Evolution viewed from physics, physiology and medicine

Abstract

Stochasticity is harnessed by organisms to generate functionality. Randomness does not, therefore, necessarily imply lack of function or 'blind chance' at higher levels. In this respect, biology must resemble physics in generating order from disorder. This fact is contrary to Schrödinger's idea of biology generating phenotypic order from molecular-level order, which inspired the central dogma of molecular biology. The order originates at higher levels, which constrain the components at lower levels. We now know that this includes the genome, which is controlled by patterns of transcription factors and various epigenetic and reorganization mechanisms. These processes can occur in response to environmental stress, so that the genome becomes 'a highly sensitive organ of the cell' (McClintock). Organisms have evolved to be able to cope with many variations at the molecular level. Organisms also make use of physical processes in evolution and development when it is possible to arrive at functional development without the necessity to store all information in DNA sequences. This view of development and evolution differs radically from that of neo-Darwinism with its emphasis on blind chance as the origin of variation. Blind chance is necessary, but the origin of functional variation is not at the molecular level. These observations derive from and reinforce the principle of biological relativity, which holds that there is no privileged level of causation. They also have important implications for medical science.

Keywords: Schrödinger's error; biological relativity; evolution and physiology; modern synthesis; neo-Darwinism; stochasticity.

Figure 1.

The robustness of heterogeneity of expression of Sca-1 protein expression in a cloned cell population. Heterogeneity detected by immunofluorescence flow cytometry (a) was significantly larger than the resolution limit of the method (b). (c) The stability of the clonal heterogeneity over a period of three weeks. Note that the spread of gene expression levels is three orders of magnitude [21].

Figure 2.

Two examples illustrating experiments in which populations were produced by cloning either from one of the peaks in a bimodal distribution (a) or from outliers in a monomodal distribution (b). In both cases, the new population initially exhibits the range of expression of the parent subpopulation. Over time (several days), however, the heterogeneity reverts to the original distribution [22]. (Online version in colour.)

Figure 3.

Schematic diagram of gene-specific targeted hypermutation in immunoglobulin gene loci. The mutation rate is greatly increased only in the variable part of the genome, which is an approximately 1.5 kb region in each of the three immunoglobulin loci. In this figure, the graph above the rearranged variable (V) and joining (J) gene segments that form the variable region of Igκ depicts the mutation domain in the κ-light chain (Igκ) locus. 3′Eκ, Igκ 3′ enhancer; Cκ, Igκ constant; iEκ, Igκ intronic enhancer; MAR, matrix attachment region [23]. (Online version in colour.)

Figure 4.

(a) Five of the Galapagos finch species were studied, the reference species Geospiza fortis and four others. The graph in (b) shows the number of genetic and epigenetic changes plotted as a function of phylogenetic distance. The epigenetic changes correlate well with phylogenetic distance, the genetic mutations do not correlate as strongly [38]. (Online version in colour.)

Figure 5.

The extended evolutionary synthesis representing the extension as extensions of Darwinism and then of the neo-Darwinist modern synthesis (from [62]).

Figure 6.

The integrated synthesis representing the extensions as extensions of Darwinism but only partially from neo-Darwinism. Darwin's view of inheritance is also represented as extending outside the boundary of neo-Darwinism/(developed for this article from [61], based on [62]).