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Zinc finger and BTB domain containing 16 (ZBTB16) play the roles in the neural progenitor cell proliferation and neuronal differentiation during development, however, how the function of  ZBTB16  is involved in brain function and behaviors unknown. Here we show the deletion of  Zbtb16  in mice leads to social impairment, repetitive behaviors, risk-taking behaviors, and cognitive impairment. To elucidate the mechanism underlying the behavioral phenotypes, we conducted histological analyses and observed impairments in thinning of neocortical layer 6 (L6) and a reduction of TBR1+ neurons in  Zbtb16  KO mice. Furthermore, we found increased dendritic spines and microglia, as well as developmental defects in oligodendrocytes and neocortical myelination in the prefrontal cortex (PFC) of  Zbtb16  KO mice. Using genomics approaches, we identified the  Zbtb16  transcriptome that includes genes involved in neocortical maturation such as neurogenesis and myelination, and both autism spectrum disorder (ASD) and schizophrenia (SCZ) pathobiology. Co-expression networks further identified  Zbtb16 -correlated modules that are unique to ASD or SCZ, respectively. Our study provides insight into the novel roles of  ZBTB16  in behaviors and neocortical development related to the disorders.

Zbtb16 regulates social cognitive behaviors and neocortical development