Machine Zygote: Causal Biparental Heredity Before Learning in a Germline--Soma Artificial Agent
arXiv:2609.17300v1 Announce Type: cross Abstract: Artificial ontogeny, developmental encodings, robot reproduction, and inherited controllers are established research directions, yet a narrower question remains: can a newborn artificial agent exhibit measurable biparental heredity before learning, and can that dependence be isolated causally rather than inferred only from parent-offspring resemblance? We introduce Machine Zygote, a computational germline-soma architecture designed to test this
Overview
arXiv:2609.17300v1 Announce Type: cross Abstract: Artificial ontogeny, developmental encodings, robot reproduction, and inherited controllers are established research directions, yet a narrower question remains: can a newborn artificial agent exhibit measurable biparental heredity before learning, and can that dependence be isolated causally rather than inferred only from parent-offspring resemblance? We introduce Machine Zygote, a computational germline-soma architecture designed to test this question. Two parental germlines are independently mutated and recombined into a zygote that parameterizes development of an initially generic eight-module soma, which is then frozen and evaluated without learning. A preregistered 4 x 4 diallel of 640 offspring shows significant dam and sire dependence for five of six behavioral traits after Holm correction, with parental and interaction components accounting for 36-53 percent of modeled variance across five principal traits. In matched-background interventions (n=60), substituting one parental germline while holding recombination and stochastic background fixed causes phenotype shifts exceeding a same-parent re-mutation control for five of six traits for both parental channels. Recombination also yields excess transgressive offspring for speed and gait frequency. A preregistered developmental-dependence hypothesis is not supported: a quasistatic no-dynamics ablation preserves the mean phenotype distribution while altering parental variance structure. Thus the study supports causal biparental pre-learning heredity in this simulation, but not the stronger claim that recurrent developmental dynamics are necessary. It does not establish physical heredity, biological genetics, or autonomous evolution. The contribution is an intervention-centered framework and reproducible benchmark for separating heredity, development, stochastic variation, and post-birth learning.
Source
Originally published at arxiv.org.
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Source: https://arxiv.org/abs/2609.17300