Mutations: How They Work and Which Worldview They Favor

chemistry-formulas-green-bg-1Does evolution point to naturalism or to intelligent design?

Before addressing this question it is always important to define terms. Evolution, at a very basic level, means change over time. We use the words evolution and evolve in this way all the time. As an example one might assert that one’s thinking about race and cross-cultural interactions evolves over time as one gains exposure to various cultures and races. In scientific language evolution can have this same basic meaning: change. But often in naturalistic explanations of the origins of life and of species this simple concept of change is misapplied to mean more than has been scientifically or mechanistically demonstrated.

Consider mutations in the cell as an example of this misapplication. Mutations are changes to the nucleic acid molecular codes that randomly occur as a result of mistakes in DNA replication or during DNA damage repair. There are many different kinds of mutations; for example, point mutations (single base substitutions), repetition of short segments (from stuttering of the polymerase during replication), and indels (insertions or deletions of bases). Spontaneously occurring mutations result from external stimuli or internal mistakes that affect cells’ processes. Mutations can also be induced through intentional exposure to chemicals or radiation. Within a given cell, some mutations have no effect, some can be detrimental to proper functioning (even resulting in cell death), and on rare occasions some can provide increased fitness in particular environments.

For haploid organisms (those possessing one complete set of chromosomes) and single-cell organisms, mutations of any kind can have a radical effect on the cell and all its progeny. The replication of single-cell organisms is haploid and asexual, and is extremely rapid compared to the reproductive cycle of sexual organisms. Therefore, a mutation that provides a fitness advantage will often spread throughout single-cell progeny and become prevalent throughout the population within a very short period of time. The fact that rapid selection of mutations provides fitness advantages is an uncontested idea at the level of single-cell microorganisms. This type of evolution is sometimes referred to as microbial evolution or microevolution and it is noncontroversial.

Similar molecular mutations and adaptations occur, emerge, and are preserved over time within multicellular organisms and populations, especially when such genetic changes correspond to fitness advantages. But the scientific mechanisms of such inheritance and spread within multicellular organisms and populations are much more complex and less frequent than for single-cell organisms.

In multicellular, diploid organisms (those possessing two sets of chromosomes) that require sexual reproduction, mutations typically occur in somatic (nonreproductive) cells and in an allele on only one chromosome. These mutations can have an immediate effect on the single cell’s function or progeny cells if it undergoes division.

Significantly, however, somatic mutations in sexual, diploid organisms are not passed on to offspring. In order for a mutation to be inherited, the mutation must occur in a gamete, the haploid cell of a sperm or egg.1 If the mutation occurs within a gamete (sperm or egg), upon fusion with the corresponding unmutated gamete (egg or sperm, respectively) the resulting diploid progeny becomes heterozygous (occurring in one chromosome) for the mutation. If a mutation is heterozygous but not dominant in its phenotype, it must occur independently and concurrently in both individual gametes of the reproductive pair in order to have a phenotypic effect in offspring and for subsequent positive selection to occur within a population. In fact, it would almost certainly need to have spontaneously occurred in multiple germ-line cells of each individual to result in a likely fertilization of a mutated sperm with a mutated egg. Therefore, in multicellular organisms, in order for a single change to be passed to progeny, such fitness mutations must be heterozygous dominant or they must occur independently and concurrently in multiple cells in each member of a reproductive pair. To add to the difficulty, they must occur within the germ-line cells, not just somatic cells. The intricate, complex nature of this nontrivial type of molecular change and germ line heredity was unknown to evolutionary champion Charles Darwin.

Furthermore, selection of advantageous mutations in large-organism populations is extensively prolonged in two ways compared to simple, single-cell organisms or asexual reproductive populations. First, selection is prolonged by the fact that the progeny or recipient of the germ-line mutation must reach reproductive age and successfully reproduce. And second, the spread of the trait throughout the population is prolonged by the previously unmutated allele’s predominance in the existing population, which would not necessarily result in an immediate inability or inhibited ability to compete for resources or mates.

Nevertheless, the existence of mutations (or variations) within human alleles that provide obvious environmental advantages for specific populations is uncontested. This molecular adaptation is often heralded as a hallmark of naturalistic evolution. In evolutionary dogma these nontrivial molecular changes are employed to explain not only the observation of complex organisms’ adaptive abilities but also the emergence of entirely new species.

However, macroevolutionary changes and advancements in complexity that are necessary for observed differences in biologically advanced organisms pose significant problems for naturalistic evolution. To employ microevolutionary (undisputed) explanations in an attempt to address macroevolutionary (highly disputed) advancement seems wholly inadequate. It is similar to citing the discovery and repeated verification of the use of stone tools as an explanation for the computer laptops and tablets humans use today.

From my perspective as a scientist, there is no rational reason why molecular adaptation should be co-opted and relegated only to naturalistic evolutionary explanations of the origin of species. In fact, what scientists observe about the mechanisms and advantages of molecular adaptation fits better in a biblically compatible, design narrative than in a neo-Darwinian one. In a design narrative, one starts with complex organisms that have the capacity for molecular adaptation. Such molecular adaptation would be expected as a mechanism of survival, persistence, and thriving. An insightful designer would anticipate various external challenges and environmental changes between different geographical climes and creatively engineer organisms with the capacity to accommodate such changes. Any species subject to such environmental stresses would be short-lived if not for an innate ability to adapt.

In an attempt to understand the world, we need to seek out the best possible explanations, clearly enunciating the scientific underpinnings of nature’s complexities. And for the sake of scientific inquiry and true advancement we must admit the areas where neo-Darwinian explanations fail to offer sufficient or viable mechanisms for observed phenomena. To force the observations to fit the paradigm just for the sake of maintaining the paradigm might truly hinder scientific progress.


  1. It’s important to note in regard to complex diploid, multicellular, sexual organisms that mutations in somatic cells are not directly passed on to offspring. Although some epigenetic changes are passed on to offspring, unless these mutations occur in the egg of the maternal parent it is difficult to imagine or articulate how these epigenetic changes are “inherited” and not rather a result of continual environmental influences resulting in individually reproducible, repeated epigenetic changes.


By Anjeanette Roberts

Dr. Anjeanette (AJ) Roberts received her PhD in cell and molecular biology from the University of Pennsylvania in 1996, and currently serves as a Visiting Fellow with the Rivendell Institute at Yale University in New Haven, CT.



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