title: Intrinsically driven changes in gene interaction complexity. I. Growth of regulatory complexes and increase in number of genes.
abstract: A two-step process, previously considered in the literature, and here named coadaptational drive, is deemed to be largely responsible for both increases in the complexity of transcriptional control and increases in the total gene number, along lines of descent leading to more complex organisms. Coadaptational drive consists in a succession of modifications in the interaction among informational macromolecules, namely, structural decay spread by genetic drift and repair spread by selection. Increased genetic complexity, drawing on the opportunities offered by gene duplication, may be considered to be a secondary effect of such processes of decay and repair. The evolution toward higher regulatory complexity is thus considered to be obligatorily founded in part on random genetic drift. Increases in this complexity would represent primarily a trend intrinsic to the internal molecular environment, with the external environment having only to concur. Direct selection of mutations that increase complexity without the intervention of a phase of genetic drift is acknowledged likely to be a significant process as well, but it is claimed that a sequence of events of direct selection cannot be unlimited and will eventually stall, and that the roots of such a sequence ultimately are to be traced to an episode of coadaptational drive. Controller gene diseases, mostly mild, therefore seem to be essential for the evolution of increased biological complexity. The attempt is made to show or to confirm that (i) a conservative force (repair) provides a mechanism for the generation of novelty, (ii) a prominent part of selection, counterpart to Darwinian selection, originates from the internal environment and derives from the mechanics of genomic processes, and (iii) this selection is at times directional and leads to increases in complexity.
authors.affiliation: Institute of Molecular Medical Sciences, P.O. Box 20452, Stanford, CA 94309, USA. EmileIMMS@aol.com
authors.forename: E
authors.initials: E
authors.lastname: Zuckerkandl
mesh_terms: D000818:Animals; D019143:Evolution, Molecular; D020440:Gene Duplication; D005786:Gene Expression Regulation; D005787:Gene Frequency; D005809:Genes, Regulator; D006801:Humans; D008957:Models, Genetic; D009154:Mutation; D010641:Phenotype; D012641:Selection, Genetic