Variations in brain defects result from cellular mosaicism in the activation of heat shock signalling

Seiji Ishii, Masaaki Torii, Alexander I. Son, Meenu Rajendraprasad, Yury M. Morozov, Yuka Imamura Kawasawa, Anna C. Salzberg, Mitsuaki Fujimoto, Kristen Brennand, Akira Nakai, Valerie Mezger, Fred H. Gage, Pasko Rakic () and Kazue Hashimoto-Torii ()
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Seiji Ishii: Center for Neuroscience Research, Children's National Medical Center
Masaaki Torii: Center for Neuroscience Research, Children's National Medical Center
Alexander I. Son: Center for Neuroscience Research, Children's National Medical Center
Meenu Rajendraprasad: Center for Neuroscience Research, Children's National Medical Center
Yury M. Morozov: Yale University School of Medicine
Yuka Imamura Kawasawa: Pennsylvania State University College of Medicine
Anna C. Salzberg: Institute for Personalized Medicine, Pennsylvania State University College of Medicine
Mitsuaki Fujimoto: Yamaguchi University School of Medicine
Kristen Brennand: Icahn School of Medicine at Mount Sinai
Akira Nakai: Yamaguchi University School of Medicine
Valerie Mezger: CNRS, UMR7216 Epigenetics and Cell Fate
Fred H. Gage: Salk Institute for Biological Studies, Laboratory of Genetics
Pasko Rakic: Yale University School of Medicine
Kazue Hashimoto-Torii: Center for Neuroscience Research, Children's National Medical Center

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Repetitive prenatal exposure to identical or similar doses of harmful agents results in highly variable and unpredictable negative effects on fetal brain development ranging in severity from high to little or none. However, the molecular and cellular basis of this variability is not well understood. This study reports that exposure of mouse and human embryonic brain tissues to equal doses of harmful chemicals, such as ethanol, activates the primary stress response transcription factor heat shock factor 1 (Hsf1) in a highly variable and stochastic manner. While Hsf1 is essential for protecting the embryonic brain from environmental stress, excessive activation impairs critical developmental events such as neuronal migration. Our results suggest that mosaic activation of Hsf1 within the embryonic brain in response to prenatal environmental stress exposure may contribute to the resulting generation of phenotypic variations observed in complex congenital brain disorders.

Date: 2017
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DOI: 10.1038/ncomms15157

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