Purpose of the Prize

“The Origin-of-Life Prize” ® is being offered to stimulate research into chaos, complexity, information, probability, self-organization, and artificial life/intelligence theories as they relate directly to biochemical and molecular biological reality. The Foundation wishes to encourage the pursuit of natural-process explanations and mechanisms of initial “gene” emergence within nature. The subject of interest is the genesis of primordial functional information itself rather than its physico-chemical matrix of retention and transmission. Bioinformation fits into the category of “prescriptive information” (“instruction,” rather than mere probabilistic combinatorics [Abel, 2000]). By what mechanisms do stochastic ensembles acquire instructive/integrative potential? In other words, what are the processes whereby random biopolymeric sequences self-organize into indirect, functional code?

Central questions of interest relate to the definition and nature of “genetic instructions” and “biomessage.” Is genetic recipe adequately represented and described by “mutual entropy” (shared, correlative uncertainty between transmitter and receiver)? At what point and by what processes do “biofunction” and “biosystem” enter into the chemical evolution of bioinformation?

What is a reasonable, empirically-accountable definition of “minimal life”?

How does nature’s genetic programming achieve such long sequences of highly functional decision-node selections?

Genes are linear, digital, quaternary decision-node strings. Nucleotide selections represent four-way algorithmic switch-settings. These switch-settings are covalently-bound into primary structure. The string’s specific sequence precedes secondary and tertiary folding. Folding results from forces such as hydrogen bonding, charge attractions/repulsions, and hydrophobicity. These forces are much weaker than the covalent binding that has already determined sequence. Folding space is primarily constrained by this pre-existing nucleotide sequencing. Ultimately, the algorithmic programming instantiated into the nucleotide-selection sequence determines biofunction.

The problem is that natural selection works only at the phenotypic level, not at the genetic level. Neither physicochemical forces nor environmental selection choose the next nucleotide to be added to the biopolymer. Mutations occur at the genetic level. But environmental selection occurs at the folding (functional) level, after-the-fact of already strongly set sequence, and after-the-fact of already established algorithmic function of the folded biopolymer.

By what mechanism did prebiological nature set its initial algorithmic switch-settings to program the first few (RNA?) genes?

How was RNA folding function anticipated when covalently-bound primary structure was forming?

Suppose a self-replicative oligoribonucleotide analog sequence occurred spontaneously out of sequence space. How did this self-replicative strand simultaneously anticipate folding needs for metabolic utility? Any evolution toward folding fitness would tend to mutate the sequencing away from self-replicative fitness. What was the bridge between both functions? How could random mutations simultaneously contribute to both disparate functions?

How did so many biochemical pathways get integrated into one coherent, unified, and sophisticated metabolic process?