| First Author | Umemura M | Year | 2021 |
| Journal | Sci Rep | Volume | 11 |
| Issue | 1 | Pages | 7295 |
| PubMed ID | 33790322 | Mgi Jnum | J:304967 |
| Mgi Id | MGI:6695652 | Doi | 10.1038/s41598-021-86442-5 |
| Citation | Umemura M, et al. (2021) ATF5 deficiency causes abnormal cortical development. Sci Rep 11(1):7295 |
| abstractText | Activating transcription factor 5 (ATF5) is a member of the cAMP response element binding protein (CREB)/ATF family of basic leucine zipper transcription factors. We previously reported that ATF5-deficient (ATF5(-/-)) mice exhibited behavioural abnormalities, including abnormal social interactions, reduced behavioural flexibility, increased anxiety-like behaviours, and hyperactivity in novel environments. ATF5(-/-) mice may therefore be a useful animal model for psychiatric disorders. ATF5 is highly expressed in the ventricular zone and subventricular zone during cortical development, but its physiological role in higher-order brain structures remains unknown. To investigate the cause of abnormal behaviours exhibited by ATF5(-/-) mice, we analysed the embryonic cerebral cortex of ATF5(-/-) mice. The ATF5(-/-) embryonic cerebral cortex was slightly thinner and had reduced numbers of radial glial cells and neural progenitor cells, compared to a wild-type cerebral cortex. ATF5 deficiency also affected the basal processes of radial glial cells, which serve as a scaffold for radial migration during cortical development. Further, the radial migration of cortical upper layer neurons was impaired in ATF5(-/-) mice. These results suggest that ATF5 deficiency affects cortical development and radial migration, which may partly contribute to the observed abnormal behaviours. |
