Answers are grounded in this paper and cite their sources.
Mathematical modeling reveals that weak natural selection drives the emergence of functional elements from non-functional DNA in eukaryotes, suggesting non-adaptive origins for genomic complexity.
How do eukaryotic genomes acquire new functional parts, such as regulatory elements and long non‐coding RNAs? Here, we propose that these parts arise from non‐functional precursors primarily through non‐adaptive processes that proliferate when selection is weak. Borrowing concepts from Markov chain theory, we represent each stage along the junk‐to‐function continuum as a discrete state with defined transition probabilities. This formalism makes clear why selection cannot act on future function, and why a part's current biochemical activity may be unrelated to its evolutionary past. We show how, under certain conditions, new intermediate states appear that increase the forward flux from junk DNA to new functional parts. These conditions—weak selection, abundant epistasis and quality control processes, and the accumulation of messiness—are characteristic of many eukaryotic genomes, allowing them to become more complex as new functional parts emerge.
No takes yet. Share an insight, caveat, or question.
Palazzo et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: