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The Ādam Paradox Hypothesis 76
Regulatory Fine-Tuning of the Genome
Building on this distinction, a second strand focuses on non-
coding DNA — the enhancers and promoters that regulate
when and where genes are expressed. Over evolutionary time,
gradual tweaks to these elements may have altered the wiring
of neural circuits. Research on human accelerated regions
(HARs) is often cited: HAR1, for example, is a rapidly
evolving non-coding RNA expressed in Cajal-Retzius neurons
during cortical layering (Pollard et al., 2006). Experimental
assays suggest that enhancers such as HAR202 show human-
specific activity patterns in progenitor cells linked to
synaptogenesis and migration. Similarly, human-specific
intronic enhancers of FOXP2 — a gene central to vocal
learning — have been shown to influence expression in
cortico-striatal circuits (Reilly et al., 2015).
Claim. Gradual changes to enhancers and promoters
modulated when/where neural genes turn on, subtly shifting
circuits for syntax, working memory, social learning,
sequencing (Pollard et al., 2006; Reilly et al., 2015).
Case studies / anchors.
HAR1: fast-evolving noncoding RNA expressed in Cajal-
Retzius neurons during cortical layering — a plausible lever
on cortical architecture (timing/lamination).
HAR enhancers (incl. HAR202): active in neural progenitors;
experimental assays show human-shifted activity for genes
tied to migration/synaptogenesis.
FOXP2 regulatory elements: human-specific intronic
enhancer activity suggests expression tuning in cortico-striatal
circuits (consistent with vocal learning/sequencing).
Takeaway. Rather than a single “language gene,
” many small
regulatory shifts accumulate toward a functional threshold.
Rather than a single
“language gene,
” many
small regulatory shifts
accumulate toward a
functional threshold.