this refers to the phenomenon where the expression of a phenotype becomes more pronounced in succeeding generations. Instability in areas of the genome underlies this phenomenon, which is seen in diseases such as myotonic dystrophy, Huntingdon disease and Fragile X syndrome. While the basic inheritance of the disorder can be explained via Mendelian inheritance, the expression of the phenotype in succeeding generations isn’t explained in a Mendelian manner.
Providing an overview of non-Mendelian genetics isn’t an
exercise in pedantry. Collyer has made a basic mistake in claiming that variations
within species are all explained by Mendel’s laws of genetics. This isn’t mere pedantry. Mistakes such as this which an
undergraduate science student would be able to pick up demonstrate that Collyer
simply does not know what he is talking about with respect to evolutionary
genetics.
