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The Mouse Hindbrain As a Model for Studying Embryonic Neurogenesis
Published on: January 29, 2018
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MafB is required for development of the hindbrain choroid plexus
Ryusuke Koshida1, Hisashi Oishi2, Michito Hamada2
1Department of Anatomy and Neuroscience, Faculty of Medicine, University of Tsukuba, Tsukuba, 305-8575, Japan.
Biochemical and Biophysical Research Communications
|December 28, 2016
Summary
MafB is crucial for embryonic hindbrain choroid plexus (hChP) development. Mafb-deficient mice show delayed hChP differentiation, hypoplasia, increased cell death, and reduced proliferation, highlighting MafB
Area of Science:
- Developmental biology
- Neuroscience
- Epithelial biology
Background:
- The choroid plexus (ChP) produces cerebrospinal fluid (CSF) and develops from the neural tube's roof plate.
- Molecular mechanisms of ChP development are less understood than neural development.
- MafB, a bZip transcription factor, is expressed in the roof plate.
Purpose of the Study:
- To investigate the role of MafB in the embryonic development of the hindbrain choroid plexus (hChP).
Main Methods:
- Utilized Mafb-deficient mice for study.
- Employed immunohistochemical analyses to examine MafB expression patterns.
- Assessed hChP development, differentiation, cell proliferation, and apoptosis in wild-type and mutant embryos.
Main Results:
- MafB expression was observed in the roof plate and early hChP cells, diminishing later in development.
- Mafb-deficient hChP exhibited delayed differentiation and hypoplasia compared to wild-type.
- Increased apoptotic cell death and decreased proliferating cells were noted in Mafb-deficient hChP at E12.5.
Conclusions:
- MafB plays a significant role in promoting embryonic hindbrain choroid plexus development.
- MafB is essential for normal hChP differentiation, growth, and cell survival during embryogenesis.
