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

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 c...

Full description

Saved in:
Bibliographic Details
Published in:FEBS letters 2008-08, Vol.582 (18), p.2811-2815
Main Authors: Miyagi, Satoru, Masui, Shinji, Niwa, Hitoshi, Saito, Tetsuichiro, Shimazaki, Takuya, Okano, Hideyuki, Nishimoto, Masazumi, Muramatsu, Masami, Iwama, Atsushi, Okuda, Akihiko
Format: Article
Language:English
Subjects:
Animals
Cell Differentiation - genetics
Conditional knockout
DNA-Binding Proteins - biosynthesis
DNA-Binding Proteins - genetics
DNA-Binding Proteins - physiology
Embryonic Stem Cells - cytology
Embryonic Stem Cells - metabolism
Gene Silencing
High Mobility Group Proteins - biosynthesis
HMGB Proteins - genetics
HMGB Proteins - physiology
Lateral Ventricles - cytology
Lateral Ventricles - embryology
Lateral Ventricles - metabolism
Mice
Multipotency
Neural stem cells
Neurons - cytology
Neurons - metabolism
Receptors, Notch - metabolism
Self-renewal
Signal Transduction - genetics
Sox2
SOXB1 Transcription Factors
Transcription Factors - biosynthesis
Transcription Factors - genetics
Transcription Factors - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2008.07.011