By quantifying EPR-generated accumulations of entangled proton qubits populating duplex microsatellite base pairs, observed as G-C → G'-C', G-C → *G-C* and A-T → *A-*T, the potential to exhibit expansion or contraction over evolutionary times can be qualitatively specified. Bold italics identify base pair superpositions of entangled proton qubits. Metastable hydrogen bonding amino (−NH2) protons encounter quantum uncertainty limits, Δx Δpx ≥ ћ/2, which generate EPR arrangements, keto-amino -(entanglement)→ enol−imine, yielding reduced energy entangled proton qubits shared between two indistinguishable sets of electron lone-pairs belonging to enol oxygen and imine nitrogen on opposite strands. When measured by Grover's-type quantum processors, δt ≤ 10 -13 s, microsatellites whose entangled proton qubits generate a preponderance of initiation codons ─ UUG, CUG, AUG, GUG ─ participate in the expansion mode of DNA synthesis, but if more stop codons ─ UAA, UGA, UAG ─ were introduced and/or the particular sequence consisted exclusively of A-T, such microsatellites would generally decrease in relative abundance over evolutionary times. This model is tested by evaluating the twenty-two most abundant microsatellites common to human and rat. From this list, predictions by "measurements of" entangled proton qubit states identify two ordered sets -eleven exhibiting expansion and eleven exhibiting contraction -of microsatellites, consistent with observation. These analyses imply Grover's-type enzyme-processor measurements of EPR-generated entangled proton "qubit pairs" can simulate microsatellite evolution, and further, identify entangled proton "qubit pairs" as the smallest "measurable" genetic informational unit, specifying particular evolution instructions with "measured" quantum information. Classical pathways cannot simulate microsatellite evolution observables.

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Transcriptase measurements of quantum expectations due to time-dependent coherent states populating informational DNA base-pair sites, designated by G-C --> *G-*C, G-C --> G'-C', and A-T --> *A-*T, provide a model for transcription and replication of time-dependent DNA lesions exhibited by bacteriophage T4. Coherent states are introduced as consequences of hydrogen bond arrangement, keto-amino --> enol-imine, where product protons are shared between two sets of indistinguishable electron lone-pairs and thus participate in coupled quantum oscillations at frequencies of ~10(13) s(-1). The transcriptase deciphers and executes genetic specificity instructions by implementing measurements on superposition proton states at *G-*C, G'-C', and *A-*T sites in an interval Δt << 10(-13) s. Decohered states participate in Topal-Fresco replication, which introduces substitutions *C --> T, *G --> A, G' --> T, and G' --> C, but superposition *A-*T states are deleted. These results imply an evolutionary shift favoring A-T richness.

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Experimental and theoretical evidence supporting the L€ owdin model of DNA specificity is presented. Molecular genetic measurements by the transcriptase demonstrate that timedependent point lesions, G-C ! G 0 -C 0 and G-C ! *G-*C, are consequences of keto-amino ! enol-imine arrangement. Product enol-imine protons are shared between two sets of indistinguishable electron lone-pairs, and thus, participate in coupled quantum oscillation at frequencies of $10 13 s À1 . Transcriptase genetic specificity is determined by components contributing to the formation of complementary hydrogen bonds, which in these cases are variable because of coupled quantum oscillations. In an interval Dt \ 10 À13 s, genetic specificities are measured and executed before an entanglement is created between coherent protons and the transcriptase. The ensuing entanglement causes a decoherent transition from quantum to classical, yielding a statistical ensemble of decohered enol and imine isomers that participate in Topal-Fresco substitution replication. Coherent states within *A-*T sites are deleted. Using approximate quantum methods for times t \ $ 100 years, the probability, P(t), of keto-amino ! enol-imine arrangement is P q ðtÞ ¼ 1 =2ðc q = hÞ 2 t 2 where c q is the energy shift between states. This model illustrates biological consequences of coherent states populating inherited (CAG) n repeats in human genomes.