THESIS
2015
xi, 86 pages : illustrations (some color) ; 30 cm
Abstract
Embryonic neurogenesis is a critical event in brain development, in which various
types of neurons are generated. During neurogenesis, the numbers and types of neurons
produced must be precisely controlled to allow the proper formation of neural circuits
and ultimately construction of a functional brain. Accordingly, impairments in embryonic
neurogenesis can lead to the production of abnormal numbers and types of neurons,
resulting in severe neurodevelopmental disorders such as microcephaly. Nonetheless,
how the fate of neurons is determined during embryonic neurogenesis remains poorly
understood. We found that the protein expression of the upper-layer but not the lower-layer
neuronal marker is significantly decreased in cyclin-dependent kinase 5 knockout
(cdk5
-/-) mouse brains...[
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Embryonic neurogenesis is a critical event in brain development, in which various
types of neurons are generated. During neurogenesis, the numbers and types of neurons
produced must be precisely controlled to allow the proper formation of neural circuits
and ultimately construction of a functional brain. Accordingly, impairments in embryonic
neurogenesis can lead to the production of abnormal numbers and types of neurons,
resulting in severe neurodevelopmental disorders such as microcephaly. Nonetheless,
how the fate of neurons is determined during embryonic neurogenesis remains poorly
understood. We found that the protein expression of the upper-layer but not the lower-layer
neuronal marker is significantly decreased in cyclin-dependent kinase 5 knockout
(cdk5
-/-) mouse brains at embryonic day 18, suggesting that Cdk5 may play a role in the
regulation of neuronal fate specification during embryonic neurogenesis. Interestingly,
according to in utero cdk5 conditional knockout experiments, the decreased expression of
upper-layer neuronal markers is regulated by the specific knockout of Cdk5 in neural
progenitors, suggesting that Cdk5 acts in neural progenitors to regulate the upper-layer
neuronal fate specification in a cell-autonomous manner. We further found that Cdk5
affects upper-layer neuronal marker expression only at protein level, implicating that Cdk5 may regulate the upper-layer neuronal marker expression through post-transcriptional
processes. In conclusion, our findings suggest that Cdk5 regulates cortical
development through modulation of the protein levels of upper-layer neuronal markers.
In the future, it will be interesting to investigate whether deletion of Cdk5 disrupts the
differentiation of the upper-layer neurons in cerebral cortical development by reducing
the expression of upper-layer neuronal markers. In addition, it is worth the effort to study
the molecular mechanism that underlies the action of Cdk5 in embryonic neurogenesis.
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