Theoretical model reveals frequency modulation of mitochondrial clocks during sexual differentiation in mammalian embryos, highlighting a quantum metabolic basis for dimorphism.
In mammalian and human embryonic development, the fertilized egg initially develops along a “default female (maternal-based) morphology” as a standard prototype, irrespective of its genetic sex (XX/XY). In this paper, we reformulate this initial developmental trajectory from physical and informational perspectives grounded in the Biological Quantum Processing Unit (Bio-QPU) hypothesis. Following fertilization, a robust “female baseline framework” is established under the fundamental quantum clock frequency (ωM) supplied by maternal mitochondria. The expression of the SRY gene on the Y chromosome at gestational weeks 6–7 acts as a “frequency modulation (FM) switch”. Through testis organogenesis and androgen secretion, optimization of the mitochondrial membrane potential (ΔVmem) and a resultant clock frequency shift (ωM → ωM+Δ) re-tune the resonance conditions between the receptive neural architecture (hardware) and the mitochondrial metabolic clock (power supply). This mechanism provides a comprehensive physical formulation for the emergence of sexual dimorphism and individual cognitive diversity.
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