The genome governs the developmental trajectory of neural circuits [1, 2], guiding processes like neurogenesis and synaptogenesis to ultimately shape the structure of the brain. Here, we study the impact of genetic variation during development on the dynamics and geometry of neural population activity in the motor cortex (MOp) of adult mice during natural feeding behavior. We focus on autism spectrum disorder (ASD) models, many cases of which are characterized by stereotypical motor impairments [3]. Specifically, we compare neural activity during a dexterous cued self-feeding task in two transgenic models of ASD---Angelman’s syndrome (AS) and Pitt-Hopkins syndrome (PS) [4]---to wild-type (WT) mice, to understand how genetic variations that disrupt neurodevelopmental processes alter neural dynamics and behavior. Analysis of paw kinematics showed that when compared to WT mice, PS mice often largely overshot their movements, whereas AS mice produced slightly shorter reach trajectories. We then analyzed MOp population activity recorded with Neuropixels. To assess the impact of abnormal neurodevelopmental trajectories in AS and PS mice, we quantified the similarity across genotypes in the geometry and dynamics of neural population trajectories using Canonical Correlation Analysis (CCA) [5] and Dynamical Similarity Analysis (DSA) [6], respectively. We found that genetically altered developmental trajectories in both ASD models led to significant differences in both the structure and dynamics of MOp neural population activity, with features specific to each genetic manipulation. Crucially, the neural dynamics of the PS mice were most dissimilar to those of the WT mice, as we anticipated based on their more extreme behavioural phenotype. By characterising the differences in neural dynamics underlying the abnormal movements produced by AS, PS mice, we provide insights into how genetic factors influence the development of motor-related neural dynamics, offering a potential mechanistic insight into the motor impairments observed in people with ASD.