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The closely related transcription factors Sox4 and Sox11 function as survival factors during spinal cord development
Daniela C Thein1, Johannes M Thalhammer, Anna C Hartwig
1Institut für Biochemie, Emil-Fischer-Zentrum, Universität Erlangen-Nürnberg, Erlangen, Germany.
Abstract:
Development of the mouse CNS was reported to be normal in the absence of either Sox4 or its close relative Sox11 despite strong and widespread expression of both transcription factors. In this study, we show that combined absence of both Sox proteins in the mouse leads to severe hypoplasia of the developing spinal cord. Proliferation of neuroepithelial precursor cells in the ventricular zone was unaffected. These cells also acquired their correct positional identity. Both glial and neuronal progenitors were generated and neurons appeared in a similar spatiotemporal pattern as in the wild-type. Rates of cell death were however dramatically increased throughout embryogenesis in the double deficient spinal cord arguing that Sox4 and Sox11 are jointly and redundantly required for cell survival. The absence of pronounced proliferation, patterning, specification, and maturation defects furthermore indicates that the decreased cell survival is not a secondary effect of one of these events. We therefore conclude that the two Sox proteins directly function as pro-survival factors during spinal cord development in neural cell types.
Insights
Sox4 and Sox11 transcription factors are essential for spinal cord development. Their combined absence in mice leads to severe spinal cord hypoplasia due to increased cell death, highlighting their role in neural cell survival.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- Sox4 and Sox11 are transcription factors with widespread expression during mouse central nervous system (CNS) development.
- Absence of either Sox4 or Sox11 alone does not cause developmental defects in the mouse CNS.
Purpose of the Study:
- To investigate the combined role of Sox4 and Sox11 in mouse spinal cord development.
- To determine the function of Sox4 and Sox11 in neural cell survival and proliferation.
Main Methods:
- Generation of double knockout mice lacking both Sox4 and Sox11.
- Analysis of spinal cord development, including cell proliferation, identity acquisition, differentiation, and cell death.
- Comparison of developmental processes between double knockout and wild-type mice.
Main Results:
- Combined absence of Sox4 and Sox11 leads to severe spinal cord hypoplasia.
- Neuroepithelial precursor cell proliferation and positional identity were unaffected.
- Neuronal and glial progenitor generation and spatiotemporal patterning were similar to wild-type.
- Cell death rates were dramatically increased in the developing spinal cord of double knockout mice.
Conclusions:
- Sox4 and Sox11 are jointly and redundantly required for cell survival during spinal cord development.
- These transcription factors function directly as pro-survival factors for neural cell types.
- The primary role of Sox4 and Sox11 in this context is promoting cell survival, not regulating proliferation or patterning.
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