Aging & Senescence · §10

Archaic and present-day aging promoters

Across a cross-sectional set of seven dated, sequenced individuals — the present-day reference, three archaic Neanderthal genomes, one archaic Denisovan, and two dated modern-human genomes — the four aging-master promoter γ values sit in a very narrow band on every gene (each per-gene range < 0.0016). The senescence/apoptosis gate TP53 and the arrest switch CDKN2A read identically in the two dated modern-human genomes and the present-day reference; TERT carries the most archaic promoter substitutions (13). This is a measured snapshot — the only claims are the measured γ in each individual, its spread per gene, and which positions differ.

The same promoter-γ pipeline (−mean SantaLucia NN ΔG37 over TSS−2000..+500) is measured in each individual, where each promoter is the GRCh37 reference plus that individual's homozygous-derived substitutions. The set is examined as a snapshot; shared genotype states are reported as observed co-occurrences, never as anything beyond the co-occurrence itself.

The cross-sectional set

Seven high-coverage genomes carry the four aging masters at a known date: the present-day modern-human reference (GRCh37), three archaic Neanderthal individuals (Altai, Vindija 33.19, Chagyrskaya), one archaic Denisovan, and two dated modern-human genomes (Ust'-Ishim ≈ 45 kya, Loschbour ≈ 8 kya). Each promoter is reconstructed as the GRCh37 reference plus that individual's homozygous-derived substitutions (genotype 1/1, FILTER pass); γ is then measured by the identical pipeline used for the node atlas (§2) and the cross-species panel (§9).

Measured promoter γ for the four aging masters in each of seven dated individuals, examined as one cross-sectional set (kya = thousand years; Chagyrskaya is TERT-only). Observation only: each value is a measured present-state.
Individualage (kya)TP53CDKN2AFOXO3TERT
Present-day human (GRCh37)01.43331.44521.59271.5537
Altai Neanderthal~1221.43251.44461.59131.5540
Vindija 33.19 Neanderthal~521.43251.44461.59281.5540
Chagyrskaya 8 Neanderthal~801.5540
Denisova 3 (Denisovan)~761.43271.44461.59211.5534
Ust'-Ishim (early modern human)~451.43331.44521.59211.5541
Loschbour (W. hunter-gatherer)~81.43331.44521.59271.5537

The senescence gate reads the same

On TP53 (apoptosis) and CDKN2A (the p16 arrest switch), the two dated modern-human genomes and the present-day reference carry an identical promoter γ — the archaic individuals differ only by two or three distal substitutions that move γ by less than 0.0009. The core senescence/apoptosis gate is, as a measured state, the same sequence in every modern-human genome in the set and nearly the same in the archaic ones.

TERT carries the most promoter substitutions

Of the four masters, the telomere-maintenance gene TERT carries the most homozygous-derived promoter substitutions across the archaic individuals (13 in total), and the same three TERT positions co-occur across all four archaic genomes. The widest γ range in the whole set, however, belongs to FOXO3 (0.001536), and even that is under 0.0016 — so “most substituted” (TERT) and “widest γ spread” (FOXO3) are distinct, both small, measured facts.

Homozygous-derived promoter substitutions carried by the archaic individuals (Neanderthal + Denisovan), and the full γ range across the seven-individual set. TERT carries the most substitutions; every per-gene γ range is below 0.0016.
Genearchaic hom-sub countγ range (set)
TP5380.000860
CDKN2A60.000624
FOXO360.001536
TERT130.000712

The cancer-promoter positions are invariant

The two recurrent TERT cancer-promoter regulatory positions (the −124 and −146 sites relative to the start codon) carry the same base in every individual in the set; every difference TERT does carry is distal to them. This invariance is a measured observation across the snapshot.

What is and is not claimed

The claims are exactly three: the measured γ in each individual, the width of the γ spread per gene, and which promoter positions differ. Why the states co-occur is out of scope and graded [O]: a cross-sectional snapshot is silent on mechanism. Per-individual γ, the γ spread, the substitution counts, and the cancer-hotspot invariance are measured [V].