Consequence of the loss of Sox2 in the developing brain of the mouse

Miyagi, Satoru; Masui, Shinji; Niwa, Hitoshi; Saito, Tetsuichiro; Shimazaki, Takuya; Okano, Hideyuki; Nishimoto, Masazumi; Muramatsu, Masami; Iwama, Atsushi; Okuda, Akihiko

doi:10.1016/j.febslet.2008.07.011

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Volume 582, Issue 18 , Pages 2811-2815, 6 August 2008

Consequence of the loss of Sox2 in the developing brain of the mouse

Edited by Jesus Avila

Satoru Miyagi
- Division of Developmental Biology, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka, Saitama 350-1241, Japan
- Department of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan
Shinji Masui
- Division of Molecular Biology and Cell Engineering, Department of Regenerative Medicine, Research Institute, International Medical Center of Japan, 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655, Japan
Hitoshi Niwa
- Laboratory for Pluripotent Cell Studies, RIKEN, Center for Developmental Biology, Chuo-ku, Kobe 650-0047, Japan
Tetsuichiro Saito
- Department of Developmental Biology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan
Takuya Shimazaki
- Department of Physiology, Keio University School of Medicine, Shinjyuku-ku, Tokyo 160-8582, Japan
Hideyuki Okano
- Department of Physiology, Keio University School of Medicine, Shinjyuku-ku, Tokyo 160-8582, Japan
Masazumi Nishimoto
- Division of Developmental Biology, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka, Saitama 350-1241, Japan
Masami Muramatsu
- Division of Developmental Biology, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka, Saitama 350-1241, Japan
Atsushi Iwama
- Department of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan
Akihiko Okuda
- Division of Developmental Biology, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka, Saitama 350-1241, Japan
- Corresponding author. Fax: +81 42 984 4763.

Received 23 June 2008; accepted 4 July 2008. published online 16 July 2008.

Abstract

The transcription factor Sox2 is expressed at high levels in neural stem and progenitor cells. Here, we inactivated Sox2 specifically in the developing brain by using Cre–loxP system. Although mutant animals did not survive after birth, analysis of late gestation embryos revealed that loss of Sox2 causes enlargement of the lateral ventricles and a decrease in the number of neurosphere-forming cells. However, although their neurogenic potential is attenuated, Sox2-deficient neural stem cells retain their multipotency and self-renewal capacity. We found that expression level of Sox3 is elevated in Sox2 null developing brain, probably mitigating the effects of loss of Sox2.

Keywords: Sox2, Neural stem cells, Self-renewal, Multipotency, Conditional knockout