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ATF5 deficiency causes abnormal cortical development.
Mariko Umemura1, Yasuyuki Kaneko2, Ryoko Tanabe2
1Laboratory of Environmental Molecular Physiology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan. mumemura@toyaku.ac.jp.
Scientific Reports
|April 1, 2021
Summary
Activating transcription factor 5 (ATF5) deficiency causes abnormal brain development in mice, leading to behavioral issues. This suggests ATF5 is crucial for proper neural progenitor cell function and migration during cortical development.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- Activating transcription factor 5 (ATF5) is a transcription factor involved in neural development.
- ATF5-deficient mice exhibit behavioral abnormalities, suggesting a role in brain function.
- The specific role of ATF5 in higher-order brain structures and cortical development is not fully understood.
Purpose of the Study:
- To investigate the underlying causes of behavioral abnormalities in ATF5-deficient mice.
- To examine the role of ATF5 in embryonic cerebral cortex development and neural cell migration.
Main Methods:
- Analysis of embryonic cerebral cortex in ATF5-deficient (ATF5-/-) and wild-type mice.
- Assessment of cortical thickness, radial glial cells, neural progenitor cells, and radial migration.
Main Results:
- ATF5-/- embryonic cerebral cortex was thinner with fewer radial glial and neural progenitor cells.
- Deficiency in ATF5 impacted radial glial cell basal processes, crucial for neuronal migration.
- Impaired radial migration of upper layer cortical neurons was observed in ATF5-/- mice.
Conclusions:
- ATF5 deficiency disrupts embryonic cortical development, specifically affecting neural progenitor cell numbers and radial migration.
- These developmental defects in ATF5-/- mice may contribute to the observed behavioral abnormalities.
- ATF5 plays a critical role in the proper development of the cerebral cortex.
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