RM & NS: The Creationist and ID Strawman
AUTHOR: Allen MacNeill
SOURCE: Original essay
COMMENTARY: That's up to you...
Creationists and supporters of Intelligent Design Theory ("IDers") are fond of erecting a strawman in place of evolutionary theory, one that they can then dismantle and point to as "proof" that their "theories" are superior. Perhaps the most egregious such strawman is encapsulated in the phrase "RM & NS". Short for "random mutation and natural selection", RM & NS is held up by creationists and IDers as the core of evolutionary biology, and are then attacked as insufficient to explain the diversity of life and (in the case of some IDers) its origin and evolution as well.
Evolutionary biologists know that this is a classical "strawman" argument, because we know that evolution is not simply reducible to "random mutation and natural selection" alone. Indeed, Darwin himself proposed that natural selection was the best explanation for the origin of adaptations, and that natural selection itself was an outcome that necessarily arises from three prerequisites:
• Variety: significant differences between the characteristics of individuals in populations);
• Heredity: genetic inheritance of traits from parents to offspring; and
• Fecundity: reproduction, often resulting in more offspring than are necessary for replacement.
Given these prerequisites, the following outcome is virtually inevitable:
• Demography: some individuals survive and reproduce more often than others, and hence their heritable characteristics become more common in their populations over time.
As I have alread pointed out in an earlier post, the real creative factor in evolution isn't natural selection per se, it's the "engines of variation" that produce the various heritable characteristics that natural selection then preserves from generation to generation. According to the creationists and IDers, the only source of such variation is "random mutations", and so there simply isn't enough variation to provide the raw material for evolutionary change.
In my earlier post on the "engines of evolution" I promised a list of the "engines of variation" that provide the raw material for evolutionary change. It's taken me a while, but here it is. This list includes "random mutation,' of course, but also 46 other sources of variation in either the genotypes or phenotypes of living organisms. Note that the list is not necessarily exhaustive, nor are any of the entries in the list necessarily limited to the level of structure or function under which they are listed. On the contrary, this is clearly a list of the minimum sources of variation between individuals in populations. A comprehensive list would almost certainly include hundreds (and possibly thousands) of more detailed processes. Also, the list includes processes that change either genotypes or phenotypes or both, but does not include processes that are combinations of other processes in the list, again implying that a comprehensive listing would be much longer and more detailed.
Anyway, here is the list of the "engines of variation", arranged according to level of structure and function (if a term is underlined, you can click on it and be taken to a definition and explanation of that term, usually at Wikipedia):
SOURCES OF HERITABLE VARIATION BETWEEN INDIVIDUALS IN POPULATIONS
Gene Structure (in DNA)
1) point mutations
2) deletion and insertion (“frame shift” / "indel") mutations
3) inversion and translocation mutations
Gene Expression in Prokaryotes
4) changes in promoter or terminator sequences (increasing or decreasing binding)
5) changes in repressor binding (in prokaryotes); increasing or decreasing binding to operator sites
6) changes in repressor binding (in prokaryotes); increasing or decreasing binding to inducers
7) changes in repressor binding (in prokaryotes); increasing or decreasing binding to corepressors
Gene Expression in Eukaryotes
8) changes in activation factor function in eukaryotes (increasing or decreasing binding to promoters)
9) changes in intron length, location, and/or editing by changes in specificity of SNRPs
10) changes in interference/antisense RNA regulation (increasing or decreasing binding to sense RNAs)
Gene Interactions
11) changes in substrates or products of biochemical pathways
12) addition or removal of gene products (especially enzymes) from biochemical pathways
13) splitting or combining of biochemical pathways
14) addition or alteration of pleiotropic effects, especially in response to changes in other genes/traits
Eukaryotic Chromosome Structure
15) gene duplication within chromosomes
16) gene duplication in multiple chromosomes
17) inversions involving one or more genes in one chromosome
18) translocations involving one or more genes between two or more chromosomes
19) deletion/insertion of one or more genes via transposons
20) fusion of two or more chromosomes or chromosome fragments
21) fission of one chromosome into two or more fragments
22) changes in chromosome number via nondisjunction (aneuploidy)
23) changes in chromosome number via autopolyploidy (especially in plants)
24) changes in chromosome number via allopolyploidy (especially in plants)
Eukaryotic Chromosome Function
25) changes in regulation of multiple genes in a chromosome as a result of the foregoing structural changes
26) changes in gene expression as result of DNA methylation
27) changes in gene expression as result of changes in DNA-histone binding
Genetic Recombination
28) the exchange of non-identical genetic material between two or more individuals (i.e. sex)
29) lateral gene transfer via plasmids and episomes (especially in prokaryotes)
30) crossing-over (reciprocal and non-reciprocal) between sister chromatids in meiosis
31) crossing-over (non-reciprocal) between sister chromatids in mitosis
32) Mendelian independent assortment during meiosis
33) hybridization
Genome Structure and Function
34) genome reorganization and/or reintegration
35) partial or complete genome duplication
36) partial or complete genome fusion
Development (among multicellular eukaryotes, especially animals)
37) changes in tempo and timing of gene regulation, especially in eukaryotes
38) changes in homeotic gene regulation in eukaryotes
39) genetic imprinting, especially via hormone-mediated DNA methylation
Symbiosis
40) partial or complete endosymbiosis
41) partial or complete incorporation of unrelated organisms as part of developmental pathways (especially larval forms)
42) changes in presence or absence of mutualists, commensals, and/or parasites
Behavior/Neurobiology
43) changes in behavioral anatomy, histology, and/or physiology in response to changes in biotic community
44) changes in behavioral anatomy, histology, and/or physiology in response to changes in abiotic environment
45) learning (including effects of use and disuse)
Physiological Ecology
46) changes in anatomy, histology, and/or physiology in response to changes in biotic community
47) changes in anatomy, histology, and/or physiology in response to changes in abiotic environment
So, next time you hear or read a creationist or IDer cite "RM & NS" as the sole explanation for evolutionary change, point out to them and everyone else that there are at least 47 different sources of variation (including "random mutations"), and at least three different processes that result from them: natural selection, sexual selection, and random genetic drift.
Comments, criticisms, and suggestions (especially additional items for the list) are warmly welcomed!
--Allen
Labels: engines of variation, evolution, genetic variation, intelligent design, phenotypic variation