It is impossible to imagine the nervous system without controllable genome instability, resulting in brain somatic mosaicism, one of the basic mechanisms of structural and functional heterogeneity of neurons. The source of such an instability is the presence of “hot spots” (repeating DNA sequences, provoking nonallelic recombination) and double-strand (DS) DNA breaks in the genome that occur in the matrix processes and physiological activity of neurons and are involved in memory formation and learning. The realization of the “norm–pathology” scenario is under epigenetic control; in particular, it depends on the parental effect of genome origin and stress. In this work, using the Williams model of drosophila carrying the agnts3 mutation in the gene for LIMK1 (the key enzyme of actin remodeling) using reciprocal hybrids with wild-type Canton-S line, we studied the contribution of maternal and paternal genomes in processes of learning and memory, as well as the formation of chromosome rearrangement in neuroblasts, determined by DS breaks and disorders of mitotic apparatus in norm and in exposure to stress impact via weak static magnetic field. The prevalent role of paternal genome in memory trace formation is shown. A patroclinous inheritance is established for frequencies of chromosome rearrangements and DS breaks, as well as chromatid bridges in anaphase neuroblasts at stress in the case of paternal agnts3 line. In the breed of agnts3 females, mitosis disorders are inherited via the maternal type. Based on previous research, we revealed microRNA contexts that can make patroclinous effects possible.